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

[Avenger]

Hi Jes,
restriction of Carbohydrates and Simple Sugars can reduce or stop the production of D-Lactic acid completely. It is possible to stop D-Lactic acidosis only using this method. It is the main treatment for D-La, but many patients fail to maintain the diet. See Dr. Luke White '' D-Lactic acidosis, more prevalent than we think''. He gives a very good explanation, Free online.

If you do not feed D-Lactic producing Bacteria Carbs and Sugars they will not produce D-Lactic acid. It is the presence and Overgowth of D-Lactic producing Bacteria in the Small Intestine (due to disease, motility or abnormality such as failed valve between Small and Large Intestine or Short Bowel Syndrome) that causes the production of D-Lactic acid which is a Neurotoxin..

Hi Jes,
restriction of Carbohydrates and Simple Sugars can reduce or stop the production of D-Lactic acid completely. It is possible to stop D-Lactic acidosis only using this method. It is the main treatment for D-La, but many patients fail to maintain the diet. See Dr. Luke White '' D-Lactic acidosis, more prevalent than we think''. He gives a very good explanation, Free online.

If you do not feed D-Lactic producing Bacteria Carbs and Sugars they will not produce D-Lactic acid. It is the presence and Overgowth of D-Lactic producing Bacteria in the Small Intestine (due to disease, motility or abnormality such as failed valve between Small and Large Intestine or Short Bowel Syndrome) that causes the production of D-Lactic acid which is a Neurotoxin..

Paul.

Paul.

Hi Jes,
restriction of Carbohydrates and Simple Sugars can reduce or stop the production of D-Lactic acid completely. It is possible to stop D-Lactic acidosis only using this method. It is the main treatment for D-La, but many patients fail to maintain the diet. See Dr. Luke White '' D-Lactic acidosis, more prevalent than we think''. He gives a very good explanation, Free online.

If you do not feed D-Lactic producing Bacteria Carbs and Sugars they will not produce D-Lactic acid. It is the presence and Overgowth of D-Lactic producing Bacteria in the Small Intestine (due to disease, motility or abnormality such as failed valve between Small and Large Intestine or Short Bowel Syndrome) that causes the production of D-Lactic acid which is a Neurotoxin..

Paul.

Hi Jes,
restriction of Carbohydrates and Simple Sugars can reduce or stop the production of D-Lactic acid completely. It is possible to stop D-Lactic acidosis only using this method. It is the main treatment for D-La, but many patients fail to maintain the diet. See Dr. Luke White '' D-Lactic acidosis, more prevalent than we think''. He gives a very good explanation, Free online.

If you do not feed D-Lactic producing Bacteria Carbs and Sugars they will not produce D-Lactic acid. It is the presence and Overgowth of D-Lactic producing Bacteria in the Small Intestine (due to disease, motility or abnormality such as failed valve between Small and Large Intestine or Short Bowel Syndrome) that causes the production of D-Lactic acid which is a Neurotoxin..

Paul.

Hi Jes,
I may have found a possible cure! At least for myself. It will take more time to be certain,.....

I am not making any promises but for the first time in 18 years I have been able to eat Carbs and Sugars without any negative effect! I can only hope this will be as useful to others on this site, please pass this on.

This has come about partly by chance.

I have recently used Prebiotics and Probiotics known to reverse D-Lactic acidosis, similar to the stand alone treatment used by the Japanese (report below). I have found a UK Probiotic manufacturer that uses a number of similar Bacteria including those recommended by Dr. Myhill, all in one high quality Probiotic; NOW Probiotic Defense from supplementsthatwork-uk (Amazon and Ebay).

The only reason for experimenting with Probiotics is because the NHS would no longer prescribe any form of Probiotic which I am told are now on the banned list and I had started to become unwell again over the last 2/3 months after using frequent cyclical Antibiotics and no Probiotics for around a year and a half. I had also gained resistance to more Antibiotics (I have been able to stop taking Antibiotics, but I can only be certain in 6 months or longer that they are no longer necessary).

I have been very lucky again, because I had made a desperate guess that the prolonged period of Antibiotics may have been the cause. I was even more lucky in the combination of Probiotics in my first experiment. I began to feel different in just 5 days in the same way that Antibiotics had stopped my illness! I had definitely not expected this after using VSL-3.

I did not have such a positive change when using VSL-3 Probiotics that were given on prescription, prior to this and I am wondering if VSL-3 may have made things worse (there are a number of controvesial reports).

There is a big debate about whether Lactic producing bacteria including VSL-3 used by the NHS can cause D-Lactic acidosis through the predominant Lactic producing strains in VSL-3.

Probiotic Treatment to Reverse D-Lactic acidosis in Report below.(which should work for other forms of Bacterial Overgrowth):

A stand-alone synbiotic treatment for the prevention of D-lactic acidosis in short bowel syndrome.
Takahashi K1, Terashima H, Kohno K, Ohkohchi N.
Author information

Abstract
Synbiotics are combinations of probiotics and prebiotics that have recently been used in the context of various gastrointestinal diseases, including infectious enteritis, inflammatory bowel disease, and bowel obstruction. We encountered a patient with recurrent D-lactic acidosis who was treated successfully for long periods using synbiotics. The patient was diagnosed as having short bowel syndrome and had recurrent episodes of neurologic dysfunction due to D-lactic acidosis. In addition to fasting, the patient had been treated with antibiotics to eliminate D-lactate-producing bacteria. After the failure of antibiotic treatment, a stand-alone synbiotic treatment was started, specifically Bifidobacterium breve Yakult and Lactobacillus casei Shirota as probiotics, and galacto-oligosaccharide as a prebiotic. Serum D-lactate levels declined, and the patient has been recurrence-free for 3 years without dietary restriction. Synbiotics allowed the reduction in colonic absorption of D-lactate by both prevention of D-lactate-producing bacterial overgrowth and stimulation of intestinal motility, leading to remission of D-lactate acidosis.

[Indexed for MEDLINE]
Free PMC Article

Wishing you all every peace and happiness, to be free from illness and the ignorance and arrogance of the NHS.

