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and why einstein is speculate on candida when a microbiologist girl said to me that candida is not scientist aproove and dosen't really exist?i'm confused maybe someone can explain me what is candida?and what kind of candida a women can have?
 

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There are two separate things when it comes to Candida infections.1) Totally accepted and scientific and medically known infections.In the vagina--Vaginal Yeast infectionsIn the mouth--Thrush, most common in babies, but others can get it (esp woman who don't wash hands well with vaginal yeast infections)And in people who are SEVERELY immuno-deficient and in whom EVERYTHING else that normally doesn't grow in people grows in them (like people with AIDS who get bird diseases and stuff like that) it can grow rampantly through the body and make you EXTREMELY ill (we aren't talking I have a bit of diarrhea and brain fog sick we are talking need to be in the hospital sick).2) The Candida Hypothesis.This got going in the 1980's and 90's and won't die.This is the pretty much everyone has Candida running rampent in their bodies but instead of making you severely ill like in the above medical thing it causes pretty much every vague and not so vague symptoms of every disease and disorder known to man.It is pretty much the latest of the things that people tell the "worried well" that they have. Before this the common one was hypoglycemia and it is probably about time we get a new one...something like every 10-20 years someone comes up with something to explain why people don't feel 100% totally perky and healthy every single moment of every single day because if you aren't in the utmost peak of health with every breath something TERRIBLE MUST BE WRONG WITH YOU!!!!!!This is the one your microbiologist friend said didn't exist.K.
 

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The candida theory's didn't begin in the 80-90's but actually started in the early 1900's.In fact, the Dr. who first believed in beneficial bacteria in the colon won the Nobel Prize in Medicine for it. Your immune does not have to be completely shut down for Yeast, bacteria, parasites or other pathogens to create GI Symtoms. Understanding the role that beneficial bacteria play & the importance to your health is beeing studied/researched as we speak. These are not some odd-ball Drs. who have these feelings.
 

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OK...al the alt med people jumped on the Candida bandwagon starting in the 1980's which was when I remember a whole bunch of articles in the lay press and a bunch of things showed up in the medical lit where doctors took a look see then dropped it.WHO SAID EVERY PATHOGEN ONLY INFECTS IMMUNO COMPROMISED PEOPLE...SHEESH.Putting frigging words in my mouth..SIGH.Some pathogens are adapted to VERY EASILY infect all of a given species. SOME infect ONE AND ONLY ONE organism...like say SMALL POX....some infect most warm blooded animals like say RABIES.Most are somewhere in between. In severely immunocompromised people you find things that DO NOT NORMALLY infect people causing big problems.Yeast normally infects VAGINA's AND MOUTHS.If you have AIDS or take cancer drugs it can get a severe hold on your whole body and land you in the Intensive Care Unit.SIGHBut you believe whatever fairy tales you like. Just STOP PUTTING STUPID IDIOTIC STATEMENTS IN MY MOUTH THANK YOU
K.
 

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DavidLA,i completely agree with you. things usually work on a continuum. it is foolishness to think that only when a person is near death that they will then be succumbed by yeast. if a person has abused antibiotics and consumed a high sugar diet combined with a dysfunctional immune system then they can easily have a yeast overgrowth condition.it is NOT an either/or proposition. rather it can just gradually happen. all the while the body is fighting it with all the resources that it can muster. this can go on for years until CFIDS set in or something else.the reason that it has not been proven YET. is because the whole issue is rather complicated. by the time the patient has the condition -- multiple other problems are well under way. the only good scientific experiment would be to lock up people for 6 to 12 months who are suspected of candida overgrowth and monitor every thing they eat and do (including antifungal drugs) so that everything is controlled. a control group would also need to be locked up and not treated.....experiments like this are out of the realm of what people are willing to put themselves through. it is infeasible. the thousands of people who have been successfully treated will have to be the evidence which is good enough for me.david keep up the good work!!!
 

