Discussion in 'The Gut: De Meirleir & Maes; H2S; Leaky Gut' started by redo, Mar 26, 2011.
I have not seen him writing it is the cause.
Well, thanks for pointing out PubMed'ing him. I've never checked what he's published before, so here that is. And please do try to poke holes into my hypothesis. All well meant hole poking attempts are welcomed. I am trying to see if the hypothesis can hold water ;-)
lansbergen. I doubt you will read that until he has evidence for it being the cause (if it is the cause). I am not sure if he thinks it is the case, I think he's thinking more broadly (if a paper lits on fire, which is the cause A) The paper B) The oxygen C) The spark which lit it). But as I have understood him he thinks the easy test of H2S in your urine is the best test to see if someone is a PWC (or more correctly, if someone is not a PWC). If you have high H2S in your urine, it means you have issues with your gut (the H2S comes from the gut, via the body, and into the urine bladder). If you have high H2S in your urine, that means there are problems in the gut area.
But then it is not the cause but a consequence.
Thank you for clarifying.
Okay but XMRV integration can cause problems on is own.
That is okay with me as long as you do not make a point of it.
I think this theory has been around for awhile in various forms, certainly enterovirus research points to a similar conclusion. There was a digestive/intestinal treatment study a few years ago with a group of CFS patients and a significant number improved. I have tried to find that study but can't, maybe someone can find or remember it? Not the yoghurt study.
I haven't heard of the enterovirus research before. I'd really like to read more on that. Interesting. If you can find those links, then please post.
You've taken that quote out of context. I wrote that there are two ways psy. stress can make one worse in this setting.
One. When someone already is a PWC, they have problems with not breaking down the catecholamines, which may make them a lot worse. That has nothing to do with being a cause.
Two. Psy. stress being a trigger for other problems arising (such as either activating a virus causing a unbalance in the gut) or working directly on the gut does not mean that I've written that psy. stress can be a cause of CFS. You have to separate between trigger and cause.
I've never written XMRV integration can't cause problems on is own. I do think it can, and I do think it does. I am saying that my hypothesis is that the main problems comes from unwanted microbes in the gut. Which XMRV may contribute to.
I'm not sure if you have read all the stuff on d-lactic acid producing bacteria, so I have put together a few links below, which you might find of interest.
firstly, I just wanted to tell you about a study taking place in Australia regarding d-lactic acid in CFS,. This study is furthering research done by a team that found d-lactic acid producing bacteria in higher amounts in the stools of CFS patients, than in healthy controls. Here is a link to the original study.
The new study will measure d-lactate in stool, urine and blood samples of CFS patients, and compared to samples of healthy controls, to see whether CFS patients have a higher level of d-lactic acid. Here is their application, together with brief discussion.
As part of this study a questionnaire was given to the CFS patients, regarding lactic acid symptoms, you can find this here:
I wanted to also point out that research has also been carried out into lactate levels in the brain fluid of CFS patients, and was found to be higher. D-lactic acid crosses the bbb, and causes neurological changes that are said to be strikingly similar to CFS symptoms. Here is an abstract of a recent study.
Increased ventricular lactate in chronic fatigue syndrome measured by 1H MRS imaging at 3.0 T. II: comparison with major depressive disorder.
Murrough JW, Mao X, Collins KA, Kelly C, Andrade G, Nestadt P, Levine SM, Mathew SJ, Shungu DC.
Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.
Chronic fatigue syndrome (CFS), a complex illness characterized by fatigue, impaired concentration, and musculoskeletal pain, is often misdiagnosed as a psychiatric illness due to the overlap of its symptoms with mood and anxiety disorders. Using proton magnetic resonance spectroscopic imaging ((1)H MRSI), we previously measured levels of the major brain metabolites in CFS, in generalized anxiety disorder (GAD), and in healthy control subjects, and found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in CFS compared to the other two groups. In the present study, we sought to assess the specificity of this observation for CFS by comparing ventricular lactate levels in a new cohort of 17 CFS subjects with those in 19 healthy volunteers and in 21 subjects with major depressive disorder (MDD), which, like GAD, is a neuropsychiatric disorder that has significant symptom overlap with CFS. Ventricular CSF lactate was significantly elevated in CFS compared to healthy volunteers, replicating the major result of our previous study. Ventricular lactate measures in MDD did not differ from those in either CFS or healthy volunteers. We found a significant correlation between ventricular CSF lactate and severity of mental fatigue that was specific to the CFS group. In an exploratory analysis, we did not find evidence for altered levels of the amino acid neurotransmitters, gamma-aminobutyric acid (GABA) and glutamate + glutamine ('Glx'), in CFS compared to MDD or healthy controls. Future (1)H MRS studies with larger sample sizes and well-characterized populations will be necessary to further clarify the sensitivity and specificity of neurometabolic abnormalities in CFS and MDD.