Paul.

 

[sb4]

@Avenger I had a look for the probiotic in question and found this. Upon looking at the ingredients it says it contains
Proprietary Blend Defense Blend of:
Fermented Greens [Barley Grass (Hordeum vulgaris), Oat Grass (Avena
sativa), Wheat Grass (Triticum aestivum), and Alfalfa (Medicago sativa)].
Freeze-Dried Probiotics Strains (1 Billion cfu) [Lactobacillus acidophilus,
Bifidobacterium lactis, Lactobacillus brevis, Lactobacillus casei, Lacto-
bacillus plantarum, Lactobacillus rhamnosus, Lactobacillus salivarius,
Lactobacillus paracasei, Lactobacillus bulgaricus, Bifidobacterium bifidum,
Bifidobacterium brevis, Bifidobacterium longum, and Saccharomyces boulardii]
Super Green Foods [Alfalfa Juice Concentrate, Atlantic Kelp
(Laminaria digitata)]

Lots of these are Lactobacillus. Wiki says
Lactobacillus acidophilus (New Latin'acid-loving milk-bacillus') is a species of gram positivebacteria in the genus Lactobacillus. L. acidophilus is a homofermentative, microaerophilicspecies, fermenting sugars into lactic acid.

So wouldn't all these probiotics be changing sugar into lactic acid causing worse tolerance of sugar???

I am very interested in improving carb tolerance so more info would be great.

 

[Avenger]

Hi sb4,
I agree that the Bacteria include L. acidophilus, which you would think would cause an increase in lactic acidosis. But these probiotics have worked for me.

There are a number of studies with totally opposing conclusions and the production of D-Lactic acid may not happen at such high levels under normal conditions for metabolizing Carbohydrates or Simple Sugars. I believe that it may be that we are experiencing abnormal conditions and the same conditions promote Overgrowth possibly due to the decrease in motility alone as found in the 'Stand Alone Treatment' (this may be the opposite for SIBO where there is an increase in motility).

There is no absolute data showing that L. acidophilus will cause problems and It may be that the other Bacteria have somehow normalized my Gut through improving Motility alone, but still early days.

The first improvement that I noticed was Motility. I have had bad problems with Motility and bad Constipation since falling ill in 1999. This was one of the first symptoms of my illness. Improved Motility may mean that the abnormal production of D-Lactic acid in the Small Intestine does not happen at abnormal levels (which the pyruvate chain cannot metabolize).

This is a complex problem and it may be that the production of D-Lactic acid only happens under certain circumstances, eg. poor motility caused by the production of Methane gasses as a bye product of abnormal fermentation which is known to decrease motility (Methane producing Bacteria are known to live off Hydrogen Producing Bacteria. Methane producing Bacteria cause constipation, Hydrogen the opposite, as in SIBO).

I should state that I started the Probitoics above shortly after using an Antibiotic combination of Tinidazole and Neomycin. If normal motility was kick started at that point, this would mean that my illness may possibly have been caused by 'self maintaining negative feedback' due to the production of Methane. This was the conclusion of the 'Stand Alone Treatment' Report in my last email.

I also used Prebiotics; the first week Galactooligosaccharides with Xylosaccharides (Jarrow Formulas), but ran out and then moved to another Prebiotic which could theoretically cause me to become ill due to 7 grams of Carbohydrate per 100 grams; Inulin (100% Fructo-Oligosaccharide 'FOS') plus 10% Glucose/Fructose/Sucrose (Make; Peak Supps 1KG www.peaksupps.com). This was free, a gift from a friend who purchased it and never used it. I used 5 grams twice a day when I took the Probiotics, to promote growth.

This was an experiment! and I was prepared to try out a number of combinations of Probiotics. I was not expecting such results on the first attempt and I was very dubious about the claims of the 'Stand Alone Report' (I am naturally very cautious and doubting after so many years of being misdiagnosed).

It was my first attempt and experiment to try something similar to the 'Stand Alone Treatment' used by Japanese Researchers that caused a reversal in a D-Lactic patient. They used Galacto-Oligosaccharides, with Bifidobacterium breve Yakult and Lactobacilus casei Shirota.

It is still early days, but I enjoyed normal Christmas food including pizza and chocolate and other rubbish over the past week, something unthinkable and resulting in serious illness for many years.

I am still waiting to be proven wrong, but I have also stopped using Antibiotics, so far so good.....

I do not yet know if the effects will stop when I stop taking Pre and Probiotics or how long this may last?

I will keep you informed.

Paul.

 

[learning]

This is all making perfect sense to me. My problem was lactic acidosis confirmed by cutting sugar and carbs out of my diet. All symptoms have been gone for 2 months. Bacterial over growth is converting glucose into lactic acid. It would make sense that the "cure" if any would involve probiotics. Perhaps overloading with other less offensive strains of bacteria to crowd out the bad ones.

 

[JES]

Thanks for the update, I always follow this thread with interest. I'm also in the process of trying similar approaches, i.e. modifying my diet to reduce starches and trying some other methods to treat bacterial imbalance and SIBO (I noticed I start to feel worse 3-4 hours after intake of starchy carbohydrates, which is the time it takes for them to pass to the small intestine). I have experienced some improvements, but the puzzle is so big that it takes a few more months for me to understand what really helps and to see if the improvement stays or is only transient, as is unfortunately often the case for many ME/CFS treatments.

@Avenger The probiotic you mentioned looks pretty much ordinary with common lactobacillus and bifidobacteria strains. The only thing which makes it special is the inclusion of fermented greens and some superfoods. Maybe they somehow potentiate the included probiotics? Who knows. I have always had constipation predominant stomach issues and these issues became worse after I cut out starchy foods, so I'll order one of these probiotics just in case it helps the constipation / slow motility.

I think gut issues and ME/CFS are a very complex puzzle and sometimes it's hard to understand exactly why there was a sudden improvement. It may well have been that as you described, something in the gut bacteria shifted, which was the reason for your better tolerance of carbs. This would actually be the ideal result for us, i.e. that the microbiome rebounds back to normal after dietary/probiotic/prebiotic/antibiotic manipulation.

