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

Avenger

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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:


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

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Hi Hip, I do not think that it is in question that humans do produce or can metabolize D-Lactic acid.

At normal levels of Bacteria this is not a problem, because it is part of the normal symbiosis of Gut flora.

This is about massive Overgrowth of Bacteria and levels of production fluctuating levels of D-Lactic acid in some humans, which I do not believe is rare, just misunderstood as rare.

I do not believe that we can metabolize D-Lactic acid at higher levels, which are known to interfere with the ability (pyruvate chain/mitochondria) to metabolize D-Lactic acid. See Luke White Consultant Gastroenterologist 'D-Lactic acidosis more prevalent than we think':

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #145 Luke White, D.O. Department of Critical Care Medicine, Memorial Hospital, South Bend, IN D-Lactic Acidosis: More Prevalent Than We Think? Luke White D-lactate acidosis, in which the D-isomer of lactate accumulates, may be more prevalent than once thought. This uncommon disorder has been reported in the setting of short bowel syndrome, and in particular, with high carbohydrate diets in children. Mental status changes and gait instability, the classic symptoms of D-lactate buildup, may not immediately lead the clinician to consider this uncommon disorder. The purpose of this article is to present information about D-lactate that will increase the readers’ level of vigilance for this disorder, which affects a broader group of patients than initially thought.

Dr. White states that anyone with Bacterial Overgrowth is at risk of developing D-Lactic acidosis.


Just as in IBS Bacterial Overgrowth is the problem. It is the cause of Overgrowth that is of concern.

My belief, just as Sheedy et al. and an increasing number of others, that forms of Bacterial Overgrowth including D-Lactic acidosis may result in the severity of neurological symptoms in at least a subset of ME/CFS. This cannot be ruled out until properly investigated.

This may concern purely levels of production of metabolites including D-Lactic acid as a cause in a very complex chain. I do not think that it is possible to make further conjecture because the issues are far too complex to be properly understood without further investigation.

I can only go on my own experience and think that it is reasonable to assume that different forms of Bacterial Overgrowth acting much like an infection, hidden in the Gut and affecting many with ME/CFS could be the cause illness in at least a subset.

Paul.
 

Hip

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The NHS similarly do not want to investigate which is appalling.
Medical research is typically carried out at universities and medical research institutions, or sometimes by highly motivated individual doctors. As far as I am aware (though I am not certain), the NHS does not have much of an internal research department, but rather utilizes research produced at universities and institutions.



I have tried to pass this to the ME association, but they are firm that ME/CFS has Viral causation
ME/CFS appears after viral infection in the majority cases, and studies have found chronic viral infection in the muscles, guts and brains of ME/CFS patients. It's quite possible though that a chronic viral infection of the gut could alter gut ecology and lead to bacterial dysbiosis.



I asked for tests for the Pyruvate Chain, which should include the enzyme.
When you say should include D-lactate dehydrogenase, did it specifically list that enzyme on the test results page analytes list? I could not find any lab tests for D-lactate dehydrogenase levels, so it's possible this test is not available.


By the way, I found a test for blood D-lactic acid levels, offered by Biolab in London. In the US, Quest offer a blood D-lactic acid test. And Mayo do a D-lactic acid urine test. The Organix Dysbiosis Profile from Genova Diagnostics measures urine D-lactic acid.

I found some patients on this forum who are high in urine D-lactate: here and here.



This is a good article: D-Lactic Acidosis: More Prevalent Than We Think?

Interestingly the article says:
D-lactate toxicity generally occurs with serum D-lactate levels over 3 mmol/L
The mechanism for D-lactate encephalopathy remains unclear. D-lactate freely passes into the cerebral spinal fluid.

Serum and urine levels do not always correlate to symptoms and healthy volunteers infused with D-lactate showed no signs of encephalopathy even when concentrations reached up to 6.7 mmol/L.

It has been proposed that given these findings, D-lactate may be a proxy for other neurotoxic organic acids that have not yet been identified. Some cases of D-lactate encephalopathy appear related to thiamine deficiency.
So those facts are very telling: even though patients suffering from D-lactate toxicity show blood levels of over 3 mmol/L, when healthy volunteers are injected with D-lactate to create blood concentrations of up to 6.7 mmol/L, no symptoms or adverse effects are observed.

Perhaps that is because most people have sufficient D-lactate dehydrogenase to protect them from the toxic effects of D-lactate. Perhaps it's only if you inject someone with D-lactate who does not have sufficient D-lactate dehydrogenase that D-lactic acidosis symptoms will appear.

Or maybe as the article suggests, D-lactate may be a proxy for other neurotoxic organic acids that have not yet been identified.

In any case, clearly it is more complicated than the simple idea that D-lactate in the blood leads to ME/CFS-like symptoms. If healthy people injected with high doses of D-lactate do not show any symptoms, there is obviously something more complex going on.


The article also states that:
Both isomers of lactate are produced by usual human colonic flora as they metabolize small amounts of CHO, protein, non-absorbable starches, and fiber.

The principal source of D-lactate production in the human gut is due to Lactobacillus and Bifidobacteri species.

E. coli, Klebsiella pneumoniae and Candida freundii also produce significant quantities of D-lactate while producing minimal amounts of L-lactate.
So this would suggest that for people who do not have sufficient D-lactate dehydrogenase, taking Lactobacillus and Bifidobacterium probiotics will make them worse (there is a subset of ME/CFS patients who become worse when taking probiotics).


Yet you found that probiotics made you better?


Have you tried vitamin B1 (thiamine) supplementation? The article says that:
Thiamine deficiency may both result from malnutrition and poor absorption, and contribute to reduced clearance of D-lactate due to impaired pyruvate metabolism. The cerebellum is particularly sensitive to thiamine deficiency. In some instances of encephalopathy associated with excess D-lactate, thiamine supplementation alone has led to symptomatic resolution.
We recommend aggressive treatment, supplementing all patients with neurologic symptoms at risk for thiamine deficiency with 500mg parenterally three times daily for 1-2 days and then 100mg orally or parentally indefinitely thereafter.
 
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@Avenger, this study says something that may be of interest to you:

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:



Though they say:

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.
Interesting that oxalate and D-lactic acid are linked.

I mentioned having to avoid carbs in my previous post; however, I've also had to eliminate histamines and oxalates, as well.

A quick search revealed that oxalate "is a strong inhibitor of the enzyme that helps rid the body of D-lactic acid..."

https://oley.org/page/DLacticAcidosis
 

Avenger

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Dear Hip and TMartin,
the Probiotic experiment has ended in disaster!!!

I had a bad recurrence of illness after some 5 weeks or more free of symptoms using normal Carbohydrates and Sugars while taking Probiotics which did contain Lactic producing Bacteria. I have been very unwell for the last few days and have had to use the exclusion diet with Antibiotics.

I will have to repeat the experiment with isolates of the Bacteria that have been used by the Japanese Gastroenterologist Researchers. I could only find similar mixed with Lactic producing in the Probiotic that I chose.

I am still not sure why I was symptom free, followed by recurrence of D-La??? or whether the Lactic producing Bacteria are to blame? I will only know for sure if I try the same Bacteria used by the Japanese or experiment with non Lactic producing mixed cultures?

Perhaps using Prokinetics and Promotility products will help remove D-Lactic Bacteria accumulate in the Small Intestine.

Symptoms came back over a few days which started with feeling bad fatigue, falling asleep at my laptop and Flu like aching pain and malaise (brain fog), then the symptoms rapidly escalated and I started to feel sick on and off, dyspepsia, slurred speech, confused, very unwell, with abnormal gait like drunk at times with rapid heartbeat. I can imagine that this may be about levels of production. It is possible that some may develop lower or higher levels of Overgrowth.

My antibiotics are no longer working and so I used three failed ones together and barely managed to stop the symptoms. Due to difficulty thinking I had further Carbohydrates by mistake and was close to going into Hospital. I am only back to normal 6 days on due to adding some Carbohydrates by mistake two days running.

I have read a lot of conflicting reports concerning Lactic producing Bacteria and do not have time to wait around another 18 years. I hope to find a way to reverse the condition. I will just have to keep experimenting.

Thank you TMartin, you reminded me to use Bicarbonate of Soda during the crisis which helped reduce my symptoms. Bicarbonate acts as a bactericide for D-Lactic producing Bacteria. It lowers the PH which D-La Bacteria thrive in, which effectively helps to reduce them and their product. I may Bicarbonate of Soda to the Antibiotics if I have another exacerbation because it can increase the ability of Antibiotics for Gut Bacteria.