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Have you heard abouf Helicobacter Pylori ?Well ok here is the rough outline - I don;t have the exact details but it's well know so you could find them anywhere.H. Pylori is a bug that has been found to be responsible for 90% of peptic ulcers and a lrage proportion of gastric ulcers also.It's easy to treat with a course of antibiotics.Before it was recognised - treatment was generally by surgery - with all sorts of nasty side effects - such as a risk of dying.Around about 1980 (ish) an Australian Doc (whose name escapes me right now) discovered the H. pylori bug. But the medical establishment would not aceppt his findings as the scientific dogma of the time was that nothing could live in the extremely acidic gastric environment.It took theis doctor something like 10 years of fighting to have his findings recognised, even though he provided evidence to support his theroy the H. pylori was responsible for causing peptic ulcers.In the end - he persuaded the setablishment - not with scientific evidence - but with the following stunt. He infected himself with a large dose of h. pylori. Sure enough he soon developed and ulcer. THen he cured himself with a course of antibiotics.Low and behold - suddenly people believed him.Incidnetally it is not thought that h pylroi itself causes peptic ulcers - merely that it is a risk factor. There are many people who walk around with h pylori and don't develop ulcers - it's jsut that they are more likely too.Now for those doubting thomas's out there - I do not have any references for this story - but it's a pretty famous one -so go look it up yourselves - I'm sure there's been a few books on the subject by now.So now - when we talk abouit candida, IBS etc. Who knows whether there is a connection or not - no-one can give a definitve answer to that - in all the talk on here - I have not seen one bit of real evidence for or against IBS. Dreamers - ask your microbiologist friend on what she bases her opinion - ask for evidence that it doesn't exist.The only thing I know is this - I was diagnosed by a GI specialist asa having IBS 7 years ago. For the past 6 months I have been treated on the basis of having a candida overgrowth - and it has worked for me. -I no longer experience the symptoms of IBS
 

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MECKLE,you bring up an excellent point about the h. pylori bacteria. actually they knew about this a long time before the 1980's but the scientists would not listen to the evidence.meckle, i am glad you are doing better. i was treated for yeast with Lamisil and nystatin back in december and i have improved about 75%. i used to experience horrible symptoms every single day, but now i am symptom free approx. 4 out of 7 days. i am still reacting to all my food intolerances that may or may not be a result of the candida in my system. i think my immune system has been beaten up pretty good and it will take a while to come back.i sometimes wonder if all of this is real. it seems to good to be true.
 

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quote:it is NOT an either/or proposition. rather it can just gradually happen.
No, you are confusing two different things. Something that exists and something that somebody just made up.
quote: But the medical establishment would not aceppt his findings as the scientific dogma of the time was that nothing could live in the extremely acidic gastric environment.It took theis doctor something like 10 years of fighting to have his findings recognised,
This is silly argument:1) Barry Marshall (the discoverer) actually documented it. Truss fabricated Candida.2) H. Pylori causes specific symptoms that make sense. Candida is blamed on lot of symptoms that don�t make a lot of sense.3) H. pylori must be treated with antibiotics while Candida can supposedly succumb to a diet low in sugar as if that has some magical antifungal property. Perhaps we should treat H. pylori the same way.That it took 10 years to establish the discovery in the medical community is a good thing. Science needs a lot of proof before it accepts something that turns current thinking around 180 degrees.
quote: actually they knew about this a long time before the 1980's but the scientists would not listen to the evidence.
They? Who are they? This is false. The evidence was first uncovered in 1983.
 

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quote:No, you are confusing two different things. Something that exists and something that somebody just made up.
Once again flux - you give your opinion -where is your definitive proof that candida overgrowth does or does not occur ? You cannot provide any can you. As with the other possible causes of IBS, the candida postulate is a theory - it is not conclusively been proved or disproved. However - you there is EVIDENCE supporting candidias in the form of 1. gut fermentation test2. stool sample tests3. colonic irrigation therapist scan see candidia whilst performing CI'sIs it the one true cuase of IBS - nobody can say - it as one of many possible causes.
quote: H. Pylori causes specific symptoms that make sense. Candida is blamed on lot of symptoms that don�t make a lot of sense.
There may be those who claim all sorts of symptoms for candidias. However I am not one - there are specific symptoms of candidias and they do make sense. You may not be aware of them - tarring all proponents of the candida postulate with the same brush. THis is your failure to edcuate yourself properly on the subject. I suggest as an introduction that you read the book I have mentioned on several occasions.
quote:3) H. pylori must be treated with antibiotics while Candida can supposedly succumb to a diet low in sugar as if that has some magical antifungal property. Perhaps we should treat H. pylori the same way.
Candida will NOT succumb to a diet low in sugar. Your symptoms will remain - however the candida will remain. You need to take antifungals in order to kill the candida. This often leads to "die-off" reactions as the dead candida gives out many toxins - and you feel awful.
quote: That it took 10 years to establish the discovery in the medical community is a good thing. Science needs a lot of proof before it accepts something that turns current thinking around 180 degrees.
A good thing huh ? Tell that to the relatives of the THOUSANDS of people who died during unnecessary surgery - and the thousands more who suffered there chronic condition when it could have been cured with a short course of antibiotics.Science needs proof, yes. It also needs scientists to be open-minded and free from vested interests in order to properly.I am not a doctor - and I am not offering medical opinion. I am merely sharing the information that has helped me to get rid of my IBS symptoms.
 