 

[Wayne]

This would actually be the ideal result for us, i.e. that the microbiome rebounds back to normal after dietary/probiotic/prebiotic/antibiotic manipulation.

Hi @JES -- Yes, that would be the ideal. In my case, I think my decades-long problems with digestion, absorption, constipation, and slow motility originated with vagus nerve impingement from an accident at age 15. The vagus nerve supplies nerve energy for the entire intestinal tract--and many other critical organs as well.

I suspect vagus nerve dysfunction--which is often mentioned in ME/CFS hypothesizing--is the source of many of my other conditions, like the ones I mentioned; and immune system dysfunction as well. I do everything I can to help out my microbiome, but it never seems to be quite enough.

 

[sb4]

(I noticed I start to feel worse 3-4 hours after intake of starchy carbohydrates, which is the time it takes for them to pass to the small intestine)

@Avenger @learning Do you experience similair symptoms? We may be experiencing diferent problems with carbs.

For me, after eating carbs I get worsening heart pounding, general POTS stuff from 30mins, peaking at around 1hr and decreasing back to baseline after 4+hrs. This suggests to me that my problem isn't with the gut handling the carbs but my cells and probably PDH. This is backed up by my experiments with MCT.

I think I am similar to @Wayne in that my vagus nerve or activation of it is malfunctioning for whatever reason (gastroparesis, dry mouth, inability to relax/meditate, etc).

I intend to try rifaximin soon. If I have sibo this may make my slow motility worse but I figure rifaximin is relatively safe to try.

 

[Avenger]

Hi, sb4, JES and Wayne,

In answer to sb4, yes I had horrendous problems with Carbohydrates in general. This actually worsened after I started the D-Lactic diet, when I could not find Carb free food.

Fast heartbeat is one of the clinical signs of D-La. It is something that I had along with arrhythmia's when I became very unwell. But it is also a sign of difficulty in digesting certain foods which I have also experienced. You need to ask for tests for intestinal enzymes, this may be due to a lack of the necessary enzymes to metabolize food which causes intolerance for different foods.

I also have frequent bouts of falling into an abnormal sleep after consuming a Carbohydrate loaded meal. I would feel knocked out, but periodically aware that I felt abnormal while sleeping during the digestion of Carbs (2 Pints of Lager with Carbs would induce this possibly 1/2 to an hour after eating). I can only vaguely remember feeling dreadful while drifting in and out of abnormal sleep until I presume digestion had stopped when I returned to normal.

After eating later in the day, I would find that Carbs would not shift from my Stomach whereas meat and vegetables would pass normally. At worst I woke during the night after choking on reflux food and would have to put my finger down my throat to eject the food so that I could sleep. Carbohydrate and Sugary meals would just sit in my stomach and I would remain full with acid like discomfort, burning and burping up food.

I also suffered periods of extreme hypoglycemia along with D-Lactic symptoms which also stopped using the D-Lactic Carb Free (very low Carb) diet. In all honesty I never managed 100% Carb free diet, but just lowering to aim for Carb Free made a huge difference (I possibly reduced my diet to 5% plus or minus).

It is possible that my hypoglycemia was due to mitochondrial problems and the inability to transfer or utilize glucose during episodes of illness and low Ph. Again this was never purely about exaccerbations which seem to be the focus of Reports, but fluctuating levels of D-Lactic acid and other Metabololites produced due to complex circumstances, which can make you feel mildly unwell and fatigued to more serious illness and problems in the worst affected, such as confusion and breathing difficulty.

For me D-Lactic producing Bacteria are known to cause neurotoxicity and are the prime candidate for ME. But I also believe that there are more than one form of Bacterial Overgrowth and two forms of dysmotility causing differences in individual presentation (see high levels of hydrogen breath test in Fibromyalgia below).

My belief is that this is not just about Bacterial Overgrowth or Motility it is about the level of production of Metabolites in Bacterial Overgrowth due to things like Motility in individuals, which may be slightly different for all of us and there may still be different underlying causation's for Overgrowth and dysmotility (eg. scleroderma, diabetes, pre-diabetes, weight loss in SIBO; within a starch overloaded culture, along with the overuse of Antibiotics, which are fed back in low quantities due to high impact farming methods).

I am now managing without dietary restriction and without antibiotics at the moment just as the patient in the Japanese 'Stand alone Synbiotic Treatment'. I have eaten Carb Laden Food and Sweets over the past week. This is the best Christmas Present ever!!!! However I will return to the Low Carb Diet because it has so many other benefits.

My main concern is what happens if I stop taking the Probiotics, and will the manufacturer start hiking the prices once they realize their potential? But I really hope that others on this site may benefit.

Below is one of the best explanations of SIBO and relation to underlying pathology, which can be caused by a wide variety of disease processes and failure of the protective mechanisms such as stomach acidity (Helicobacter infections in the stomach and duodenum exist in approximately 50% of humans and is known to reduce stomach acidity). I believe that pre & probiotics have the potential to redress the balance, but finding the cause and redressing the underlying issues is of paramount importance. For whatever reasons I have been very lucky!

Small intestinal bacterial overgrowth syndrome
Jan Bures, Jiri Cyrany, Darina Kohoutova, Miroslav Förstl, Stanislav Rejchrt, Jaroslav Kvetina, Viktor Vorisek, and Marcela Kopacova
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

Go to:
Abstract
Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Keywords: Bacterial overgrowth, Breath test, Hydrogen, Methane, Small intestine
Go to:
INTRODUCTION
Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. The duodenum and proximal jejunum normally contain small numbers of bacteria, usually lactobacilli and enterococci, gram-positive aerobes or facultative anaerobes (< 104 organisms per mL). Coliforms may be transiently present (< 103 bacteria per mL) and anaerobic Bacteroides are not found in the jejunum in healthy people. Up to one third of jejunal aspirates might be sterile in healthy volunteers. The distal ileum is a transition zone between sparse populations of aerobic bacteria of the proximal small intestine and very dense populations of anaerobic micro-organisms in the large bowel[1-3]. The epithelial surface of the small intestine in a healthy human is not colonised. Occasional groups of bacteria can be found in low concentrations within the lumen. Bacteria do not form clusters and spatial structures, and the luminal contents are separated from the mucosa by a mucus layer[4].

Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequences for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO).

Fibromyalgia
Pimentel et al[14] found that 42/42 (100%) patients with fibromyalgia had an abnormal lactulose hydrogen breath test. This was a significantly higher rate compared to patients with irritable bowel syndrome (93/111, 84%) and clinically healthy persons used as a control (3/15, 20%). Patients with fibromyalgia also had a higher hydrogenic profile that correlated with somatic pain[14].

CONCLUSION
SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. The aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders.

SIBO is often misdiagnosed and generally underdiagnosed. Clinical symptoms might be non-specific (dyspepsia, bloating, abdominal discomfort). Nevertheless, SIBO can cause severe malabsorption, serious malnutrition and deficiency syndromes. Non-invasive hydrogen and methane breath tests after glucose or lactulose challenge are most commonly used for the diagnosis of SIBO. Therapy of SIBO must be complex and should include treatment of the underlying disease, nutritional support and cyclical gastrointestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Paul.

 

[Wayne]

I am now managing without dietary restriction and without antibiotics at the moment just as the patient in the Japanese 'Stand alone Synbiotic Treatment'. I have eaten Carb Laden Food and Sweets over the past week. This is the best Christmas Present ever!!!!

Thanks @Avenger for your ongoing in-depth description of the things you're discovering--very helpful. -- Hmmm, four exclamation points--now that says something! Many CONGRATULATIONs on your hard-fought health improvements. May they continue into the next year--and the rest of your life. It must feel good to be getting back a semblance of control over your life! -- Best!

 

[Avenger]

Thanks for the update, I always follow this thread with interest. I'm also in the process of trying similar approaches, i.e. modifying my diet to reduce starches and trying some other methods to treat bacterial imbalance and SIBO (I noticed I start to feel worse 3-4 hours after intake of starchy carbohydrates, which is the time it takes for them to pass to the small intestine). I have experienced some improvements, but the puzzle is so big that it takes a few more months for me to understand what really helps and to see if the improvement stays or is only transient, as is unfortunately often the case for many ME/CFS treatments.

@Avenger The probiotic you mentioned looks pretty much ordinary with common lactobacillus and bifidobacteria strains. The only thing which makes it special is the inclusion of fermented greens and some superfoods. Maybe they somehow potentiate the included probiotics? Who knows. I have always had constipation predominant stomach issues and these issues became worse after I cut out starchy foods, so I'll order one of these probiotics just in case it helps the constipation / slow motility.

I think gut issues and ME/CFS are a very complex puzzle and sometimes it's hard to understand exactly why there was a sudden improvement. It may well have been that as you described, something in the gut bacteria shifted, which was the reason for your better tolerance of carbs. This would actually be the ideal result for us, i.e. that the microbiome rebounds back to normal after dietary/probiotic/prebiotic/antibiotic manipulation.

Hi Jes,

Thanks for the update, I always follow this thread with interest. I'm also in the process of trying similar approaches, i.e. modifying my diet to reduce starches and trying some other methods to treat bacterial imbalance and SIBO (I noticed I start to feel worse 3-4 hours after intake of starchy carbohydrates, which is the time it takes for them to pass to the small intestine). I have experienced some improvements, but the puzzle is so big that it takes a few more months for me to understand what really helps and to see if the improvement stays or is only transient, as is unfortunately often the case for many ME/CFS treatments.

@Avenger The probiotic you mentioned looks pretty much ordinary with common lactobacillus and bifidobacteria strains. The only thing which makes it special is the inclusion of fermented greens and some superfoods. Maybe they somehow potentiate the included probiotics? Who knows. I have always had constipation predominant stomach issues and these issues became worse after I cut out starchy foods, so I'll order one of these probiotics just in case it helps the constipation / slow motility.

I think gut issues and ME/CFS are a very complex puzzle and sometimes it's hard to understand exactly why there was a sudden improvement. It may well have been that as you described, something in the gut bacteria shifted, which was the reason for your better tolerance of carbs. This would actually be the ideal result for us, i.e. that the microbiome rebounds back to normal after dietary/probiotic/prebiotic/antibiotic manipulation.

Thanks for the update, I always follow this thread with interest. I'm also in the process of trying similar approaches, i.e. modifying my diet to reduce starches and trying some other methods to treat bacterial imbalance and SIBO (I noticed I start to feel worse 3-4 hours after intake of starchy carbohydrates, which is the time it takes for them to pass to the small intestine). I have experienced some improvements, but the puzzle is so big that it takes a few more months for me to understand what really helps and to see if the improvement stays or is only transient, as is unfortunately often the case for many ME/CFS treatments.

@Avenger The probiotic you mentioned looks pretty much ordinary with common lactobacillus and bifidobacteria strains. The only thing which makes it special is the inclusion of fermented greens and some superfoods. Maybe they somehow potentiate the included probiotics? Who knows. I have always had constipation predominant stomach issues and these issues became worse after I cut out starchy foods, so I'll order one of these probiotics just in case it helps the constipation / slow motility.

I think gut issues and ME/CFS are a very complex puzzle and sometimes it's hard to understand exactly why there was a sudden improvement. It may well have been that as you described, something in the gut bacteria shifted, which was the reason for your better tolerance of carbs. This would actually be the ideal result for us, i.e. that the microbiome rebounds back to normal after dietary/probiotic/prebiotic/antibiotic manipulation.

Dear Jes,
I am certain that the change is due to these Probiotics. I do not think that anything else contributed (although I took them with Prebiotics). But I am uncertain whether this change will continue if I stop taking the Probiotics. All I can be certain of is that this blend work for me.