I have seen a new dietitian who has changed my diet somewhat, to a low FODMAP which I hope will work even better for me (avoidance of foods high in Polyols, Lactose, Oligosacharides, Fructose), which is far more complex and I will need time to mentally digest! I will copy these to you later.

I am also seeing another Consultant Gastroenterologist and Microbiologist, to help with Antibiotic, Probiotics and Fecal Transplant and will keep you informed. I will ask him about the specific Enzyme investigations for the Pyruvate Chain and also Digestive and Biliary Enzymes, motility investigations and Kidney and Liver Function etc. Finding the cause of Bacterial Overgrowth is the main goal, then correcting it and replacing the abused Gut Flora Dysbiosis (abused by antibiotics and possibly Probiotics).

I have realized that I had been given VSL-3 Probiotic for some years, high in Lactic Producing Bacteria. This may have worsened the Overgrowth if all Lactic producing Bacteria do in fact add to the load or Overgrowth. Sheedy found specific D-Lactic Bacteria in their CFS patients.

The NHS have stopped the use of Probiotics such as VSL-3, perhaps they realize that they may be dangerous and are distancing themselves? It is possible that Antibiotic Selection for Overgrowth and even Lactic Probiotics could be contributing to ME/CFS, but this badly needs investigation.

There are so many possible factors!!!!

Paul.
 
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Dear Hip and TMartin,
the Probiotic experiment has ended in disaster!!!

I had a bad recurrence of illness after some 5 weeks or more free of symptoms using normal Carbohydrates and Sugars while taking Probiotics which did contain Lactic producing Bacteria. I have been very unwell for the last few days and have had to use the exclusion diet with Antibiotics.

I will have to repeat the experiment with isolates of the Bacteria that have been used by the Japanese Gastroenterologist Researchers. I could only find similar mixed with Lactic producing in the Probiotic that I chose.

I am still not sure why I was symptom free, followed by recurrence of D-La??? or whether the Lactic producing Bacteria are to blame? I will only know for sure if I try the same Bacteria used by the Japanese or experiment with non Lactic producing mixed cultures?

Perhaps using Prokinetics and Promotility products will help remove D-Lactic Bacteria accumulate in the Small Intestine.

Symptoms came back over a few days which started with feeling bad fatigue, falling asleep at my laptop and Flu like aching pain and malaise (brain fog), then the symptoms rapidly escalated and I started to feel sick on and off, dyspepsia, slurred speech, confused, very unwell, with abnormal gait like drunk at times with rapid heartbeat. I can imagine that this may be about levels of production. It is possible that some may develop lower or higher levels of Overgrowth.

My antibiotics are no longer working and so I used three failed ones together and barely managed to stop the symptoms. Due to difficulty thinking I had further Carbohydrates by mistake and was close to going into Hospital. I am only back to normal 6 days on due to adding some Carbohydrates by mistake two days running.

I have read a lot of conflicting reports concerning Lactic producing Bacteria and do not have time to wait around another 18 years. I hope to find a way to reverse the condition. I will just have to keep experimenting.

Thank you TMartin, you reminded me to use Bicarbonate of Soda during the crisis which helped reduce my symptoms. Bicarbonate acts as a bactericide for D-Lactic producing Bacteria. It lowers the PH which D-La Bacteria thrive in, which effectively helps to reduce them and their product. I may Bicarbonate of Soda to the Antibiotics if I have another exacerbation because it can increase the ability of Antibiotics for Gut Bacteria.

I have seen a new dietitian who has changed my diet somewhat, to a low FODMAP which I hope will work even better for me (avoidance of foods high in Polyols, Lactose, Oligosacharides, Fructose), which is far more complex and I will need time to mentally digest! I will copy these to you later.

I am also seeing another Consultant Gastroenterologist and Microbiologist, to help with Antibiotic, Probiotics and Fecal Transplant and will keep you informed. I will ask him about the specific Enzyme investigations for the Pyruvate Chain and also Digestive and Biliary Enzymes, motility investigations and Kidney and Liver Function etc. Finding the cause of Bacterial Overgrowth is the main goal, then correcting it and replacing the abused Gut Flora Dysbiosis (abused by antibiotics and possibly Probiotics).

I have realized that I had been given VSL-3 Probiotic for some years, high in Lactic Producing Bacteria. This may have worsened the Overgrowth if all Lactic producing Bacteria do in fact add to the load or Overgrowth. Sheedy found specific D-Lactic Bacteria in their CFS patients.

The NHS have stopped the use of Probiotics such as VSL-3, perhaps they realize that they may be dangerous and are distancing themselves? It is possible that Antibiotic Selection for Overgrowth and even Lactic Probiotics could be contributing to ME/CFS, but this badly needs investigation.

There are so many possible factors!!!!

Paul.
Hi, Paul:

Thanks for the update.

It's unfortunate that your probiotic choice didn't work out, but at least you successfully proved that you could "reset" to a baseline using antibiotics - and that's encouraging.

I've got everything on order for the protocol I've designed; something that may help you were some of the options I found for probiotics. While not exact matches to the Japanese researchers, here's some I considered:

1. B. Breve

https://www.customprobiotics.com/b-breve-custom-probiotic-powder.html

2. L. Casei

https://www.customprobiotics.com/l-casei-probiotic-powder.html

I was going to use the options listed above; however, I chose to go in a different direction when I spotted a specific, D-Lactic Acid-free combination (low histamine, as well):

https://www.customprobiotics.com/d-lactate-free-probiotics.html

The prices may seem steep, but the D-Lactic Acid-free combo is available in a sample size that might ease the burden on some, while allowing successful trial periods:

https://www.customprobiotics.com/custom-probiotics-d-lactate.html

Additionally, you mentioned an increased resistance to antibiotics. Is this due to using the same ones over and over again? If so, this group may be able to help you. They offer a wide array of the antibiotics that match the Japanese team and Dr. White's recommendations:

https://www.inhousepharmacy.vu/p-453-trichozole-200mg-metronidazole.aspx

They're based in the UK (I believe you are, as well?). They were recommended by someone on this board; I've used them many times, even though I'm in the US, with flawless service.

Hopefully, some of my notes will offer you help in your path forward.

Please continue to keep us posted, I've drawn heavily on this thread when designing my own protocol - I'll post updates on my experiences, as they develop.

Best Regards.

Terry
 

Avenger

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Dear Hip and TMartin,
the Probiotic experiment has ended in disaster!!!

I had a bad recurrence of illness after some 5 weeks or more free of symptoms using normal Carbohydrates and Sugars while taking Probiotics which did contain Lactic producing Bacteria. I have been very unwell for the last few days and have had to use the exclusion diet with Antibiotics.

I will have to repeat the experiment with isolates of the Bacteria that have been used by the Japanese Gastroenterologist Researchers. I could only find similar mixed with Lactic producing in the Probiotic that I chose.

I am still not sure why I was symptom free, followed by recurrence of D-La??? or whether the Lactic producing Bacteria are to blame? I will only know for sure if I try the same Bacteria used by the Japanese or experiment with non Lactic producing mixed cultures?

Perhaps using Prokinetics and Promotility products will help remove D-Lactic Bacteria accumulate in the Small Intestine.

Symptoms came back over a few days which started with feeling bad fatigue, falling asleep at my laptop and Flu like aching pain and malaise (brain fog), then the symptoms rapidly escalated and I started to feel sick on and off, dyspepsia, slurred speech, confused, very unwell, with abnormal gait like drunk at times with rapid heartbeat. I can imagine that this may be about levels of production. It is possible that some may develop lower or higher levels of Overgrowth.

My antibiotics are no longer working and so I used three failed ones together and barely managed to stop the symptoms. Due to difficulty thinking I had further Carbohydrates by mistake and was close to going into Hospital. I am only back to normal 6 days on due to adding some Carbohydrates by mistake two days running.

I have read a lot of conflicting reports concerning Lactic producing Bacteria and do not have time to wait around another 18 years. I hope to find a way to reverse the condition. I will just have to keep experimenting.

Thank you TMartin, you reminded me to use Bicarbonate of Soda during the crisis which helped reduce my symptoms. Bicarbonate acts as a bactericide for D-Lactic producing Bacteria. It lowers the PH which D-La Bacteria thrive in, which effectively helps to reduce them and their product. I may Bicarbonate of Soda to the Antibiotics if I have another exacerbation because it can increase the ability of Antibiotics for Gut Bacteria.