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Antibiotics and antifungals can cause side effects that could make you feel bad beyond any "die off" reaction. They are poisons after all, just ones that hurt other organisms more than they hurt you.Yep, people get hurt with traditional medicine, but at least it learns from those mistakes and moves on. People also get hurt all the time by alt. med practices as well, but the mechanism for change seems to be less rigorous. When people get hurt, nothing seems to change. I have always found the logic that the sicker the treatment makes you the more it must be working rather stange...but many practices include that mostly IMO as an article of faith. All treatments must make you much worse before you get better.Science won't believe you the first time you say "the hoofbeats you hear are a unicorn" Science says prove it. When the definitive experiments get done Scientific types go "wow, that really is a unicorn".In alt med/pseudoscience no matter how much you show that they horn is glued on, the DNA is identical to a horse, and that the photos were doctored they still seem to say "I don't care what evidence you have, I it is a unicorn".But that is just my experience of both processes.K.
 

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quote:Antibiotics and antifungals can cause side effects that could make you feel bad beyond any "die off" reaction. They are poisons after all, just ones that hurt other organisms more than they hurt you.
No doubt - I completely agree. But what about the side effects of pharmaceutical drugs ? Personally I would rather take antifungals for a couple of months and havbe my problem solved - than take HT3, or Ach antagonists in order to merely control my symptoms - ie with no end in site. Thes drugs also have their side effects.
quote:Yep, people get hurt with traditional medicine, but at least it learns from those mistakes and moves on. People also get hurt all the time by alt. med practices as well, but the mechanism for change seems to be less rigorous. When people get hurt, nothing seems to change.
Again I completely agree. But you tar all alternative meds with the same brush. Alt meds - have a lot to offer - but if they are not taken seriously and properly evaluated by trad med - than trad med are failing in their objectivity. My point is - you don't dismiss all of alternative medicine because you don;'t like the way they work.
quote:I have always found the logic that the sicker the treatment makes you the more it must be working rather stange...but many practices include that mostly IMO as an article of faith. All treatments must make you much worse before you get better.
No idea what your talking about - nobody here said anything about having to get worse before you get better. It just happens to be the case when experienced candida die-off. It also happen s to be the case when yu get chemotherapy.
quote: Science won't believe you the first time you say "the hoofbeats you hear are a unicorn" Science says prove it. When the definitive experiments get done Scientific types go "wow, that really is a unicorn".
No I wouldn't expect it to either. But when they evidence is there - I do expect science to listen. I sugegst you get over your image that science is an objective establishment. It isn't. Scientists are human - they have their preconceptions, their vested interests and their bigotries just like anyone else. 10 years to accept h. pylori when the evidence for h pylori was clear is unacceptable. The evidence was there - it was scientifc DOGMA that prevented it's acceptance - the idea that nothing could survive in such a higly acidic environment - it was NOT science FACT.A quote I heard a few years back - though I forget who it was that said it (nnot good with names I'm afriad !!!) I think it was a physicist.
quote: Science progresses one funeral at a time.
 