Lactobascillus rhasmosus has been used to stop potential overgrowth of harmful Bacteria. Bifidobacterium breve and Lactobascillus casei are similar to the Probiotics used to reverse D-Lactic acidosis in the Japanese report. I chose this Probiotic for these three alone. I just got lucky for whatever reason and I now believe that this product is special in some way. It may be that it is just special for me.

There are also huge differences in similar Probiotics and survival after freeze drying. This product may be better for unknown reasons or slight difference in DNA within Bacteria? I obviously cannot guess, but I intend to use this gift. I am now afraid to take Antibiotics in the future, and would hate to mess this up.

But this also shows that taking Lactobascillus acidophillus does not increase the Overgrowth of D-Lactic producing Bacteria, at least not for me. I have been using this Probiotic with no discernable production of D-Latic acid (I am certain because even mild production affects me). There is something else going on here.

It is just possible that just the change in motility or some quality in these Bacteria that I am unaware of is happening.

I am hoping that at least some of you may benefit.

Paul.

 

[sb4]

@Avenger Can you say if you felt negative effects from carbs soon after eating (0-2hrs) or if they didn't kick in until later (3hrs+)?

 

[TMartin]

Hi Jes,




Dear Jes,
I am certain that the change is due to these Probiotics. I do not think that anything else contributed (although I took them with Prebiotics). But I am uncertain whether this change will continue if I stop taking the Probiotics. All I can be certain of is that this blend work for me.

Lactobascillus rhasmosus has been used to stop potential overgrowth of harmful Bacteria. Bifidobacterium breve and Lactobascillus casei are similar to the Probiotics used to reverse D-Lactic acidosis in the Japanese report. I chose this Probiotic for these three alone. I just got lucky for whatever reason and I now believe that this product is special in some way. It may be that it is just special for me.

There are also huge differences in similar Probiotics and survival after freeze drying. This product may be better for unknown reasons or slight difference in DNA within Bacteria? I obviously cannot guess, but I intend to use this gift. I am now afraid to take Antibiotics in the future, and would hate to mess this up.

But this also shows that taking Lactobascillus acidophillus does not increase the Overgrowth of D-Lactic producing Bacteria, at least not for me. I have been using this Probiotic with no discernable production of D-Latic acid (I am certain because even mild production affects me). There is something else going on here.

It is just possible that just the change in motility or some quality in these Bacteria that I am unaware of is happening.

I am hoping that at least some of you may benefit.

Paul.

Hi, Paul:

I genuinely appreciate you sharing your experiences; our stories are quite similar.

About me:

I've been riding this dragon for a little over 22 years now; proton pump inhibitors and anti-depressants have been all that modern science has offered me - obviously, both of no use.

My primary symptoms include: arrhythmia, tachycardia, psoriasis, fibromyalgia, numerous chemical sensitivities, alternating IBS-C and -D, and a distinct intolerance for carbohydrates - sugars and starches being the worst offenders.

I have other symptoms, as well; however, those are the most prominent. All the symptoms listed are potentiated by carbohydrate intake; in short, diet represents the most powerful tool I've run across - zero carb being relatively effective with symptom control, with fasting producing the best results.

21 years ago, I tried to explain to an MD that I displayed the classic symptoms of D-Lactic Acidosis; he scoffed at such a notion while stating that only people on death's doorstep experience acidosis - he clearly was not drawing a distinction between D-Lactic Acidosis and Diabetic Keto Acidosis.

So began my 22 year journey of frustration with the medical profession....

Regardless, I'm very encouraged that this topic has surfaced as it represents a potential area of treatment that I have not yet explored - mostly due to incompetent MDs being the only conduit through which to obtain treatment.

Fortunately, that is no longer the case for me.

With that said, I'd like to examine potential treatment protocols. Having read this thread, and it's attachments, I have some questions for you:

1. You mention that you used neomycin as an antibiotic. What made you chose this compound? I ask this considering that Dr. White's article lists neomycin as being reported to provoke D-Lactic Acidosis.

2. Was neomycin the only compound you used during the antibiotic phase?

3. What was your antibiotic dosing protocol? Example: "XXX"mgs * "X" times per day * "XX" days.

4. At what point did you add probiotics: once completing the neomycin course, halfway through, at the beginning?

4. Did you consider any other probiotics (E.Coli Nissle, etc.)?

I'm really interested to hear your input on the above items, given the similarity in our cases.

Thanks for reading!

Terry

 

[Belbyr]

Wow, I really need to follow this and am just now seeing it.

Was on tetracycline for a year or two before getting ill, 70% of symptoms are gut related and no meds work. The rest of my illness is body wide muscle pain/trigger points and fatigue. I know I don't have SIBO after doing testing for it 2 different times though...

https://www.healthrising.org/blog/2016/03/01/lactate-fibromyalgia-chronic-fatigue-syndrome/

https://www.healthrising.org/blog/2015/10/12/lactic-acidosis-causing-cfs-fm-symptoms/

 

[Belbyr]

https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2014/06/Parrish-September-15.pdf

Symptoms of congenital pyruvate deficiency are similar to those seen in D-lactate toxicity.11 D-lactate (and acidosis itself) impairs the action of pyruvate dehydrogenase (PDH), interfering with pyruvate metabolism and inhibiting utilization of L-lactate as a fuel in the brain. As cerebellar PDH is already reducedrelative to the serum, a relatively low concentration ofD-lactate may lead to clinical symptoms, even as serum levels of PDH remain adequate.6,3

Pyruvate acts as an intermediate product inD-lactate metabolism. Thiamine, a cofactor in pyruvate metabolism, may be deficient in patients suffering from malnutrition. Thiamine deficiency has been associatedwith lactic acidosis.9 Patients suffering from SBS, abnormal gut flora and/or malabsorption syndromes are at increased risk for thiamine deficiency. This deficiency,when paired with the elevated lactate production fromabnormal gut flora, may lead to large amounts of excesslactate that cannot be effectively metabolized.

 

[Avenger]

Hi, Paul:

I genuinely appreciate you sharing your experiences; our stories are quite similar.