I have seen a new dietitian who has changed my diet somewhat, to a low FODMAP which I hope will work even better for me (avoidance of foods high in Polyols, Lactose, Oligosacharides, Fructose), which is far more complex and I will need time to mentally digest! I will copy these to you later.

I am also seeing another Consultant Gastroenterologist and Microbiologist, to help with Antibiotic, Probiotics and Fecal Transplant and will keep you informed. I will ask him about the specific Enzyme investigations for the Pyruvate Chain and also Digestive and Biliary Enzymes, motility investigations and Kidney and Liver Function etc. Finding the cause of Bacterial Overgrowth is the main goal, then correcting it and replacing the abused Gut Flora Dysbiosis (abused by antibiotics and possibly Probiotics).

I have realized that I had been given VSL-3 Probiotic for some years, high in Lactic Producing Bacteria. This may have worsened the Overgrowth if all Lactic producing Bacteria do in fact add to the load or Overgrowth. Sheedy found specific D-Lactic Bacteria in their CFS patients.

The NHS have stopped the use of Probiotics such as VSL-3, perhaps they realize that they may be dangerous and are distancing themselves? It is possible that Antibiotic Selection for Overgrowth and even Lactic Probiotics could be contributing to ME/CFS, but this badly needs investigation.

There are so many possible factors!!!!

Paul.
Just a general comment: From the way that the planet is going, it now seems that we are the Overgrowth!
A bunch of nasty Warring, Genocidal, Selfish Ape's. We are not the most Intelligent Species as was Self Ordained, just the most Aggressive, eating and using our way through every other Species and usable Material. We are now consuming our own Metabolites and are a Planetary Dysbiosis! Where is the love? Well at least there is some to be found here in this little community! (Sorry this comes from studying Philosophy and Sculpture before I became ill, where I nearly lost my head in my own backside!).
Anyway my love to you all, who are lost in this maze.

Paul.
 

Avenger

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This is for everyone on the site please pass this on!
Dear All,

I have just found the reason that it took so long for me to be diagnosed!

Anyone with multiple undiagnosed symptoms for two years which remain unexplained under the ICD or DSM classifications for Somatization may be diagnosed with Somatization!

Please check and ask for a copy of your 'Significant Medical History' for all Doctors and Services where it may be found if diagnosed.


If placed in your Clinical Record, it will mean that no one will take you seriously for any of the symptoms or illness, even during severe breathing difficulty (this happened to me frequently when I was told that I was hyperventilating while suffocating due to D-Lactic acidosis, which causes natural hyperventilation to get rid of the increased acid in the blood stream). On one of many occasion when I had serious exacerbations I was left to suffocate in a room on my own for over 9 hours without observation or investigation and not offered any fluids which were necessary for D-Lactic acidosis, which can be either mild or fatal.

(I have just read a very good report from the Oley Foundation that states that milder symptoms may go undiagnosed, which I believe is what happening for a subset of ME/CFS. It is also possible for a mild Overgrowth to worsen).

Everyone can ask for a copy of their 'Significant Medical History' which is the first document seen on screen by all Doctors and Services. It introduces you as a patient and if you have Somatization, then you may not be taken seriously for anything for the rest of your life as happened to me for 18 years. My 'Significant Medical History' has only recently been annotated, but it has been an 18 years fight!

D-Lactic acidosis and forms of Bacterial Overgrowth will cause multiple symptoms. D-La causes multiple neurological systemic symptoms and is ripe if undiagnosed for Somatization as will other forms of Bacterial Overgrowth. Psychologists are now including Gut symptoms as criteria for diagnosis!

This will affect many if not all of you!

Concerning my D-Lactic illness that remained undiagnosed for 18 years (having to make the diagnosis myself and pay Privately for a D-Lactic Gastrointestinal Consultant who I now see under the NHS);

I was diagnosed with Somatization disorder with 'lack of insight', which was placed in my 'Significant Medical History' for all Doctors and Services which caused many Doctors, especially A&E not to believe me or take symptoms seriously even when confused, with slurred speech and breathing difficulty!

Please read some of the articles on Somatization by Professor Malcolm Hooper (who I am indebted to, because he personally helped me through this and gave me the strength to challenge and investigate for myself. He is noted in Wikipedia as one of the main challenges to Simon Wessely's ideology concerning Somatization and ME/CFS, cognitive behavioral therapy and graded exercise. The knighthood given to Wessely by the Government for suppressing organisations such as the ME association, should be snatched back and given to the few including Professor Hooper who have stood up for us. As far as I am concerned the Psychiatrists who have taken part in ICD or DSM concerning Somatization should be brought before the law courts on similar grounds as war criminals, they are doing serious harm both physically and mentally and it is possible that some of the fatalities may be due to Bacterial caused Acidosis.

Simple logic dictates that anyone with undiagnosed multiple symptoms is ripe for Somatization, to be neglected and for there to be no further need for investigations, because the Somatization will be taken as your diagnosis and the cause of all of your symptoms. Psychiatrists are setting themselves up as our mental betters, when they dictate such nonsense and poor thinking! This is nothing but Shamanism and will destroy the basis of Psychiatry which is supposedly based on Scientific Principle not poor thinking!

Please also go to Dr. Myhills online site concerning ME/CFS and Abuse! Dr. Myhill is another who should be given a knighthood for her services to ME/CFS.


This has to be challenged!!!!! It is abuse and an abuse of our human rights to fair medical treatment and duty of care!!!! A nice cheap way of dealing with us by the NHS, just ignore us we are all Somatizing.
 

Avenger

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Just an addition to my last rant!

We do not hang people on the same grounds!

If you make a mistake and hang someone who is innocent.....

This poor childish logic used in Somatization may have hanged many thousands already.

For me personally, the use of Somatization was as bad psychologically as rape, because it took so much away from me and caused me to suffer years of traumatic illness, pain, abuse and Post Traumatic Problems after 18 years of fighting just to be taken seriously due to the Somatization diagnosis. I do not know if I will ever overcome what has happened.


There is no Legal Challenge, because any Psychologist is within 'his' rights to diagnose under ICD or DSM, this is a Human Rights issue and I am not sure what rights we will have once we leave Europe! Litigation due to misdiagnosis may not be possible for Somatization because of this. We have no rights!
 

Avenger

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@Avenger I strongly suspect that I have somatization on my medical record or something similar. How do you go about getting your medical record? Ask the GP?
Hi, just ask your Doctor for a copy of your 'Significant Medical History' for all Services (UK).

It is the first thing that a Doctor, Ambulance or 'Out of Hours' will see. It is the most influential document, and if it contains Somatization, highly prejudicial (Search Professor Malcolm Hooper and Somatization in ME/CFS, also See 'Mislabeling Medical Illness as a Medical Condition, Allen J. Frances MD, DSM5 in distress).


This diagnosis means effectively that you do not need to be taken seriously and you do not need investigation unless you have a very enlightened Doctor.

If you are seen by someone who has not got to know you, then Somatization is your diagnosis and the reason for all of your problems. You may not be taken seriously and they may even make things worse by putting down 'Classic Somatization' in their letter as happened to me when I went to see a Neurologist.

I saw 4 Neurologists in all, two were 'World Class' leaders in Neurology. Investigations were never performed while I had exacerbations!

Neurologists are not trained to understand that Gut Bacteria can cause seriously abnormal Neurology. I now suspect that other forms of Bacterial Overgrowth may cause different fluctuating neurological symptoms through the metabolites (toxins) produced. There may be a number of other Metabolites involved in D-La alone according to Sheedy et al.

This is more about Shamanism than the good Science purported by Psychologists.
 

Avenger

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I am seriously thinking about taking on a Degree in Pychology, I was actually offered one, but funding is impossible to obtain.

It is hard to just walk away from this when you can see so many people suffering and Somatization greatly adds to the load of physical illness and can cause mental illness due to the stress and depression caused by Doctors who just ignore the illness, and in patients like myself who have spent 18 years fighting the misdiagnosis while very unwell.

For the genuinely ill, Somatization is a serious burden.


I already have my Thesis based upon my own story and the dangerous and negative effects of Somatization in ME/CFS.

The situation is just ridiculous, and the misuse of Somatization needs to be challenged.

In multi-system diseases like Multiple Sclerosis, Behçet’s syndrome or Systemic lupus, it can take several years before a diagnosis is arrived at.