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COMMENT: LOL ___________________________________"Putting frigging words in my mouth..SIGH." ____________________________________AND _____________________________________"Just STOP PUTTING STUPID IDIOTIC STATEMENTS IN MY MOUTH THANK YOU " _____________________________________At least be assured you are not the Lone Ranger!TontoNL
PSThis thought comes to my mind whenever anyone takes soemthing I said and morphs it into something else, then sets it (the metamorphosed item) forth as "evidence" of my supposed ignorance or that of my "teachers":"What is character, but the determination of incident?And what is incident, but the determination of character?"Henry James
 

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Oh now THIS was REALLY GOOD!!! ______________________________"Science progresses one funeral at a time." ______________________________I only wish everyone could see for themselves at least once in their lives what I have seen during that part of my career which was "in hospital", so as to realize how chillingly true this statement is. The Grim Reaper really is the most omnipresent bedside instructor I ever met in my entire life. ...and the most articulate.MNL
 

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It's my impression that this argument about alternative approaches is ike beating a dead horse with a stick? Doctors are accepting that which works ad the evidence supports. if you look at the recent mainstream article in Archives of Internal medicine, for example, you'll see what's been proven and what hasn't yet. it seems ike it's up to the rest of alternate medicine to get with the agenda.. Its like what happened with hypnosis. It's now proven itself, the evidence is there, it's part of non-alternative medicine.tom
 

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Yeah Mike.No doubting your experience there - but I believe the subtlety of my point has eluded you.The point was this - the preferred paradigm in a given field is rarely overturned until the scientific "big names" in that field pass to the great beyond. Thus giving other theories a chance to proliferate without fear of ridcule from either - the big name him/herself - or his or her dogmatic supporters.TomYou are assuming the science actually wants to examine alternative medicines. Don't get me wrong - I think most of alternative medicine is horse-**** - but I've seen enough to know that some of it isn't. Most scientists are unwillinging to challenge ther own preconceptions though regading alternative medicines. Further - what funding body will actually devote funds into investigating alternative meds - they might discover something important - but they might not. They can't be seen to be wasting money - so they take the safer bet. So once again baby gets thrown out with the bath water.
 

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quote:Once again flux - you give your opinion -where is your definitive proof that candida overgrowth does or does not occur ? You cannot provide any can you. As with the other possible causes of IBS, the candida postulate is a theory - it is not conclusively been proved or disproved. However - you there is EVIDENCE supporting candidias in the form of 1. gut fermentation test 2. stool sample tests 3. colonic irrigation therapist scan see candidia whilst performing CI's
It is up to the people who claim that it exists to provide proof it. Barry Marshall did this for H. plyori, but no one has documented Candida. Your statement is pure fabrication.
quote:there are specific symptoms of candidias and they do make sense.
No, all the claims are for a lot of nonspecific symptoms which do not make sense.
quote:Candida will NOT succumb to a diet low in sugar. Your symptoms will remain - however the candida will remain. You need to take antifungals in order to kill the candida.
What's the logic in altering diet at all? Why not alter the diet for H. pylori in the same way?
quote:Science needs proof, yes. It also needs scientists to be open-minded
That's why we now have accepted H. pylori has primary cause of ulcers.
quote:But what about the side effects of pharmaceutical drugs ? Personally I would rather take antifungals for a couple of months and havbe my problem solved - than take HT3, or Ach antagonists in order to
But you have no evidence for having Candida other than that bogus test.
quote:But you tar all alternative meds with the same brush. Alt meds - have a lot to offer - but if they are not taken seriously and properly evaluated by trad med
Nope. There is only one medicine. What works. If it works, it eventually does become incorporated in medicine. Most of the alternative stuff had been abandoned ages ago because it was found not to work. On occasion, something gets past and is rediscovered: arsenic for cancer, which is an ancient Chinese remedy.
quote:It also happen s to be the case when yu get chemotherapy.
No, chemotherapy is toxic and it always hurts you.
 