About me:

I've been riding this dragon for a little over 22 years now; proton pump inhibitors and anti-depressants have been all that modern science has offered me - obviously, both of no use.

My primary symptoms include: arrhythmia, tachycardia, psoriasis, fibromyalgia, numerous chemical sensitivities, alternating IBS-C and -D, and a distinct intolerance for carbohydrates - sugars and starches being the worst offenders.

I have other symptoms, as well; however, those are the most prominent. All the symptoms listed are potentiated by carbohydrate intake; in short, diet represents the most powerful tool I've run across - zero carb being relatively effective with symptom control, with fasting producing the best results.

21 years ago, I tried to explain to an MD that I displayed the classic symptoms of D-Lactic Acidosis; he scoffed at such a notion while stating that only people on death's doorstep experience acidosis - he clearly was not drawing a distinction between D-Lactic Acidosis and Diabetic Keto Acidosis.

So began my 22 year journey of frustration with the medical profession....

Regardless, I'm very encouraged that this topic has surfaced as it represents a potential area of treatment that I have not yet explored - mostly due to incompetent MDs being the only conduit through which to obtain treatment.

Fortunately, that is no longer the case for me.

With that said, I'd like to examine potential treatment protocols. Having read this thread, and it's attachments, I have some questions for you:

1. You mention that you used neomycin as an antibiotic. What made you chose this compound? I ask this considering that Dr. White's article lists neomycin as being reported to provoke D-Lactic Acidosis.

2. Was neomycin the only compound you used during the antibiotic phase?

3. What was your antibiotic dosing protocol? Example: "XXX"mgs * "X" times per day * "XX" days.

4. At what point did you add probiotics: once completing the neomycin course, halfway through, at the beginning?

4. Did you consider any other probiotics (E.Coli Nissle, etc.)?

I'm really interested to hear your input on the above items, given the similarity in our cases.

Thanks for reading!

Terry

Hi, sorry have not been on line for a while.
You seem to have a very good understanding from your questions and this is all very complex and perhaps slightly different for everyone with forms of Bacterial Overgrowth (anyone with Bacterial Overgrowth can develop D-Lactic acidosis, much depending on underlying causes of Overhrowth. Diabetes can cause Bacterial Ovegrowth as well as a number of other underlying disease processes )

First Proton Pump Inhibitors can cause Overgrowth by lowering stomach acid at the gateway to the Gut and allow unwanted Bacteria to enter.
You obviously have some Gut discomfort relieved by Proton Pump Inhibitors. Please Read the work of Chris Kresser below.

At least 50% of the population have Helico-bacter which leads to the use of Proton Pump Inhibitors.

There may be a chain of problems or contributing factors which evolve to Bacterial Ovegrowth and Reflux symptoms secondary to the increased pressure from Overgrowth, and depending on the underlying causation which has to be established to treat Bacterial Overgrowth and D-Lactic acidosis.

Helico-bacter was the first Gut problem through my teens and eventually releved by Proton Pump Inhibitors for some years before being given a partial treatment for Helico-bacter that left it Resistant and necessitating the use of multiple attempts to destroy it, which would also have damaged my Gut Flora Balance. I believe that my chain started here. Then I developed bad abdominal pain, reflux bringing up food and even choking on reflux food during the night and developing serious illness from D-Lactic acidosis.

Most of my problems stopped within days after lowering my Carbohydrates aiming for 0% but in reality having around 5% in a few foods including yogurt. My Reflux stopped almost instantly and problems after using Carbohydrates including Hypoglycemia stopped within days! If I use Carbohydrates (eg. Chips) when I cannot find suitable low Carb foods, then I go into an abnormal sleep as if knocked out while the food is digesting (highs and lows of insulin and glucose).

In answer to your question concerning Neomycin, yes they can either help or make things worse depending on the type of Overgrowth (you need a microbiologist to identify). For me Neomycin failed to work on its own and I did have D-Lactic symptoms back after two days of use. I only tried it again when I started to become resistant to Tinidazole. I combined both Tinidazole and Neomycin in desperation and found that they worked together despite Tinidazole losing its potency. This was pure luck!

Non absorbable Antibiotics such as Rifaximin are supposed to be the best, but I found Metronidazole to be
the quickest and longest lasting until I developed resistance. I started using Probiotics after an absence of a year and a half, because the NHS Doctors had advised me that they do not have any efficacy and have banned them on prescription, which is crazy when you are using frequent antibiotics.

I have had great success with the probiotics that I put online some time ago and I am still not using any antibiotics so far. This all needs urgent research, but the NHS does not seem interested and none of their Doctors have a clue about these issues and will prescribe Proton Pump Inhibitors, treating the symptoms but not understanding the dangers, the underlying problems or chains of causation. Their last move to ban probiotics shows how poorly they understand these problems when some Gastrointestinal disease has been reversed with the use of probiotics alone including E. Coli.

If using Antibiotics, I would only take the Probiotics when not using Antibiotics and two days after so that no further Bacterial Resistance will result from Probiotics gaining resistance. I have considered E.Coli, but have not needed any other than the Probiotics that I referred to so far. I would also consult Dr. Myhill's website for advice on the best Probiotics.

This may all be slightly different for everyone with Bacterial Overgrowth. Finding any underlying cause is the key and then treating the cause as well as the symptoms with a mind to not making things worse. You need a good Consultant Gastroenterologist and possibly a Microbiologist. It may even be possible to get a reversal through fecal transplant, but getting a diagnosis is important. Many Doctors do not understand these symptoms and will make things worse by treating discomfort with Proton Pump Inhibitors when the source of the problems needs to be properly investigated and underlying causation treated.