I only studied Psychology to A-Level, but the first thing that was taught concerned many of the now illegal and immoral experiments and actions of Psychologists and the many failures in terms of diagnosis and how the misuse of statistical data has led to so many mistakes (eg. Pace Trials and Graded Exercise concerning ME/CFS; See Professor Malcolm Hooper, who believes that the data did not reflect the proposed outcomes and was fixed to make the Pace Trials look successful, so that many with ME/CFS would be put through nothing but torture!).

Psychology has been used in everything from War and Effective Interrogation and Torture, in Frontal Labotomy of Offenders from the 1930's. In homosexuality frontal labotomy was used to render them 'Moraly Sane' and even delinquent children and those in the care of Asylums were labotomised to make them quiet and easy to manage. You could even have your wife labotomised (strepfordized). And there are many immoral experiments that the findings are still relied upon today. It would make a good book on its own.

But the use of Somatization in ME/CFS should be met some day in the Law Courts as Human Right Abuse.


Paul.
 

Avenger

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Email to Professor Malcolm Hooper early last year below;

I need to add before the email, that since reading a number of reports that I believe that at least for a Subset of ME/CFS that this is all about the level of production of metabolites in Bacterial Overgrowth. It is possible that those only having milder problems will only report varying fatigue and muscle pain and problems as Chronic Fatigue or ME without full D-Lactic symptoms. I only had mild symptoms of fatigue, sleep problems and muscle pain for a number of years before the illness worsened.

For Hip and all interested; D-Lactic/Mitochondrial/Pyruvate Report below letter. Direct investigations on Rats which may give more insight.


Dear Professor,

I am sending a list of reasons that Bacterial Overgrowth/D-Lactic acidosis may be one of the causes of ME/CFS which may be helpful to others with serious symptoms such as Hypoglycemia and Breathing Difficulty/Hyperventilation in ME/CFS (researched by Professor Belch). Many of these symptoms are experienced in ME/CFS such as gastrointestinal symptoms and when seen together there are many similarities between D-La and ME/CFS, and Bacterial Overgrowth alone can cause fatigue and milder CFS symptoms.


1.Neurological Symptoms that ME patients have stated for decades are also caused by D-Lactic fluctuations due to Overgrowth (which acts not unlike an infection, but without any raise in temperature because only the Metabolites enter the Blood Stream) and can be mild or prove fatal. I had multiple symptoms which you already know were diagnosed as Somatization because Doctors were unable to understand because many investigations were normal.


2. Hypoglycemia can also be caused by Bacterial Overgrowth. I had frequent and sometimes serious Hypoglycemia which stopped when I started the 0% (very low) Carbohydrate and Simple sugar exclusion diet. I was told by the Gastroenterologist, Dr. Ray Shidrawi that Hypoglycemia is caused by competition for food in the Small Intestine. But I am also wondering if it can be caused or worsened by Neurological changes due to D-Lactic poisoning or at the Mitochondrial level? (inability to process or transfer glucose in the brain due to D-Lactic acid).

3. Breathing difficulty; including Hyperventilation is a natural response to acidosis. I had experienced fluctuating and sometimes serious breathing problems due to fluctuating levels of D-Lactate (Wessely's statement that he had established no relationship between Hyperventilation and ME/CFS would be incorrect because he would not have investigated acidosis/blood gasses during exacerbations of D-La in patients or the possibility of other Metabolites).

4. Flu or Infection like Symptoms without Temperature;
I now believe that D-Lactic acidosis is a form of infection but without giving rise to any temperature, and this may be why it has been misunderstood for so long in ME/CFS. Many ME/CFS describe Flu like or infection symptoms as I had.


The 'infection' is an Overgrowth of Bacteria that are normal to the Gut, which remains in the Gut and metabolites such as D-Lactate poison the host but without an immediate immune or temperature response (although autoimmune problems will happen due to Bacterial Overgrowth damaging the mucosal lining and causing 'Leaky Gut') .

With D-La the host feels the symptoms of infection (Flu like) without any change in temperature. Doctors who are trained to look for temperature are blind to the underlying cause, because D-La breaks the rules and appears as though nothing is happening except psychologically and will then blame the patient.


5. Muscle Pain and Weakness; is also caused by D-La and I also suffered post activity fatigue along with frequent increased heart rate and tachyarrhythms after activity. I suffered frequent tachyarrhythms during exacerbations of illness. D-La is known to cause increased heart rate and tachyarrhythms.


6. Abdominal Symptoms such as pain and bloating, Reflux and gastrointestinal symptoms; My frequent Reflux and gastrointestinal symptoms also stopped along with Hypoglycemia soon after the exclusion diet was implemented. The problems lies in both digesting Carbohydrates and Simple Sugars as well as abnormal inability to Metabolize. These foods seem to decrease motility and stomach emptying and cause reflux.


7. Brain Fog and Confusion; I had periods of what I described as feeling dopey, dizzy or light headed to periodic confusion with slurred speech when most ill and seizure. This also stopped after treating D-La with the exclusion diet.


The picture may be very complex because D-Lactic acidosis is always secondary to other problems such as Motility, Diabetes and a number of other disorders, but I am hoping that you may be able to help those with similar symptoms and that this may help change the belief that this is all Somatic.


The ME Association is not interested in investigating and have stated that ME/CFS is most definitely caused by Viral Outbreaks.


For me there seems to be so many similarities between ME/CFS and D-Lactic acidosis or Overgrowth symptoms and according to statistics many ME/CFS have Bacterial Overgrowth and there are so many ways in which Bacterial Overgrowth can be caused including a number of frequently used medications including antibiotics, and proton pump inhibitors such as Omeprazole may be contributing (I had used Omeprazole frequently due to Helicobacter infection which is found in around 50% of the population) and there may be a chain of possible contributors.


I am also being investigated again for Mitochondrial dysfunction (found to be abnormal by Dr. Myhill and during two other investigations) which may be related to D-La.


Best wishes, Paul.


D-Lactate altered mitochondrial energy production in rat brain and heart but not liver
Binbing Ling,1 Fei Peng,1 Jane Alcorn,1 Katharina Lohmann,2 Brian Bandy,1 and Gordon A Zello
1
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This article has been cited by other articles in PMC.

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Abstract
Background
Substantially elevated blood D-lactate (DLA) concentrations are associated with neurocardiac toxicity in humans and animals. The neurological symptoms are similar to inherited or acquired abnormalities of pyruvate metabolism. We hypothesized that DLA interferes with mitochondrial utilization of L-lactate and pyruvate in brain and heart.

Methods
Respiration rates in rat brain, heart and liver mitochondria were measured using DLA, LLA and pyruvate independently and in combination.

Results
In brain mitochondria, state 3 respiration was 53% and 75% lower with DLA as substrate when compared with LLA and pyruvate, respectively (p < 0.05). Similarly in heart mitochondria, state 3 respiration was 39% and 86% lower with DLA as substrate when compared with LLA or pyruvate, respectively (p < 0.05). However, state 3 respiration rates were similar between DLA, LLA and pyruvate in liver mitochondria. Combined incubation of DLA with LLA or pyruvate markedly impaired state 3 respiration rates in brain and heart mitochondria (p < 0.05) but not in liver mitochondria. DLA dehydrogenase activities were 61% and 51% lower in brain and heart mitochondria compared to liver, respectively, whereas LLA dehydrogenase activities were similar across all three tissues. An LDH inhibitor blocked state 3 respiration with LLA as substrate in all three tissues. A monocarboxylate transporter inhibitor blocked respiration with all three substrates.

Conclusions
DLA was a poor respiratory substrate in brain and heart mitochondria and inhibited LLA and pyruvate usage in these tissues. Further studies are warranted to evaluate whether these findings support, in part, the possible neurological and cardiac toxicity caused by high DLA levels.

Keywords: D-Lactate, Mitochondrial function, Rat, Brain, Heart
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Introduction
Lactate exists as two stereoisomers, L-lactate and D-lactate. Under healthy physiological conditions, L-lactate is the major enantiomer found in blood whereas D-lactate is normally present in very low concentrations [1]. However, supra-physiological levels of D-lactate have been found in several disease states such as diarrhea, short bowel syndrome, and diabetes [2,3]. Most research in this area focus on the cause and the consequences of extremely high levels of D-lactate (> 3 mM D-lactate in plasma, resulting in D-lactic acidosis) in the body [3-7]. Although sub-clinical levels of D-lactate (high D-lactate levels, no acidosis) have been reported in several chronic diseases including diabetes and chronic fatigue syndrome [8,9], few studies explore the potential negative outcomes of such sub-clinical concentrations of D-lactate circulation in the body [10]. Interestingly, the clinical symptoms due to high levels of D-lactate (D-lactic acidosis) are similar to inherited or acquired abnormalities of pyruvate metabolism [11]. Therefore, D-lactate may directly or indirectly interfere pyruvate metabolism pathways, which are essential for mitochondrial energy production [12]. Any disturbance in pyruvate metabolism pathways may eventually impair mitochondrial energy generation and thus affect organs that are more highly energy dependent [13,14].

