FYI:The role of faecal Candida albicans in the pathogenesis of food-intolerant irritable bowel syndrome. Middleton SJ, Coley A, Hunter JO Department of Gastroenterology, Addenbrooke's Hospital, Cambridge, UK. Candida albicans was sought in stool samples from 38 patients with irritable bowel syndrome and 20 healthy controls. In only three patients with irritable bowel syndrome was C. albicans discovered and these patients had either recently received antibiotics or the stool sample had been delayed more than 24 hours in transit. C. albicans was isolated from none of the control stool samples. We conclude that C. albicans is not involved in the aetiology of the irritable bowel syndrome. Comments: Comment in: Postgrad Med J 1993 Jan;69(807):80 PMID: 1437926, UI: 93065844 ------------------ http://www.ibshealth.com/
The role of faecal Candida albicans in the pathogenesis of food-intolerant IBS
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Here's Some newer Stuff...Even the Europeans Are not Studying It. And they Study Everything!-----------------------------------Fortschr Med 1996 Sep 20;114(26):319-21 [Pathogenicity of Fungi in the Intestines--Current Status of the Discussion]. [Article in German]Scheurlen M Medizinische Poliklinik, Universitat, Wurzburg.The hypothesis that colonization of the intestinal tract by yeasts (e.g. Candida albicans) can lead to disease in immunocompromised individuals is currently being discussed controversially. Proponents assume that toxins produced by the fungi can trigger such complaints as irritable bowel syndrome of the chronic fatigue syndrome, and that such chronic or recurrent infections may be caused by an intestinal reservoir of yeasts. Opponents of the hypothesis, however, point out that no hard data on the pathogenetic significance of an intestinal reservoir of yeasts are available, controlled studies have failed to demonstrate the effectiveness of antifungal treatment. Discussions are however, hampered by a lack of objective data. The postulated pathomechanisms therefore need to be clarified, diagnostic criteria developed, and the efficacy of the proposed therapeutic measures shown by controlled studies. Until this has been done, assumption about the pathogenicity of yeasts in the bowel, cannot be taken as a basis for binding therapeutic recommendations.-------------------------------------The only place chronic diarrhea and candida is being studied, therefore one cannot say much about it, is in immunocompromised patients (opportunistic infection):--------------------------------Sante 1997 Nov-Dec;7(6):349-54 Related Articles, Books, LinkOut [A clinical and biological study of parasitic and fungal diarrhea in immunosuppressed patients in an urban and suburban area of Yaounde]. [Article in French]Same-Ekobo A, Lohoue J, Mbassi A Laboratoire de parasitologie, mycologie et immunologie parasitaire, CHU de Yaounde, Cameroun.We studied 66 cases of intestinal mycosis and parasitosis in patients infected with the human immunodeficiency virus with chronic diarrhea. All subjects were from the Yaounde urban area and were followed between February and December 1996. They were recruited from 3 hospitals in the center of Yaounde and were aged between 2 and 52 years. There was weight loss in 80.3% and severe dehydration in 72.3% of cases. Feces consisted mostly of watery stools similar to those of cholera patients (50% of cases) and loose stools (43.9% of cases). Parasitic agents were detected in 31.8% and fungal agents in 80.5% of cases. The opportunistic Protozoans detected included Cryptosporidium parvum (15.8%), microsporidia (8.8%) and Isospora belli (3.5%). Six cases of helminthiasis were also identified. Candida albicans was the most common opportunistic mycosis agent (39.1%). Other fungal species detected included Geotrichum candidum, Candida pseudotropicalis and Trichosporon sp. but all of these were less common.---------------------------------Nobody is even looking for it as related to IBS except that it can occur as a complication (superimposed mycotic infection). At least I have had it twice, (actually probably once, and the initial course of antifungal therapy was probably insufficient and it recolonized) if no one else ever has (on this planet). But it did not cause my IBS it aggravated it. And some IBS patients come up reactive to candida, which they should not (not pathogenic) unless infected (or post-infection if it became allergenic). This is unclear. Do not know if the rate is higher than in the general population (ie: no epidemiologic data). ------------------------MNL____________________________________ www.leapallergy.com [This message has been edited by Mike NoLomotil (edited 09-21-2000).][This message has been edited by Mike NoLomotil (edited 09-21-2000).]