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Scientific PROOF! Candida does not cause IBS.Everybody on the bb here who has IBS should log into medscape which requires a password, but it is TOTALLY FREE,They do not spam email you and they send IBS and gastroenterology updates in the email and have an IBS resource center with all new current IBS information.Its really easy to get into it and way worth the valid and important information on IBS!Irritable Bowel Syndrome: Taking Concepts Into Clinical Practice CMEChairperson: Michael D. Gershon, MD; Faculty: Kevin W. Olden, MD; Walter L. Peterson, MD; Nicholas J. Talley, MD, PhD; Gervais Tougas, MD, CM, FRCPC http://www.medscape.com/viewprogram/1985
 

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some highlights of the above information, for those that can get into medscape.Dr Michael D. Gershon, MD is the worlds leading authority on the enteric nervous system and the person directly responsible for learning about the role of serotonin in the enteric nervous system and the role it plays in the functioning of the gut and the role it plays in communicating to the brain. http://www.hosppract.com/issues/1999/07/gershon.htm Quotes from the Medscape information."Return to Irritable Bowel Syndrome: Taking Concepts Into Clinical PracticeIntegrating Current Concepts of Causality: Towards a Unifying HypothesisGervals Tougas, MDPhenomenology, Pathophysiology, and Symptomatology of Irritable Bowel SyndromeSlide 1. Integrating Current Concepts of Causality: Towards a Unifying HypothesisSlide 2. OutlineMy brief is to review 6 main points:Look at how a phenomenon, a set of symptoms, relates to, or at least begins to relate to, a definable pathophysiologyTry to see to some extent how and why patients with irritable bowel syndrome IBS experience visceral painGet back to this area of mind and gut, and how events that seem to influence primarily psychological constraints, such as stress and psychological factors, will play a role in the perception of symptoms originating from the gutRemind us that in addition to these factors, primarily luminal and enteric factors, such as certain food types, infection, or inflammation, can also interact with these central nervous system CNS factors to produce painBegin to look at the role and the place of serotoninergic mechanisms in the modulation of these thingsLook at this in the broader sense of IBSSlide 3. Phenomenology and PathophysiologyWe know that in terms of its phenomenology, IBS is a condition that's associated with altered brain-gut communication. Pain plays a major role so that we have alterations, or at least generation of abnormal sensation within the gut. Emotions can modulate these symptoms to a large extent, but at the end they also have alterations of function characterized in general by either constipation or diarrhea. This is largely due to alterations of neuromodulation at the level of the enteric neurons and also at the level of central and autonomic pathways.""Return to Irritable Bowel Syndrome: Taking Concepts Into Clinical PracticeIntegrating Current Concepts of Causality: Towards a Unifying HypothesisGervals Tougas, MDPhenomenology, Pathophysiology, and Symptomatology of Irritable Bowel SyndromeSlide 1. Integrating Current Concepts of Causality: Towards a Unifying HypothesisSlide 2. OutlineMy brief is to review 6 main points:Look at how a phenomenon, a set of symptoms, relates to, or at least begins to relate to, a definable pathophysiologyTry to see to some extent how and why patients with irritable bowel syndrome (IBS) experience visceral painGet back to this area of mind and gut, and how events that seem to influence primarily psychological constraints, such as stress and psychological factors, will play a role in the perception of symptoms originating from the gutRemind us that in addition to these factors, primarily luminal and enteric factors, such as certain food types, infection, or inflammation, can also interact with these central nervous system (CNS) factors to produce painBegin to look at the role and the place of serotoninergic mechanisms in the modulation of these thingsLook at this in the broader sense of IBSSlide 3. Phenomenology and PathophysiologyWe know that in terms of its phenomenology, IBS is a condition that's associated with altered brain-gut communication. Pain plays a major role so that we have alterations, or at least generation of abnormal sensation within the gut. Emotions can modulate these symptoms to a large extent, but at the end they also have alterations of function characterized in general by either constipation or diarrhea. This is largely due to alterations of neuromodulation at the level of the enteric neurons and also at the level of central and autonomic pathways.Slide 4. The Many Facets of IBSIBS has many dimensions. The symptom complex itself is characterized by abdominal discomfort associated with altered bowel habits. In addition to these, though, there is a substantial psychological comorbidity in many patients. At the same time, we have frequent extraintestinal manifestations associated with poor sleep, fatigue, changes in libido, and loss of energy, and a number of other symptoms, that often overlap with symptoms in the gut, outside of the colon, such as dyspeptic symptoms or noncardiac chest pain.We also know from increasing literature that many of these patients have other