The brain and heart are metabolically active organs with substantial energy requirements. The major cellular pathways of energy production are glycolysis and mitochondrial oxidative phosphorylation [15]. During glycolysis, glucose is converted to pyruvate, which is accompanied by the production of ATP and NADH [15]. In mammalian cells, the enzymes responsible for pyruvate metabolism are located in the mitochondria [16]. Thus, pyruvate generated during glycolysis is transported into the mitochondria via monocarboxylate transporters (MCTs) particularly MCT1 [17]. In the mitochondria, pyruvate breakdown irreversibly funnels the products of glycolysis into the Krebs cycle to produce ATP and a large quantity of NADH [12]. NADH produced by both processes is then used to fuel mitochondrial ATP synthesis via oxidative phosphorylation or mitochondrial respiratory chain phosphorylation [15,16].

In some tissues, L-lactate oxidation can provide cellular energy in addition to glycolysis [18,19]. For example, L-lactate has been identified as the preferential oxidative energy substrate for the brain during excitation [20]. The Astrocyte-Neuron Lactate Shuttle hypothesis suggests that fuel for increased energy requirement of neurons during excitation is supplied by L-lactate from the surrounding astrocytes rather than glucose [18,21]. Following its transport into the cell, cytosolic L-lactate is converted to pyruvate by L-lactate dehydrogenase (LDH), an enzyme using NAD as a cofactor [18], which subsequently enters the TCA cycle in the mitochondria for further energy production. In addition, mitochondria also contain significant amounts of LDH, located largely in the inter-membrane space [18]. L-lactate transported into the mitochondria via MCTs is metabolized to pyruvate for energy production. Therefore, mitochondrial utilization of both L-lactate and pyruvate is crucial for cellular bioenergetics.

D-Lactate, recognized by MCTs [22], can competitively inhibit L-lactate and/or pyruvate transport via MCTs at the cellular level. For example, D-lactate inhibited L-lactate uptake into erythrocytes and brain cells and pyruvate uptake into cardiac myocytes [23,24]. Once D-lactate has entered the cells, it can affect the transport of L-lactate and/or pyruvate into the mitochondria and thus affects the usage of pyruvate and/or lactate. In fact, D-lactate interference of pyruvate metabolism has been postulated based on the clinical similarities between D-lactic acidosis and inherited or acquired abnormalities of pyruvate metabolism [25]; however, no experimental data are available to support this inference.

Cellular D-lactate is metabolized by mitochondrial D-lactate dehydrogenase (DDH) using FAD as cofactor [26,27]. The expression of DDH is tissue dependent and therefore affects the usage of D-lactate in different tissues [26,27]. For example, due to low expression levels of DDH in the brain, the rate of oxidation of D-lactate in the brain is considerably slower compared to that of L-lactate [26,27]. D-Lactate accumulation, then, may compromise energy metabolism by interfering with the mitochondrial usage of its more efficient energy substrates pyruvate and/or L-lactate and thus lead to toxicity. Energy deficiency in the brain of chickens has been reported following intracerebral infusion of D-lactate which suggests D-lactate's involvement in altered substrate utilization and ATP generation [28]. In this study, we hypothesized that D-lactate interferes with mitochondrial utilization of L-lactate and pyruvate.

The objectives of this study were to compare the mitochondrial utilization of D-lactate to L-lactate and pyruvate in mitochondria from rat heart, liver and brain tissues. We also investigated the effects of D-lactate on mitochondrial respiration with L-lactate or pyruvate as substrates. The D- and L-lactate dehydrogenase activities from different tissue mitochondria were also measured. To test the role of LDH on the mitochondrial respiration of L-lactate, a LDH inhibitor, oxamate (OX) was used in rat liver and brain. Our investigations also employed an MCT inhibitor, α-cyano-4-hydroxycinnamate (CINN), to identify the role of mitochondrial MCTs in D-lactate, L-lactate and pyruvate metabolism in rat liver and brain.

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Materials and methods
Animals and Chemicals
Male Wistar rats were obtained from Charles River Canada (St. Constant, PQ) and were housed in a temperature and humidity controlled facility (22°C ± 2°C) on a 12-hour light: dark cycle (0700 h - 1900 h). Rats had free access to food and water and were allowed a 7-day acclimatization period. Rats were provided a nutritionally adequate rat diet (Prolab® RMH 3000, Purina, Inc., Richmond, IN) ad libitum. This work was approved by the University of Saskatchewan's Animal Research Ethics Board, and adhered to the Canadian Council on Animal Care guidelines for humane animal use. Chemicals, unless specified, were purchased from Sigma-Aldrich.

Mitochondrial Isolation
Mitochondria were isolated from rat (250-300 g body weight, n = 6) brain, heart and liver following humane euthanasia (isoflurane anaesthesia and exanguination) and rapid removal of organs. Briefly, freshly isolated organs were homogenized using a glass-teflon homogenizer (brain and liver) or a Polytron homogenizer (heart) with an isolation medium containing 250 mM sucrose, 10 mM HEPES and 1 mM EGTA (pH 7.2). In the case of brain, the mitochondria were isolated in the presence of 0.1% fat-free bovine serum albumin (BSA). The homogenate was then centrifuged at 1000 g for 8 min at 4°C. The supernatant was collected and centrifuged at 10000 g for 10 min at 4°C. The pellet was collected and washed twice with washing medium containing 250 mM sucrose, 10 mM HEPES and 0.1 mM EGTA. The final pellets of mitochondria were suspended in 2 mL of isolation medium without EGTA [29-32].

Oxygen Uptake Studies
Mitochondrial protein was measured as described by the biuret method using bovine serum albumin as standard [33]. Respiration rates of isolated mitochondria were measured with a Clark-type electrode (DW1; Hansatech Instruments Ltd, Norfolk, England) in a water-jacketed glass chamber with magnetic stirring. An oxygen electrode was used and the respiration chamber was kept constant at 30°C. Oxygen uptake measurements were carried out in 1 mL of medium containing 210 mM mannitol, 70 mM sucrose, 0.1 mM EDTA, 20 mM Tris/HCl, 3 mM MgCl2, 5 mM KH2PO4/K2HPO4 and 0.2% BSA (pH 7.4) [34]. Assays were performed in duplicate using fresh mitochondria. The respiratory parameters of the mitochondria were tested using a respiratory cocktail (containing 62.5 μM each of malate, glutamate, alpha-ketoglutarate and pyruvate), pyruvate + malate, L-lactate + malate, or D-lactate + malate. Pyruvate (10 mM) and D/L-lactate (5 mM) were added alone or in combination. To inhibit the mitochondrial monocarboxylate transporter (mMCT), 5 mM α-cyano-4-hydroxycinnamate (CINN) was used. To inhibit mitochondrial LDH, 50 mM oxamate (OX) was used. Respiration was initiated by the addition of 1 mg protein of the mitochondrial suspension to the reaction medium, and a conventional respiratory experiment with transitions from state 4 to 3 was performed.

Mitochondrial respiratory state 4 is the resting state which is differentiated by relatively slow oxygen uptake and no availability of ADP [35]. On the other hand, mitochondrial respiratory state 3 is the active state with high rates of oxygen uptake and sufficient ADP supply [35]. Thus, state 3 was initiated by adding ADP (final concentration 0.1 mM). Mitochondrial function was assessed by the respiratory control ratio (RCR) and ADP:O ratios [36]. These two parameters are well accepted as indicators of electron transport chain coupling to ATP synthesis and efficiency of oxidative phosphorylation in the presence of different substrates. The RCR values were calculated as the ratio of the respiratory rate in state 3, after addition of ADP, to the rate of oxygen uptake without ADP (state 4). The ratio between the amount of ADP phosphorylated and oxygen consumed (ADP/O ratio) was also calculated [37].