All I have to say is this:1. I was slow-transit IBS diagnosed while on birth control pills over 20yrs. ago.2. I had frequent soft stooling, and bloating epsiodes while on antibiotic therapy for over a year. This continued for a few years until diagnosed by an allergist M.D. findings of a high sensitivity to candida molds. Diflucan (antifungal) took care of the frequent soft-stooling and proctalgia pain associated with it (which I believe was actually proctitis, but they unfortunately did not do a biopsy at the time of my colonoscopy). They also failed to take me off the antibiotic - duh! I finally took myself off when my gyno scraped the yeast from my vagina post hyster for endometriosis.3. I also have fibromyalgia, which quite possibly began as chronic fatigue syndrome, but undiagnosed (their symptoms are over-lapping, and mine began with fatigue and flu-like symptoms).4. Both endometriosis and fibro/cfs site Candida as a fairly common occurrence in books/literature containing research. It has been suggested that cfs/fms may stem from an HHV-6 virus as this also shows up frequently but has not been proven as yet. This would put them in the autoimmune category (they are listed on some autoimmune sites on the web). It has also been suggested that Endo may be caused by PCB toxins which may compromise the immune system.Does this mean Candida caused my IBS? Not necessarily. It is possible that some people have been misdiagnosed with IBS, when if they would have been treated for candida or a different bacterial over-growth or parasite, their bowel symptoms would have subsided.Another possibility for the cause might be that an autoimmune response precipitated by the use of a medication causing the fungal/other microbrial overgowth makes ones system overly sensitive to it. They say if one keeps ignoring a sensitivity response/continues to be exposed to a substance, the immune system may eventually over-load.Be it a toxin, virus, bacteria, parasite, or genetic predisposition of a sensitivity to a substance, it remains unclear. At any rate, the sensitivity or a immune response often involves spasming to occur. Spasming of the colon can cause stool and gas to be trapped which can be painful. This can result in slow transit or constipation. The other result of continual spasming may result in fast transit or frequent stooling.The argument as I see it is: Does IBS initially stem from a biological genetic defect in the brain/gut causing the spasm response, or does the CNS become aggravated or even altered from a substance introduced from the environment as mentioned above either acquired after birth or passed on in utero? We could argue back and forth about these, but the fact is that scientists are not sure of the answer yet.Some people have success controlling their symptoms with meds like antispasmotics. Some have better results with diet. I was able to control my symptoms of slow transit with nothing other than a higher fiber diet for twenty years until antibiotics. For this the antifungal worked to balance out my flora again, along with a low sugar/no fermented/aged foods diet for what I would guess might be due to a malabsorption of sugars resulting from the over-growth. I hope to eventually control it with probiotics and diet only. Each individual has there own degree of bodily/mind "disfunction" whether genetic, sensitivity to a substance, or infection. We all have different factors to a degree, which makes it all the more complicated to figure out.In short eric, what else can I say? It fits my profile, but maybe not yours or others on this board. If you notice, it doesn't dispute the fact that candida exists or can cause problems. It just states it is not implicated in the majority of IBS patients. It is possible for the two to co-exist in some patients, however.
I was diagnosed (or rather misdiagnosed) with Candida ten years ago by a number of alternative MD's. One of them put me on yeast injections to build up my immune system. I was also given anti-fungal meds. Theses treatments, the shots in particular had the effect of worsening my IBS considerably. In the intervening ten years, I haven't seen anything to raise my opinion of this "diagnosis".