Dr. Dikoma Shungu "will build on a preliminary study showing that brain fluid of CFS patients contains significantly elevated levels of lactic acid, or lactate, a substance important in metabolism." "If this study is successful, brain lactate levels could provide an objective diagnostic biomarker for CFS and evidence of a metabolic problem in these patients."
D-lactic acidosis is a condition that is almost exclusively taught to gastroenterologist's, however they only see it in patients with a shortened bowel, as these patients cannot fully digest carbohydrates due to surgery or disease of the small intestine. It is caused by d-lactic acid producing bacteria fermenting carbohydrates, which changes the pH of the bowel, favouring acid loving bacteria at the expense of other gut bacteria. D-lactic acidosis can present without a change in the anion gap, making it invisible in blood tests, unless specifically testing for. See below:
"There are two major ways acidosis is defined from routine laboratory data. First, organic acids may be added to the body so quickly that both the H and the anion are retained; this results in metabolic acidosis and an elevated value for the plasma anion gap. Second, metabolic acidosis may be present without a rise in the plasma anion gap. In this latter setting, either the D-lactate anion was retained in the lumen of the GI tract (with the H being absorbed or titrated by bicarbonate in the lumen of the GI tract), or it was excreted in the urine, but in either case, the cation lost with it was Na and/or K ion (not a H or NH4 ion). This latter type of metabolic acidosis is akin to the over-production of hippuric acid in glue sniffers. Since D-lactate anions are reabsorbed by the kidney much less readily than is L-lactate, as time progresses, the anion gap may decline without resulting in a rise in the plasma bicarbonate concentration-that is, D-Iactate is excreted as its Na or K salt (Fig. 6). Hence there are a number of mechanisms that may contribute to the presentation whereby the rise in the plasma anion gap might not match the fall in the plasma bicarbonate concentration. Not only might this lead to a diagnostic problem, it has implications for therapy because, once the organic anions are excreted as their Na or salts, these anions are no longer available for metabolism to regenerate bicarbonate, and the patient might have developed a deficit of Na and/or K4."
Path labs are not able to test for d-lactic acid, as they do not have the d-lactate assy kit required and would have to ship a test in, however I believe d-lactic acid can also be screened for in urine tests.
On a CFS discussion group I found the post below, from a lady saying she had tested for high levels of d-lactate, but this testing was not done through a GI, and I am presuming that the significance was lost on their doctors. Normal levels of d-lactate are between 0.0-0.25 in healthy individuals, and her levels were around 2.4mmol/L, which is the level that neurological changes occur in short bowel patients suffering from dla. They should have been urgently referred to a GI, for formal testing, treatment and monitoring of their d-lactic levels, until the levels returned to normal. It is seen as a serious condition. Treatment is antibiotics, sodium bicarbonate, either orally or IV and a low carb diet, in cases where there is a recurrence of d-lactic. It can be a case of trial and error, before the correct antibiotics are found, depending on the resistance of the bacterial overgrowth.
Here are some papers regarding d-lactic acidosis, however they are all in patients with a shortened bowel. The first one has a good graph of symptoms, which are very similar to some CFS symptoms. I would imagine that in a short bowel patient, their symptoms would be very severe, more so than in CFS.
This paper talks of the possibility that d-lactic acidosis may occur in a human with a complete bowel, when they were investigating d-lactic acidosis in a calf model. "The mechanism is likely similar to that documented for D-lactic acidosis in SBS in humans except the etiology of the malabsorption is viral infection induced villous atrophy rather than surgical removal of the small intestine."
It goes on to say
"There is a possibility, although it has not been described, that a similar scenario could occur in diarrheic monogastrics, including humans"
This one talks about d-lactate having a circadian rythm, so afternoon testing might show it up. Typically, patients would have normal serum lactate, but high urinary lactate, in an afternoon test, the high urine test would suggest d-lactate.
The main symptoms of d-lactic acidosis are severe lethargy, changes in gait and co-ordination, slurred speech, or difficulty in speaking, blurred vision, headaches, blunted judgement, abusive or aggressive behaviour, irritability, inability to concentrate, the feeling of being drunk in the absence of alcohol, hyperventilation, craving carbohydrates, nausea and nystagmus.