L- and D-Lactate Dehydrogenase (LDH and DDH) Assay
The LDH and DDH assays were performed photometrically by means of a 96 well spectrophotometer at 600 nm [38] at 25°C. Briefly, the mitochondrial sample was incubated for 2 min in 2 mL of standard medium consisting of 0.2 mM sucrose, 10 mM KCl, 20 mM Hepes/Tris, pH 7.2, 1 mM MgCl2 in the presence of 30 μM phenazine methosulphate (PMS) and 50 μM dichloroindophenol (DCIP). DDH activity was determined by measuring the decrease in absorbance at 600 nm (A600) due to DCIP reduction when 15 mM D-lactate was added. The activity was expressed as nmol of DCIP reduced per min per mg of protein.

In conclusion, our study identified that D-lactate is a poor substrate for rat brain and heart mitochondria, but an efficient substrate for liver mitochondrial respiration. Low levels of DDH activity in rat brain and heart likely explain its poor utilization by mitochondria of these tissues. Additionally, D-lactate inhibited brain and heart mitochondrial respiration caused by pyruvate and L-lactate. L-Lactate also inhibited pyruvate induced mitochondrial respiration in liver, brain and heart but could maintain heart and brain mitochondrial respiration via LDH mediated conversion of L-lactate to pyruvate. Furthermore, an inhibitor of monocarboxylate transporters completely inhibited mitochondrial respiration in all tissues regardless of substrate. Collectively, these data suggest D-lactate inhibition of pyruvate and L-lactate mitochondrial utilization may be due, in part, to competitive inhibition of the monocarboxylate transporters responsible for the transport of pyruvate and lactate into the mitochondria. Since mitochondrial oxidative phosphorylation is the main source of ATP production in various tissues, disruption of mitochondrial respiratory function in brain and heart may compromise cellular energy status and result in toxicity. Hence, D-lactate mediated reductions in mitochondrial energy production may contribute to the neurological and cardiac toxicity associated with D-lactic acidosis. L-Lactic acidosis would not result in a cellular energy deficiency due to LDH mediated conversion of L-lactate to pyruvate by liver, brain, and heart mitochondria. Further investigation is warranted to determine the relationship between reductions in mitochondrial energy production to cellular energy deficiency and organ dysfunction.



Paul.
 

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Malcolm
Thu 12/04/2018 12:02
You


PAUL,
Sorry i have been late in replying to your emails I have had a bad time, health wise, since mid December and am only now getting up to speed again.
WELL DONE AGAIN!
Your thesis makes good sense. If you have the names the bacterial species providing D lactate I would very much like to receive them.
The involvement of some yeasts is also interesting. Some bacteria and viruses are adept at avoiding the immune system defences so it is not so surprising that you have found another one that uses a different mechanism.
Best wishes
Malcolm

Malcolm Hooper PhD, B Pharm., MRIC, C Chem.
Emeritus Professor of Medicinal Chemistry
University of Sunderland, UK

Phone
Moblle
Email

On 10 Apr 2018, at 09:21, Paul Smith <> wrote:

Dear Professor, this was written as part of an online discussion;

I now believe that D-Lactic acidosis is a form of infection but without giving rise to a temperature and this may be why it has been misunderstood for so long in ME/CFS. Many ME/CFS describe Flu like or infection symptoms as I had.

Criteria for infection is the invasion of an organism's body tissues by disease causing agents, their multiplication and the reaction of the host tissues to infectious agents and the toxins they produce. In D-La the infection is due to Overgrowth multiplication that remains in the Gut, but the toxins that cannot be metabolised invade the hosts tissues without giving rise to any temperarure because the immune system is not activated as it would normally be in an infection. I had frequently described infection to my Doctor but without it being understood.

With D-La the host feels the symptoms of infection (Flu like) without any change in temperature. Doctors who are trained to look for temperature are blind to the underlying cause, because it breaks the rules and appears as though that nothing is happening except psychologically and will then blame the patient.

With D-La the infection is caused by Overgrowth of a particular Species producing the toxin D-Lactic acid (and there may also be other metabolites involved with unknown attributes found by Sheedy).

The reason that this has been misunderstood for so long is that although you get the symptoms of an infection such as Flu like, or Infection like symptoms, D-Lactic acidosis generates no change in temperature (I have also describes for 18 years as Flu like, Infection and poisoning). Every time that i was unwell Doctors took my temperature. I diagnosed my own problem when I realized that no one would help me or was even interested in what they perceived as a psychological problem.

Doctors do not understand infection unless it comes with temperature. In D-La you have all the symptoms but no temperature. Many of you have reported the same lack of temperature in this thread.

My belief is that Bacterial Overgrowth barely describes the condition and should be viewed as an infection (and there may be more than one form of Overgrowth. IBS is also a form of Bacterial Overgrowth). Sheedy found two D-Lactic producing Bacteria, but Fungal infections such as Candida also produce D-Lactic acid. It may be the toxins or metabolites produced by Bacterial Overgrowth that causes illness and Flu like symptoms in ME/CFS for at the least a Subset (and possibly more).
D-Lactic acidosis is also a cause of Breathing Difficulty often seen as Hyperventilation. Simon Wessely had established the lack of relationship between Hyperventilation and CFS. Hyperventilation is a natural response to D-Lactic acidosis and my belief the cause of both neurological symptoms and cause of Flu or infection like illness without temperature.
Yours Sincerely, Paul D. Smith

Paul.
 

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Email from Professor Malcolm Hooper (look up Simon Wessely in Wikipedia and Professor Hooper. Professor Hooper and the Countess of Mar are his opponents and have made frequent criticisms of Wessely). They are the heroes of ME/CFS who should be awarded knighthoods when this is all over. Dr. Myhill is another. Without their help I would not have had the strength to survive or fight.
Professor Hooper has spent a great deal of his life supporting and writing on ME/CFS and is the Head of the Gulf War Vets (see his shared writing with Margaret Williams, sheer genius!)

Malcolm
Thu 12/04/2018 12:02
You


PAUL,
Sorry i have been late in replying to your emails I have had a bad time, health wise, since mid December and am only now getting up to speed again.
WELL DONE AGAIN!
Your thesis makes good sense. If you have the names the bacterial species providing D lactate I would very much like to receive them.
The involvement of some yeasts is also interesting. Some bacteria and viruses are adept at avoiding the immune system defences so it is not so surprising that you have found another one that uses a different mechanism.
Best wishes
Malcolm

Malcolm Hooper PhD, B Pharm., MRIC, C Chem.
Emeritus Professor of Medicinal Chemistry
University of Sunderland, UK

Phone
Moblle
Email

On 10 Apr 2018, at 09:21, Paul Smith <> wrote:

Dear Professor, this was written as part of an online discussion;

I now believe that D-Lactic acidosis is a form of infection but without giving rise to a temperature and this may be why it has been misunderstood for so long in ME/CFS. Many ME/CFS describe Flu like or infection symptoms as I had.

Criteria for infection is the invasion of an organism's body tissues by disease causing agents, their multiplication and the reaction of the host tissues to infectious agents and the toxins they produce. In D-La the infection is due to Overgrowth multiplication that remains in the Gut, but the toxins that cannot be metabolised invade the hosts tissues without giving rise to any temperarure because the immune system is not activated as it would normally be in an infection. I had frequently described infection to my Doctor but without it being understood.

With D-La the host feels the symptoms of infection (Flu like) without any change in temperature. Doctors who are trained to look for temperature are blind to the underlying cause, because it breaks the rules and appears as though that nothing is happening except psychologically and will then blame the patient.

With D-La the infection is caused by Overgrowth of a particular Species producing the toxin D-Lactic acid (and there may also be other metabolites involved with unknown attributes found by Sheedy).

The reason that this has been misunderstood for so long is that although you get the symptoms of an infection such as Flu like, or Infection like symptoms, D-Lactic acidosis generates no change in temperature (I have also describes for 18 years as Flu like, Infection and poisoning). Every time that i was unwell Doctors took my temperature. I diagnosed my own problem when I realized that no one would help me or was even interested in what they perceived as a psychological problem.

Doctors do not understand infection unless it comes with temperature. In D-La you have all the symptoms but no temperature. Many of you have reported the same lack of temperature in this thread.

My belief is that Bacterial Overgrowth barely describes the condition and should be viewed as an infection (and there may be more than one form of Overgrowth. IBS is also a form of Bacterial Overgrowth). Sheedy found two D-Lactic producing Bacteria, but Fungal infections such as Candida also produce D-Lactic acid. It may be the toxins or metabolites produced by Bacterial Overgrowth that causes illness and Flu like symptoms in ME/CFS for at the least a Subset (and possibly more).
D-Lactic acidosis is also a cause of Breathing Difficulty often seen as Hyperventilation. Simon Wessely had established the lack of relationship between Hyperventilation and CFS. Hyperventilation is a natural response to D-Lactic acidosis and my belief the cause of both neurological symptoms and cause of Flu or infection like illness without temperature.
Yours Sincerely, Paul D. Smith

Paul.
 