symptoms including irritable bladder, chronic fatigue, fibromyalgia, headaches, and a number of other symptoms. This is related to a number of abnormalities, some of them having to do with autonomic dysregulation and visceral hypersensitivity, altered pain modulation, abnormal health-seeking behavior and, to some degree, iatrogenesis.""Slide 5. Symptoms, Pathophysiology, and Pathogenesis in IBSIf we try to integrate this into a coherent map, we have symptoms that are subjectively definable, which then are associated with a series of complaints, either diarrhea, constipation, or abdominal pain, the whole spectrum of IBS. There is a pathophysiological basis to these symptoms that will vary in individual patients but seems to involve abnormalities of perception, epithelial function, and in some patients, motility, which then leads to symptom generation, and involves both external stressors, psychological stress, as well as genetic abnormalities and inflammation at the peripheral level.""Return to Irritable Bowel Syndrome: Taking Concepts Into Clinical PracticeIntegrating Current Concepts of Causality: Towards a Unifying HypothesisGervals Tougas, MDPhenomenology, Pathophysiology, and Symptomatology of Irritable Bowel SyndromeSlide 1. Integrating Current Concepts of Causality: Towards a Unifying HypothesisSlide 2. OutlineMy brief is to review 6 main points:Look at how a phenomenon, a set of symptoms, relates to, or at least begins to relate to, a definable pathophysiologyTry to see to some extent how and why patients with irritable bowel syndrome (IBS) experience visceral painGet back to this area of mind and gut, and how events that seem to influence primarily psychological constraints, such as stress and psychological factors, will play a role in the perception of symptoms originating from the gutRemind us that in addition to these factors, primarily luminal and enteric factors, such as certain food types, infection, or inflammation, can also interact with these central nervous system (CNS) factors to produce painBegin to look at the role and the place of serotoninergic mechanisms in the modulation of these thingsLook at this in the broader sense of IBSSlide 3. Phenomenology and PathophysiologyWe know that in terms of its phenomenology, IBS is a condition that's associated with altered brain-gut communication. Pain plays a major role so that we have alterations, or at least generation of abnormal sensation within the gut. Emotions can modulate these symptoms to a large extent, but at the end they also have alterations of function characterized in general by either constipation or diarrhea. This is largely due to alterations of neuromodulation at the level of the enteric neurons and also at the level of central and autonomic pathways.Slide 4. The Many Facets of IBSIBS has many dimensions. The symptom complex itself is characterized by abdominal discomfort associated with altered bowel habits. In addition to these, though, there is a substantial psychological comorbidity in many patients. At the same time, we have frequent extraintestinal manifestations associated with poor sleep, fatigue, changes in libido, and loss of energy, and a number of other symptoms, that often overlap with symptoms in the gut, outside of the colon, such as dyspeptic symptoms or noncardiac chest pain.We also know from increasing literature that many of these patients have other symptoms including irritable bladder, chronic fatigue, fibromyalgia, headaches, and a number of other symptoms. This is related to a number of abnormalities, some of them having to do with autonomic dysregulation and visceral hypersensitivity, altered pain modulation, abnormal health-seeking behavior and, to some degree, iatrogenesis.Slide 5. Symptoms, Pathophysiology, and Pathogenesis in IBSIf we try to integrate this into a coherent map, we have symptoms that are subjectively definable, which then are associated with a series of complaints, either diarrhea, constipation, or abdominal pain, the whole spectrum of IBS. There is a pathophysiological basis to these symptoms that will vary in individual patients but seems to involve abnormalities of perception, epithelial function, and in some patients, motility, which then leads to symptom generation, and involves both external stressors, psychological stress, as well as genetic abnormalities and inflammation at the peripheral level.Slide 6. Visceral Pain in IBS"To summarize, we know that there is alteration of visceral perception. There are good data to that effect and increasingly sophisticated ways to measure this, but in most patients, visceral hypersensitivity seems to play a role. In a substantial group of patients, luminal events, in particular infection and some degree of mild irritation, can alter visceral perception and lead to symptoms. Psychological factors also play a role in altering visceral perception and the vigilance to symptoms originating from the gut.""Slide 7. Increased Sensitivity to Balloon Distention in IBS PatientsOne of the most convincing studies was done by Bradette and coworkers. This was a simple study that looked at differences in visceral perception to balloon distension in patients with IBS and compared it to healthy subjects. Both the threshold to discomfort and the threshold to pain were much lower in patients with IBS than in healthy controls, suggesting that, in fact, there was visceral