Please read Chris Kessler below, plus abstract on underlying causation further below:


The hidden causes of heartburn and GERD
on APRIL 1, 2010 by CHRIS KRESSER 410 comments

Facebook555TweetPinGoogle+LinkedIn

iStock.com/egal
This is the second article in a series on heartburn and GERD. If you haven’t read the first one, I’d suggest doing that first.The idea that heartburn is caused by too much stomach acid is still popular in the media and the public. But as Daniel pointed out in the comments section of the last post, anyone familiar with the scientific literature could tell you that heartburn and GERD are not considered to be diseases of excess stomach acid. Instead, the prevailing scientific theory is that GERD is caused by a dysfunction of the muscular valve (sphincter) that separates the lower end of the esophagus and the stomach. This is known as the lower esophageal valve, or LES. The LES normally opens wide to permit swallowed food and liquids to pass easily into the stomach. Except for belching, this is the only time the LES should open. If the LES is working properly, it doesn’t matter how much acid we have in our stomachs. It’s not going to make it back up into the esophagus. But if the LES is malfunctioning, as it is in GERD, acid from the stomach gets back into the esophagus and damages its delicate lining. Here’s the key point. It doesn’t matter how much acid there is in the stomach. Even a small amount can cause serious damage. Unlike the stomach, the lining of the esophagus has no protection against acid.

We’ve been asking the wrong question
In a recent editorial published in the journal Gastroenterology, the author remarked (continued...)


New Abstract
Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Keywords: Bacterial overgrowth, Breath test, Hydrogen, Methane, Small intestine
Go to:
INTRODUCTION
Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. The duodenum and proximal jejunum normally contain small numbers of bacteria, usually lactobacilli and enterococci, gram-positive aerobes or facultative anaerobes (< 104 organisms per mL). Coliforms may be transiently present (< 103 bacteria per mL) and anaerobic Bacteroides are not found in the jejunum in healthy people. Up to one third of jejunal aspirates might be sterile in healthy volunteers. The distal ileum is a transition zone between sparse populations of aerobic bacteria of the proximal small intestine and very dense populations of anaerobic micro-organisms in the large bowel[1-3]. The epithelial surface of the small intestine in a healthy human is not colonised. Occasional groups of bacteria can be found in low concentrations within the lumen. Bacteria do not form clusters and spatial structures, and the luminal contents are separated from the mucosa by a mucus layer[4].

Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequences for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO).


Paul.

 

[unicorn7]

Is there any experience with a fecal transplantation in people with d-lactic acidose?

 

[Hip]

I have been trying to make others aware of the similarity of ME/CFS to D-Lactic acidosis that Sheedy et al have written about and reported on after finding D-Lactic producing bacteria in CFS patients (report below).

A very interesting story, Avenger.

My first thought on reading it was that although full D-lactic acidosis like you experienced might be quite rare, and is almost certainly not the cause of ME/CFS in general, it is quite possible that some ME/CFS patients might have D-lactic acid-producing bacteria in their guts which may be exacerbating their ME/CFS symptoms.

Indeed, one study by KDM et al found that ME/CFS patients have higher amounts of D-lactic acid-producing bacteria.


It has been demonstrated in this study that D-lactic acid acts to block energy metabolism in brain and heart (but not liver) mitochondria. It is hypothesized this is due to D-lactic acid interfering with the utilization of L-lactate and pyruvate in mitochondria, leading to impairments in mitochondrial energy metabolism.

And this likely explains why D-lactic acid produces symptoms that closely resemble those of ME/CFS, since there is evidence to indicate mitochondrial energy metabolism is also impaired in ME/CFS.


So could lots of ME/CFS patients have D-lactic acid-producing bacteria in their guts which are adding to the burden of their symptoms?

Well, this interesting article about D-lactic acid ME/CFS says:

When D-lactic acid then enters the cell, it can be preferentially taken up in the place of L-lactic acid, compromising mitochondrial function, leading to toxicity, acidity and resultant symptoms. Controversy still exists around this story, however, as research has revealed that despite this past hypothesis, most humans do produce D-lactate dehydrogenase and only a very small portion of the population are unable to.[1]

So it seems that most people do possess the D-lactate dehydrogenase enzyme which breaks down D-lactate dehydrogenase, and would thus not be susceptible (or less susceptible) to D-lactic acid toxicity.

In other words, even if you have high levels of D-lactic acid-producing bacteria in your guts, and D-lactic acid in your bloodstream, this may not on its own cause problems, unless you are also one of the very small percentage of the population who are unable to properly metabolize D-lactic acid, because you don't have sufficient mitochondrial D-lactate dehydrogenase.

Thus it might be interesting to do some further research, and find out if there are any known SNP genetic alleles (mutations) which lead to impaired D-lactate dehydrogenase production.

It would be good if people could look up their D-lactate dehydrogenase SNPs on 23andme.com, and work out whether they are one of the very small percentage of the population who are at risk of developing D-lactic acidosis, or milder issues with D-lactic acid, because they do not produce sufficient D-lactate dehydrogenase.

 

[Avenger]

Is there any experience with a fecal transplantation in people with d-lactic acidose?

I am

Is there any experience with a fecal transplantation in people with d-lactic acidose?

Hi, it is theoretically possible to have a reversal of D-La or any form of Bacterial Overgrowth through Fecal Transplant. I am pushing for a trial, my Gastroenterologist agrees that reversal is possible.

I am having to push for everything and effectively have had to ask for all investigations which have led to diagnosis.

There is so little known that I am experimenting myself. I have just been very lucky so far, but i am expecting from all of the literature available that both Probiotics and Fecal Implant may be either temporary or permanent, there is no guarantee. But either can be repeated and are better than the use of antibiotics unless you do not have that choice. I am gaining resistance one after the other, so it is necessary to try to reverse the condition.

I believe that Bacterial Overgrowth and D-Lactic acidosis have been overlooked for so long as possible causes for ME/CFS, because most Doctors believe that D-La only exists in the very ill.... Many with ME. are very ill and suffer the same neurological symptoms as D-La.... Others may be experiencing other forms of Bacterial Overgrowth. Doctors do not understand Bacterial Overgrowth, they have not been trained. Most Consultants do not understand D-Lactic acidosis, just a few specialist Gastroenterologists and many of them have only seen one patient. My belief is that D-La is far more common and may affect at different levels (depending on individual production of metabolites which will depend on things like underlying pathology and things like motility that have led to the problem).