Avenger

Senior Member
Messages
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Somatization in undiagnosed Illness including ME/CFS. Very Good article:

Allen J Frances M.D.
DSM5 in Distress

Mislabeling Medical Illness As Mental Disorder
The eleventh DSM 5 mistake needs an eleventh hour correction.

Many readers of my previous blog listing the ten worst suggestions in DSM 5 were shocked that I failed to mention an eleventh dangerous mistake- that DSM 5 will harm people who are medically ill by mislabeling their medical problems as mental disorder. They are absolutely right. I apologize for my previous failure to attend to this danger and hope it is not now too late to influence the process.

For an update on this issue see http://www.psychologytoday.com/blog/dsm5-in-distress/201301/bad-news-dsm...

Adding to the woes of the medically ill could be one of the biggest problems caused by DSM 5. It will do this in two ways: 1) by encouraging a quick jump to the erroneous conclusion that someone's physical symptoms are 'all in the head'; and 2) by mislabeling as mental disorders what are really just the normal emotional reactions that people understandably have in response to a medical illness. UK health advocate, Suzy Chapman, has closely monitored every step in the development of DSM 5. Her website is the best available resource for finding just about everything you need to know about DSM 5 and ICD-11. Ms Chapman sent me a troubling email that summarizes where DSM 5 has gone wrong and the many harmful consequences that will follow. More details are available at: 'Somatic Symptom Disorder could capture millions more under mental health diagnosis' (http://wp.me/pKrrB-29B )

Ms. Chapman writes, "...The DSM-5 Somatic Symptom Disorders Work Group is planning to eliminate several little used DSM-IV Somatoform Disorders and replace them instead with an extremely broad new category that is likely to be wildly overused ('Somatic Symptom Disorder' – SSD).

"A person will meet the criteria for SSD by reporting just one bodily symptom that is distressing and/or disruptive to daily life and having just one of the following three reactions to it that persist for at least six months: 1) 'disproportionate' thoughts about the seriousness of their symptom(s); or 2) a high level of anxiety about their health; or, 3) devoting excessive time and energy to symptoms or health concerns.

"Unless DSM-5 changes these incredibly over inclusive criteria, it will greatly increase the rates of diagnosis of mental disorders in the medically ill – whether they have established diseases (like diabetes, coronary disease or cancer) or have unexplained medical conditions that so far have presented with somatic symptoms of unclear etiology.

"The diagnosis of mental disorder will be based solely on the clinician's subjective and fallible judgment that the patient's life has become 'subsumed' with health concerns and preoccupations, or that the response to distressing somatic symptoms is 'excessive' or 'disproportionate,' or that the coping strategies to deal with the symptom are 'maladaptive'.

"These are inherently unreliable and untrustworthy judgments that will open the floodgates to the overdiagnosis of mental disorder and promote the missed diagnosis of medical disorder.

"The DSM-5 Work Group is taking a flying leap into the unknown. There are no published research data on the likely prevalence rates, clinical characteristics or treatment of 'Somatic Symptom Disorder,' or its validity and safety as a construct. Decisions to code or not to code will hang on the arbitrary and subjective perceptions of DSM end-users who often spend very little time with the patient and lack training in psychiatry.

"The DSM-5 field trials produced results that should have scared off the Work Group. One in six cancer and coronary disease patients met the criteria for DSM-5 'Somatic Symptom Disorder.' Do we really want to burden and stigmatize seriously ill people with an additional diagnosis of mental illness, just because they are worried about being sick and are vigilant about their symptoms? Might patients with life threatening diseases become reluctant to report new symptoms that might be early indicators of recurrence, metastasis or secondary disease – for fear of attracting a diagnosis of 'SSD'?

"The Work Group is not proposing to classify Chronic Fatigue Syndrome, Irritable Bowel Syndrome, and Fibromyalgiawithin the DSM-5 'Somatic Symptom Disorders' section, but these patients and others with conditions like chronic Lyme disease, interstitial cystitis, Gulf War illness and chemical injury will now become particularly vulnerable to misdiagnosis with a DSM-5 mental health disorder. In the field trials, more than one in four of the irritable bowel and chronic widespread pain patients who comprised the 'functional somatic' study group were coded for 'Somatic Symptom Disorder.'

"To meet requirements for Somatization Disorder (300.81) in DSM-IV, a considerably more rigorous criteria set needed to be fulfilled. There had to be a history of many medically unexplained symptoms before the age of thirty, resulting in treatment sought or psychosocial impairment. The diagnostic threshold was set high – a total of eight or more medically unexplained symptoms from four, specified symptom groups, with at least four pain and two gastrointestinal symptoms.

"In DSM-5, the requirement of eight symptoms is dropped to just one. And the requirement of 'medically unexplained' symptoms is replaced by much looser and more subjective 'excessive thoughts, behaviors and feelings' and the clinician's perception of "dysfunctional illness belief' or 'excessive preoccupation' with the bodily symptom.

"That, and a duration of at least six months, is all that is required to tick the box for a bolt-on diagnosis of a mental health disorder – Colorectal cancer + SSD; Angina + SSD; Type 2 diabetes + SSD; IBS + SSD.

"I would like to put to Dr Dimsdale: what percentage increase in mental health diagnoses across the entire disease spectrum is estimated to result from implementation of his group's ad hoc proposals and has he also considered the increased costs to US health care providers and payers?"

"Incautious, inept misapplication of these highly subjective and catch-all criteria will likely result in frequent inappropriate psychiatric diagnosis with far-reaching implications for both the health care industry and diverse patient populations. Harms include:

• Stigma

• Missed diagnoses through failure to investigate new or worsening somatic symptoms.

• Patients will be prescribed inappropriate psychotropic drugs with consequent side effects, complications, and costs.

• There may be limits imposed on the types of medical tests and treatments offered for patients misdiagnosed as having a mental disorder.

• Misdiagnosed patients may be disadvantaged in employment, medical and disability reimbursement.

• An additional diagnosis of 'SSD' in a patient's medical history may negatively influence decisions made by agencies involved with social and medical services, disability adaptations, education and workplaceaccommodations.

• An inaccurate SSD diagnosis will skew the person's view of herself and her illness and perceptions of family and friends.

• In multi-system diseases like Multiple Sclerosis, Behçet’s syndrome or Systemic lupus, it can take several years before a diagnosis is arrived at. In the meantime, patients with chronic, multiple somatic symptoms who are still waiting for a diagnosis would be vulnerable to misdiagnosis as psychiatrically ill.

• DSM-5 allows for a diagnosis of 'Somatic Symptom Disorder' when a parent is considered 'excessively concerned' about a child's symptoms. Families caring for children with any chronic illness may be placed at risk of wrongful accusation of 'over-involvement' with their child's symptomatology or of encouraging 'sick role behavior.' By what means will a practitioner accurately assess an individual's response to illness within the context of the patient's personal, family and economic circumstances and reliably determine what might be considered 'excessive preoccupation' versus a positive coping strategy for that patient and family?

• The burden of the DSM-5 changes will fall particularly heavily upon women who are more likely to be casually dismissed when presenting with physical symptoms and much more likely to receive inappropriate antidepressants and anti anxiety medications for them.

"The Work Group is well aware that patients, families, caregivers and advocacy organizations are strongly opposed to the DSM-5 changes. During the second DSM-5 public review, the 'Somatic Symptom Disorders' proposals attracted more responses than almost any other category.

"At the APA's 2012 Annual Meeting, Work Group Chair, Joel Dimsdale, MD, admitted his committee has struggled from the outset with the 'SSD' criteria set. But rather than revising in favor of less inclusive requirements or subjecting the entire section to independent, external scientific review, the Work Group's puzzling response has been to lower the threshold even further from 'at least two from the B type criteria' to 'at least one' – placing even more medical patients at grave risk of attracting an inappropriate mental health diagnosis.

"Despite the APA Trustees signing off on DSM-5, work on specific wording is still not complete. Psychiatric and non psychiatric clinicians, primary care practitioners and specialists, allied health professionals, psychologists, counselors, social workers, medical lawyers and patient advocacy organizations all need to look very hard and quickly at these proposals, consider their safety and the implications of an additional diagnosis of 'SSD', and weigh in vigorously to the Work Group Chair with a call for urgent revision of this section... while there is still time."