hypersensitivity in those patients.""Slide 8. fMRI Imaging With Rectal Distension in IBSThings have progressed a fair bit since then and we can demonstrate that, in addition to symptomatic abnormalities, there are significant differences that we can see between IBS patients and control subjects using functional magnetic resonance imaging fMRI, brain imaging, during colonic distension. These abnormalities are in 2 main parts. One is the somatosensory areas of the brain and the other is the prefrontal cortex region of the brain, each of which deals with different aspects of pain symptomatology.""Slide 9. Altered Pain Perception in IBSUp to 95% of patients with IBS will have altered pain perception. They will have lower thresholds, so they experience symptoms at much lower volumes than healthy controls. They also have an increased intensity of the sensation elicited by distension at a given volume, and they have increased referral of these sensory perceptions in response to rectal distension when compared with healthy patients.This is not something that we see very often in normal subjects and there's also different somatic pain perception in a subset of IBS patients, but by no means all.""Slide 10. Different Sensations, Different DestinationsWhy would that be? There are 2 regions in the brain that are involved with the perception of visceral sensation. The first one is the somatosensory cortex that is associated with the perception of noxious stimulation and painful stimuli. This region closely interacts with the limbic system, which is the part of the brain that is involved with the neuroendocrine and autonomic responses associated with the perception of pain. This is more of a hard-wired reflex area, but it plays a very important role in modulating responses in areas involved more directly with pain perception. These areas are also associated with aspects such as mood, hedonic behavior, and motivation, which play a very important role in the psychological make-up and modulation of these visceral sensations.""Slide 11. Visceral Pain and the Autonomic PathwayA lot of this is mediated through autonomic responses, and the important aspect here is that perception of pain in itself elicits responses that will then, in turn, alter the response and the reactivity of the gut. Eliciting painful visceral sensation will involve activation of sympathetic spinal afferents that, in turn, will lead to homeostatic visceral responses that will be associated with vagal afferent responses leading to symptoms such as satiety, nausea, and even bloating. These afferent pathways will then lead to efferent responses that are associated with visceral perception. And this is important because these pathways can in turn modulate the intensity of the afferent input.""Slide 12. Key ConceptsTo summarize, IBS patients display evidence of a central hyperresponsiveness to visceral stimuli and events, and this occurs at the level of the brain. In response to these pain stimuli, IBS patients have a visceral hyperresponsiveness to luminal events and also to central, more psychologically derived events, and this is occurring at the level of the gut. The understanding of these mechanisms is still evolving and begins to explain the 2 dimensions that we see with IBS patients, pain and altered bowel function.""Slide 13. Emotions and Visceral PerceptionEmotions modulate pain perception by several dimensions. One of them is that if you've experienced unpleasant or uncomfortable symptoms, you will have an increased vigilance to these visceral stimuli. And to some degree, the same seems to be occurring at the level of visceral pain. This involves both cortical and brain stem nuclei and a large degree of autonomic modulation. The central nervous system increases the perception of symptoms at the level of the gut. There is a clear presence of visceral hyperalgesia that can be related in many situations and experimental paradigms to very early trauma during childhood or infancy, and also seems to be associated with very stressful, psychological events, such as abuse or posttraumatic stress disorder. This raises the issue of whether there is an element of neuroplasticity involving altered perception in addition to the cortical activation that comes from altered symptoms.Furthermore, a number of studies have shown that patients with IBS have altered autonomic activity. While this is not completely described yet, it is associated with an increase or altered visceral responsiveness in many of these patients. A final aspect is that these symptoms lead to increased health-seeking behavior and use of healthcare.""Slide 14. Auditory Stress Alters Perceptual and Emotional Ratings of Visceral StimuliOne of the best studies looking at this is a study that looked at auditory stress and showed that an unpleasant external stressor, a noise in this case, altered both the perceptual and emotional rating that you experience in response to a visceral stimulus. In this study published a year ago, a control subject had responses that were measured in response to either a relaxing stimulus or a stressful stimulus, a conflicting sound in both ears. In patients with IBS, the same stimulus led to an increased degree of unpleasantness at set pressure distension. Similarly, it had the same effect on the anger rating, a psychological measure of psychological stress.""Slide 16. Enteric Factors and IBS