I believe that there is likely to be more than one form of Bacterial Overgrowth. D-La is just one of them, and it is likely that the Bacteria involved produce more than one form of Metabolite.

A fecal implant is my best hope of permanent reversal and will give me a wider range of natural Gut Flora that should help reverse the Overgrowth.

Fecal Transplantation Successfully Treats Recurrent D-Lactic Acidosis in a Child With Short Bowel Syndrome.
Davidovics ZH1, Vance K1, Etienne N1, Hyams JS1.
Author information

Abstract
D-lactic acidosis can occur in patients with short bowel syndrome (SBS) when excessive malabsorbed carbohydrate (CHO) enters the colon and is metabolized by colonic bacteria to D-lactate. D-lactate can be absorbed systemically, and increased serum levels are associated with central nervous system toxicity manifested by confusion, ataxia, and slurred speech. Current therapy, usually directed toward suppressing intestinal bacterial overgrowth and limiting ingested CHO, is not always successful. Fecal transplantation, the infusion of donor feces into a recipient's intestinal tract, has been used for decades to treat recurrent Clostridium difficile infection, and case reports document its use in the successful treatment of constipation, diarrhea, and abdominal pain. The exact mechanism of action is unknown, but it is surmised that the alteration of the intestinal microbiome, as well as the reintroduction of potential beneficial microbes, helps mediate disease. Here we present the case of a child with SBS and recurrent, debilitating D-lactic acidosis, which was successfully treated with fecal transplantation.

KEYWORDS:
enteral formulas; gastroenterology; nutrition; research and diseases; short bowel syndrome

PMID:

26616138

DOI:

10.1177/0148607115619931
[Indexed for MEDLINE]


Paul.

 

[Hip]

@Avenger, this study says something that may be of interest to you:

Humans can effectively metabolise large amounts of D-lactate. Hove and Mortensen [15] confirmed that humans have the enzyme D-2-hydroxy acid dehydrogenase (D-2-HDH) to enable conversion of d-lactate to pyruvate.

Certain conditions such as increased oxalate and low pH can inhibit the activity of D-2-HDH enzymes, as shown in animal tissue [107].

The kidney and liver have the highest concentrations of D-2-HDH. Therefore, kidney and liver impairments can reduce effective metabolism of d-lactate indicated by d-lactate accumulation in patients with renal dysfunction [40] and liver cirrhosis [108]. The presence of adequate D-2-HDH is required for d-lactate metabolism.

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

So ensuring that you don't have high oxalate from diet, and possibly an alkalizing protocol (eg bicarbonate supplementation) are things you might look into to help ensure your D-2-HDH enzyme works efficiently to neutralize the D-lactic acid.

It might also be worth looking at your kidney and liver health and functioning, since these organs have the highest concentrations of D-2-HDH, and so are the organs which should be doing the most work to metabolize D-lactic acid. Maybe part of the problem might be in the kidneys and liver.

(Note that D-lactate dehydrogenase is part of the D-2-HDH family of enzymes).


It's interesting that the paper concludes:

Our review of the D-la literature has led us to propose the hypothesis that D-la and ME/CFS may lie on a continuum

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.

Though they say:

Increased prevalence of D-lactate producing bacteria in an ME/CFS sample compared with controls [4] provides the only clear evidence supporting D-lactate theory in ME/CFS.

So it seems that nobody has measured the amount of D-lactate in the blood of ME/CFS patients as yet; they have only noted increases in D-lactate producing bacteria.

 

[Avenger]

Hi Hip,
I asked for tests for the Pyruvate Chain, which should include the enzyme. This was normal.

But from further reading the production of D-Lactic acid may inhibit the Pyruvate chain at high levels as a form negative feedback. There is a lot of contradictory information. The Pyruvate chain may be a cause of problems in some people, but I don't think that it has caused my problems directly, although it may be involved in the complex chain which badly needs research.

I did get bad Kidney pain intermittently at the height of the worst symptoms, but i had pain everywhere.

This is the point at which you cannot make any further assumptions. I am going on whatever has worked for me and then applying what I have learnt, but most of the 'experts' are at the edge of their understanding and need to invest in research.

They need to take a number of us with known D-Lactic problems and then run experiments to fully ascertain what is going on and then check the results and compare with ME/CFS patients especially those who have become critically ill from unknown illness. In the past when they are confronted with these problems the main goal has been to normalize a patient during an exaccerbation of serious illness.

My belief is that the multiple symptoms of ME/CFS are being taken for the different DSM forms of Somatization that are identical to the Symptoms of Bacterial Overgrowth and D-Lactic acidosis if left undiagnosed and at least a subset of ME/CFS are being left without treatment for complex overgrowth symptoms.

I do not think that these Consultants understand that this is about levels of D-Lactic and metabolite production. I have lived through fluctuating months of milder symptoms, months, days weeks, hours of much worse and periods in which I had expected to die when I was producing the worst levels. This may be different but similar for every one of us who have different forms and combinations of Overgrowth.

ME is a neurological illness, D-Lactic acidosis I believe is one of the most likely causes of these symptoms due to fluctuating levels of poisoning from a neurotoxin D-Lactic acid. I cannot say that this includes everyone, because there are a number of other causation's including Lyme disease that cause similar neurological illness. But this badly need research to find out how many are affected.

I believe that this problem can fluctuate wildly even with the same Carbohydrate intake as it did for myself. It is possible that some people only have fluctuating milder symptoms affecting, or more serious symptoms as those who are seriously ill may have died from D-Lactic and possibly the production of other metabolites. D-Lactic acidosis is not necessarily tested for if Lactic acidosis is suspected.

It is possible for a number of people to experience different variations and symptoms.

I think that the most important thing so far is that I am having reversal of hideous systemic symptoms by using Probiotics and Prebiotics alone. For me that poses further questions.

I have tried to pass this to the ME association, but they are firm that ME/CFS has Viral causation, they seem more interested in their campaign than the possibility of a subset of patients having such illness and this has made me question their motivation. The NHS similarly do not want to investigate which is appalling.

Paul.