Ms Chapman has provided a devastating and compelling critique. It is crucial that DSM 5 tighten its over-inclusive wording to prevent what could otherwise be the wholesale dismissal of real medical symptoms as psychiatric illness- leading to missed diagnoses, incorrect treatment, stigma, and patients understandably feeling greatly misunderstood.

I first became personally and painfully aware of the risks of misdiagnosis of somatic symptoms when, as a new psychiatric resident, I treated a man for depression for two months before discovering that his problems were in fact caused by the brain tumor I had previously missed.

The golden rule: an underlying medical illness or medication side effect has to be ruled out before ever deciding that someone's symptoms are caused by mental disorder. And the underlying medical illness may take time to declare itself. Uncertainty is hard to live with, but much better than jumping to false and risky conclusions.

The boundary between medical and psychiatric illness is inherently difficult to draw, especially since many psychiatric disorders do present with prominent somatic symptoms that are often mistaken for medical illness. Best example- people with panic attacks often get far too many medical tests for the dizziness, shortness of breath, and palpitations that are really just part of the hyperventilation caused by the panic attack. And the emotional distress some people have in reaction to real or feared illness does sometimes get out of all proportion enough to require psychiatric attention.

But there are serious risks attached to over-psychologizing somatic symptoms and mislabeling the normal reactions to being sick- especially when the judgments are based on vague wording that can't possibly lead to reliable diagnosis. DSM 5 as it now stands will add to the suffering of those already burdened with all the cares of having a medical illness.

DSM 5 must emphasize that physical symptoms deserve the respect of a thorough work-up before assuming their cause is psychiatric. And people with defined medical illnesses should not be casually mislabeled as also mentally ill just because they are upset about being sick.

There is a possible solution to the problems we have identified. Somatic Symptom Disorder should be removed from the main body of DSM 5 that is meant to describe the various mental disorders. Instead, unexplained physical symptoms or problematic responses to illness should be covered in the V Code section of the manual that includes Other Conditions That May Be A Focus Of Clinical Attention. This would remove the stigma and risks of mislabeling somatic concerns as mental disorders, while still providing clinicians with a code to describe the presentation. Second best solution- tighten the wording of the criteria set to make it less wildly over inclusive. As Ms Chapman points out, time is running out because DSM 5 is being rushed to press half baked.

For additional information see Toni Bernhard's wonderful blog at: https://cdn.psychologytoday.com/blo...llnesses-may-soon-be-labeled-mental-disorders

Be sure to read the following responses to this post by our bloggers:

Silver Linings of the New DSM Playbook is a reply by Victoria L. Dunckley M.D.

Paul.
 

Avenger

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@Avenger I strongly suspect that I have somatization on my medical record or something similar. How do you go about getting your medical record? Ask the GP?
Hi SB4,
I have only recently been made aware that the premise for Somatization stands as a Human Right abuse:

Somatization itself is diagnosed on the premise that a patient appears to have satisfied the criteria for Somatization Disorder as defined in the ICD Classificaion of Mental illness and behavioral disorders; The main features of Somatization disorder are multiple, recurrent and frequently changing physical symptoms of at least two years duration.

This means that many patients like myself with undiagnosed multiple sytemic symptoms undiagnosed after two years will be put to a serious disadvantage and danger if diagnosed with Somatization, which is a highly prejudicial diagnosis.

It also means that patients who have multiple changing symptoms that on average take more than two years to diagnose such as MS, Bechet's and Systemic Lupus, are more likely to be misdiagnosed with Somaization disorder (evidence below my email).

For patients who have real illness, Somatization is then taken as the diagnosis for their symptoms and illness and can cause many years of delay in diagnosis and treatment as happened to myself. I have only recently been given a copy of my 'Significant Medical History for all Doctors and Services' which is where the Somatization diagnosis was placed on 14th June 2001 and the cause of Doctors not believing or taking my illness seriously.


I was frequently abused and left without treatment due to a Somatization diagnosis for 18 years and left without a diagnosis for a serious illness that had been misdiagnosed as Somatization. I was also frequently told by Doctors that I had ME. or Chronic Fatigue that they stated were caused by Somatization. The illness that I had caused multiple systemic neurological symptoms, which Doctors had not been able to diagnose and so misdiagnosed Somatization.

How many more?

Paul.
 

Avenger

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Email to Professor Hooper concerning other Bacteria found in Overgrowth as causation of D-Lactic acidosis:

Dear Professor,
other Bacteria and Yeast found in causation of D-Lactic acidosis. Which means that there may be many Bacteria which in Overgrowth can cause D-Lactic acidosis; which increases the probability of D-Lactic acidosis causation. The reason for Overgrowth is better understood in Short Bowel Syndrome, but there must be other causes in ME/CFS.

August 1982 · European Journal of Pediatrics
Two cases of D-lactic acidosis associated with short bowel syndrome are described. The administration of kanamycin to the patients showed a decrease in D-lactate in blood and urine in parallel with disappearance of metabolic acidosis. Bacteriological analyses of the fecal flora showed an increase in Lactobacillus buchneri in the first patient and Lactobacillus fermenti IVa in the second; both bacteria were sensitive to kanamycin. Quantification of in vitro production of D-lactate by each species of bacteria isolated from the feces revealed that Lactobacillus produced more D-lactate than other species of bacteria. These observations indicate that Lactobacillus may play an important role in the induction of D-lactic acidosis in patients with short bowel syndrome.
Read more
March 1990 · The Quarterly journal of medicine

Two patients, both with short bowel syndrome, presented with severe D-lactic acidosis associated with subacute small bowel obstruction and bizarre neurological signs. In neither patient were D-lactic acid-producing organisms isolated from the upper intestine. In both, upper intestinal aspirates yielded a glucose-fermenting yeast, Torulopsis glabrata. Although intestinal aspirates from both contained significant quantities of ethanol alcohol could not be detected in concomitant blood samples. A glucose load test produced a rise in blood D-lactic acid in both. One patient has evidence of mild persisting renal tubular damage. The same patient responded to oral antibiotics but the other relapsed frequently despite continuous antibiotic treatment. He was shown to be thiamine deficient and since the administration of oral thiamine he has had no recurrence of symptoms or of D-lactic acidosis.


Paul.
 

Hip

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@Avenger, would you like to comment on my earlier post in which I pointed out that:
healthy volunteers infused with D-lactate showed no signs of encephalopathy even when concentrations reached up to 6.7 mmol/L.
You are proposing that D-lactate may be a cause of ME/CFS, but why don't D-lactate injections cause symptoms in healthy people?
 

Avenger

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Dear Hip, I think that is the whole point! We are not healthy individuals.

I am looking for an underlying cause of Bacterial Overgrowth causing D-La. What i have related is likely to be the tip of the iceberg. But it is reasonable to assume that a Subset may have different forms of Overgrowth including D-La, which is one of the few known causations of neurotoxicity which fits with ME as do many of the symptoms, which was why I was diagnosed ME/CFS and Fibromyalgia.

I am not saying that D-La is the one and only cause!

To answer your question properly, someone like me, who has D-La, should be injected to see how I handle, presumably pure D-Lactic acid, and follow up this in finding out why, if i do or do not respond to D-Lactic acid. This would give more insight; If i do not respond then it may be as you have assumed that D-La is only a proxy for other metabolites. If I can tolerate D-Lactic acid then that would show that the other metbolites must be the real cause of illness and neurotoxicity.

I have not seen your report or whether it has been verified by other researchers. But a lot of other researchers including Sheedy et al. believe that D-Lactic acid is unlikely to be the only metabolite produced as you have already noted.

There is always an underlying cause of Bacterial Overgrowth and there may be a number of contributing factors.

I have lived with D-La, and understand that it is not as simple as your statement infers. I also understand that at this stage it is not properly researched, controversial and contradictory and that it is possible that there are a number of forms of Bacterial Overgrowth that may produce a number of variants due to different metabolites produced. I have noted a number of D-Lactic producing Bacteria have recently been found.

It seems possible that both Viral infections and Antibiotics may be associated with the proliferation leading to Overgrowth in the Gut. We have set up an education program for inspired bacteria through low doses of Antibiotics that we are exposed to in farm animals and this is highly unlikely not to have consequence. My belief is that for a Subset of ME/CFS we are the consequence.


Paul.