SymptomsWhen we look at the other dimension, enteric factors, many patients tell us that certain foods will produce symptoms. It is difficult to determine whether this is a pharmacological, a chemical, or even an immune mechanism. Also, low-grade inflammation is present in a small subset of patients with functional symptoms. There is increasing awareness that in the substantial group of patients, although the proportion remains to be determined, infectious events seem to lead to the subsequent development of IBS. Sometimes this occurs as a single precipitant, but in many studies the biggest predictor of the subsequent development of symptoms following an enteric infection is other factors, such as psychological stress or an adverse life event a few weeks or a few months preceding the infection. Clearly, there is a role for infections but this is in association with central factors.Slide 16. Enteric Factors and IBS SymptomsWhen we look at the other dimension, enteric factors, many patients tell us that certain foods will produce symptoms. It is difficult to determine whether this is a pharmacological, a chemical, or even an immune mechanism. Also, low-grade inflammation is present in a small subset of patients with functional symptoms. There is increasing awareness that in the substantial group of patients, although the proportion remains to be determined, infectious events seem to lead to the subsequent development of IBS. Sometimes this occurs as a single precipitant, but in many studies the biggest predictor of the subsequent development of symptoms following an enteric infection is other factors, such as psychological stress or an adverse life event a few weeks or a few months preceding the infection. Clearly, there is a role for infections but this is in association with central factors.""Slide 17. Pathophysiology of Postinfectious IBSIn postinfectious IBS patients, there is accelerated gut transit in many patients, increased visceral sensitivity, and evidence for alteration of intestinal permeability, something very relevant to chronic diarrhea in these patients. There's clear evidence in many patients of increased presence of enterochromaffin EC cells in the colon. Therefore, there is the possibility of increased release of serotonin 5-HT in these patients.""Slide 18. Serotonin and the Neural Control of Digestive FunctionsSerotonin is involved at just about every level of the communication between gut and brain, both going from gut to brain and then from brain to gut. One appealing therapeutic avenue is to focus on the site where most of the 5-HT is being released and try to affect outcome and symptoms by modulating symptoms at the level of the gut trying to avoid the possible side effects that may come with more central modulation of serotoninergic pathways.""Slide 19. Plasma 5-HT Levels in IBS vs ControlsWe know that 5-HT release is actually increased in IBS patients with the diarrhea-dominant component, suggesting that, again, 5-HT may play a role in subsets of patients with IBS.""Slide 20. Serotonin and EC Cells in Altered GI MotilityThis may be further demonstrated in the sense that there is increased circulating 5-HT in patients with diarrhea-dominant IBS and increased EC cell population in the gut, whereas in some subgroup of patients with chronic constipation, there appears to be a decreased number of EC cells suggesting that, if we stimulate serotoninergic pathways, we might be able to improve symptoms in these patients.""Slide 21. SummaryIn summary, IBS is affected and modulated by many factors. Some of them have to do with emotional dimensions, others are more related to visceral function and sensation. This is probably, to some extent, associated with a dysfunction or a disorder of gut-brain communication involving both afferent and efferent pathways going to and from the gut. There is good evidence to suggest that 5-HT is a central mediator in the regulation of these visceral functions, and its modulation may provide an appealing form of therapy for a proportion of patients with IBS."
 

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Eric,How exactly is that scientific proof that candida does not play a role in IBS ?First off - it's not a piece of primary reseacrh - but a synopsis of various sources.Secondly - it doesn't even mention candida.How exactly do you understand the concept of scientifc proof ?
 

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quote:How exactly is that scientific proof that candida does not play a role in IBS ?
I think what Eric is trying to say is that Candida is not on the radar of IBS experts. The reasons for that are as described above that 1) nobody has been formally documented to suffer from it, 2) that it causes symptoms that often don't make sense and the 3) some of the treatments couldn't help if it somehow were true.And of course, actual evidence.. http://www.ncbi.nlm.nih.gov:80/entrez/quer...2&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...6&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...1&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...3&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...0&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...7&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...6&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/quer...7&dopt=Abstract
 
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