Sorry about the long post, hope it does not tire you out too much
How does this hypothesis account for those of us who do not have GI issues?
A minor point -- HHV-6 is an unlikely trigger because 98% (or more) of the population is infected with HHV-6 before the age of 2 and most, if not all, of us have the ME/CFS triggering event much later in life. All herpesviruses (HSV, chicken pox, EBV, HHV-6, CMV) remain latent in our bodies after the original, often minor, infection. Immune suppression allows herpesviruses to reactivate, which is probably the most common reason we see a disproportionate number of active herpesvirus infections in PWCs.
I wonder that too.
@Glynnis. That's news to me. Thanks for posting. Now a real interesting question would be; what would happen to the PWCs d-lactic acid levels if they were to get a faecal transplanation?
@SickofCFS thanks for asking. I am one of those (many) who don't feel any GI issues. I don't think we have to actaually feel the GI issues. If we were to have clostridium diff., (which we don't) the we would feel GI issues. But other clostridium bacteria (and other unwanted gut bacteria) doesn't have to make us symptomatic in the GI tract...
I don't know much about HHV6, my point was really that most immune surpressing events could possibly be triggers, because they may interfere with the body's ability to keep unwanted bacteria at bay in the gut. If you're saying HHV6 ain't one, then I'm buying that.
Then it is not all in the gut.
Sickofcfs asked: How does this hypothesis account for those of us who do not have GI issues?
I second that.
lansbergen. Just like newspapers normally keep the headlines simple and tabloid, I did the same. The headline is written "It's all in the gut. Why we get ME/CFS", just like Clinton's presidental campaign had the slogan "It's the economy. Stupid". Of course it's not just the economy.
So, what I did later on in my original post, was to specify:
"So, what if it's all (or mostly, is a more appropriate word) in the gut?"
As for the catecholemines not being broken down in PWCs, making symptoms worse, that was mentioned in the first post as a possible result of a dysfunctional gut flora (meaning harmful microbes inside there), and this was used as a source for that (the fact that gut problems can cause problems with breaking down the catecholamines)
There are several assumptions here that need to be addressed, such as whether or not their GI tests are accurate and whether or not the individuals really have CF/ME or some other subset or similar condition that is being misdiagnosed. There's too many variables to be able to address this theory with any conviction, especially using anecdotal evidence on an Internet forum.
It's an interesting discussion, and I am of the opinion that GI issues do indeed play a big part in this condition, but it's not like we are going to establish any definitive answer here.
I definitely agree with the gut hypothesis. I have had this condition for 18yrs. My onset was caused by EBV and I never thought that I had any major gut problems or food intolerances. I have now been a patient of KDM since November. Through hydrogen breath testing I now know that I am highly lactose intolerant and slightly fructose intolerant. Through his detailed testing (15 vials of blood sent to 5 labs in Europe and the U.S., plus saliva, urine and stool testing), I now know that I have ... in his words "a chronic inflammatory disorder, possibly associated with a gut-immune-neurotoxic disorder... fructose malabsorption and lactose intolerance, a gut dysbiosis and severel immune abnormalities. There seems to be an increased bacterial transfection from gut to blood (high sCD14)." I am also xmrv+ by serology. Since I started his treatment (end Jan), with a course of antibiotics every month interspersed with probiotics, plus a very rigid diet and also Nexavir and GcMAF, I have seen a lot of improvement. (plus high doses of VitB12, Chlorella and stomach meds).... I have lost 12kgs in weight (which I'm very glad to be rid of) and just feel so much more comfortable!!
KDM's theory is that we build up food intolerances which cause these gut problems, which in turn compromise our immune system making us vulnerable to these viral infections. I really believe he's on the right track.
Hope this makes sense as it's almost 1am here and I'm not thinking straight!!!
I thought we were discussing a hypothesis. Throwing out data simply because it doesn't fit the hypothesis is very, very far from the scientific way of evaluating the hypothesis.
I'll take your word for it for the moment since I don't feel like doing the background research tonight.
I still feel that the more straightforward explanation lies with a root cause that directly impairs the immune system allowing other infections to take hold. Over and over we find PWCs with infections that they should be able to clear or keep in latency -- Lyme, herpesviruses, unwanted gut bacteria and so on. I believe any postulated cause needs to address the question of why we are unable to suppress "normal" infections.
I suspect that the events we have historically called "triggers" are simply whatever immune insult finally overwhelmed an already dysfunctional immune system. For some of us it may be the time when the "bad" gut bacteria won out of the good; for others it may have been an infection. Persistent stress and vaccinations also tax the immune system and could, at the wrong time, overwhelm an overtaxed immune system.
So I don't disagree that unwanted gut microbes are a major player for many PWCs and that treating them will improve their quality of life. I believe the same is true for many other infections associated with ME/CFS -- if we were all effectively treated for (what I believe to be) secondary infections, we'd feel a lot better. Unfortunately, we're not getting that consistently.
I was actually encouraging the discussion by saying that we shouldn't get hung up on details that may not exactly fit...
Look for the research by Dr Montoya and Dr John Chia, plenty of discussions here on the forum. Coxsackie or some other polio-type eneterovirus. (Yes, polio is an enterovirus that causes neurologic damage). There are plenty of good viral candidates for a gut explanation for CFS.
GI issues may not be noticeable, don't always produce obvious symptoms. Many autistic and ADHD children, for example, have very serious GI issues but don't know about them, and unless someone looks they won't find them. I believe this is also related to the stage of CFS. I did not have any gut 'symptoms' for the first few years of my CFS, but I had already been partly disabled for over a year. when I had a severe biologic stress the gut symptoms and carbohydrate intolerance emerged.
I too think KDM is on the right track, but not sure about the food intolerance explanation. I believe the 'flu-like' illness is a better angle to explore this hypothesis. There are many flu-like illnesses that are GI infections, enteroviruses, etc. Some are pretty serious. There is evidence that CFS patients have B-cell abnormalities (immune cell problem), which can create problems fighting off enteroviruses.
B-cell abnormalities can be genetic, or acquired. If they are genetic, that can be a root cause. Maybe there are multiple scenarios, there was a study a few years back that showed 7 major subtypes of CFS. There might be many ways to get to the common CFS endpoint. That is pretty much the current thinking in Parkinson's disease, which now may be connected with CFS (the proteomic study). There is a small subset that has genetic Parkinson's, a family trait, or it can be acquired by neurologic injury, or by various triggers including many if not most of the CFS triggers (yes, Parkinson patients can have stress, viral infection, accident, random illness, etc as their trigger with or without the genetic traits). But in Parkinson's all the triggers lead to a common endpoint problem with dopamine regulation, etc.
I still think it's a legitimate question of the hypothesis, but let me be clear -- I do not consider it a denial of the hypothesis, just a question about how it might accommodate some of the data.
I agree with you that we're not going to make any ground-breaking discoveries with a small selection of "anecdotal evidence on an Internet forum". Nevertheless, I was born with a scientific mind and so I usually enjoy general discussions about the "why" of things. If other people are seeing this discussion as something else, I apologize for my casualness.
Yes, that could certainly be a root cause, whether genetic or acquired, although we would still need an explanation for how the B-cell abnormalities were acquired.
Possibly, but the argument of multiple scenarios doesn't stand up to Occam's Razor (http://science.howstuffworks.com/innovation/everyday-innovations/occams-razor.htm -- a simple discussion of Occam's Razor for those interested).
Yes, we know that Parkinson's Disease and ME/CFS appear to initiate with multiple triggers. Those triggers do not explain the root cause of the disorders, which is still unknown. Everyone who has stress, viral infection, accidents, etc, doesn't get PD or ME/CFS. Until we know why some fall victim while others don't, we have not come upon the root cause.
My comments were directed at another user that I thought was actually trying to find fault with the theory proposed here and I guess I was trying to get him to back off in what was probably a somewhat convoluted manner.
I certainly prefer these types of discussions to the incessant yammering on about XMRV, which I tend to believe isn't the cause of CFS/ME but an opportunistic bug... that is, if it even really exists.
Doctor's aren't really interested in helping patients out so much as they are in getting kickbacks and free trips to Hawaii for pushing drugs that are of questionable value. The medical industry has become completely degenerate to the point of being useless for anything other than enriching the shareholders of corrupt corporations. We're pretty much on our own here and need to figure this out the best we can.
I've been actively following Freddd's protocol, which I think is very promising, and feel that these sorts of user generated experiments are probably our best, maybe only, hope. A member named Catseye made numerous posts about how she worked with doctor Gary Farr on healing her digestive system for at least a year before moving on to other treatments like Methylation. I think this is potentially a very vital topic.
You can also try a Google Site Search
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