I am sorry for your misfortune badfoot of falling into the hands of perhaps unqualified alternative practioners. I really don't know how the procedure went 10 yrs. ago. Perhaps, unfortunately, some learned by the mistakes of others.I went intitally to an unqualified "quack", I will call him, as I later found out he was formerly a Psychiatrist switched to an Integrative Medicine Wannabe. Although he studied under my allergist and later opened his own practice in a different city, his techniques were not near the same. I was fortunate I didn't give him the chance to treat me, because of a gut/suspicious feeling.My allergist is an M.D. who started out as a Family Practitioner and then went on to school to be an Allergist and has practiced for over 25yrs, starting his own team of allergists.Candida is a very potent irritant for those who are sensitive, and the calculations need to be as precise as possible for each individual. I was given the antigen drops customized for me and seem to handle them well. The testing was a double-blinded provocative sublingual challenge which is the gold standard today.Antifungals are another treatment that seems to be variable by many practioners. Some are not on enough, some too much, and not monitored properly. Of course if one does not have Candida in the first place, just like if one does not have C. Difficile in the first place, the treatment can do much more harm than good. Unfortunately many doctors prescribe without the proper medical testing and investigation of the medical history that goes along with the diagnosis. I am not surprised that you are less enthused about the notion of candida. Just as good results have made me a believer, harmful results made you a disbeliever.
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MOLDIE.You wrote: "It is possible for the two to co-exist in some patients, however."Ditto. I am another one wherein intestinal candidiasis PATHOGENICALLYwas a complication I suffered which episodically worsened my IBS. An agressive antifungal course remediated it. You are not the only case on the planet, though badfoot is correct that it can be misdiagnosed without too much trouble by one who uses the wrong indicators to arrive at a diagnosis. And treatment when candida is not pathogenic to the person can do more harm.----------------Only to remark on one other area of your prior speculation...chicken vs egg relationship between neuroimmune reactivity and the hypersensitive gut in IBS (esp. D type predominant).Various findings of certain intracellular (granular), and synthyseized mediators associated with both immunologic and non-immunologic mediated hypersensitivity reactions have been published as findings at various times in groups of patients with 'IBS" symptomologic sets. The findings have been variable as to the % of patients noted to have, say, prostaglandin E2 in the feces, or leukotrines or cytokines in the sera or extravascular fluid. In large part technologic limitations of some of the methods available have made it difficult to get consistent findings. PArt is also due to the simple lack of mass-funding for this research angle as it is non-pharamceutically directed, whereas focusing in neurotransmission instead of what elicits the abnormality produces drug products as the end game. While the mechanics of signal exchange between the CNS and peripheral structures and the gut structures can be looked at and analyzed, this does not reveal why there is "excessive reactivity" (ie: lowered stimulus threshoild to elicit a repsonse, and excesive reponse of the smooth muscle to the stimuli, for example).However, that being said, newer technology applied to whole blood analysis of patients with IBS symptomologic sets (and a numbser of others)which I have the opportunity to personally witness on a daily basis shows end-point (quantitative not qualitative) reactions to one or more foods and chemicals in every IBS patient sample. This is an exciting finding, and the basis for interest among the practitioners I get to work around...granulocytic cells selectively destabilizing and discharging their contents into the plasma (along with lymphocytes and platelt reactions) is the source of the circulating immunologic and cytotoxic reaction mediators in question which trigger a known series of reactions within the body which produce known responses. these are seen in "IBS" (reactive gut would be a better nam could we start over).Their effects when elicited are well established systemically and locally on neuromuscular structure and function.The last step, which we will be working with the likes of Dr. Brostoff, Sandberg, Gilderman and other experienced and respected investigators on during the next 18 months, will be to match the quantitative reactions found with the preferred methods of quantification of the specific mediators (leukotrines, cytokines, etc) being released by IBS patients (and other symptom sets)which elicit the "twitchy gut phenom" of IBS,(or migraine, or fibro) both by local direct effect and via systemic effects on the CNS.These observations suggest strongly that the hypersensitivity reaction chemical products provide the underlying stimulus which increses the reactivity of the neuromusculature affeberently, efferently and the intrinsic contributions to motor control in the gut. These are released directly in the gut circulation and in the systemic circulation. This makes even more sense in the context of the newly evidenced interconnectivity of the gut with the immune systems structural elements.This is why I have said before I feel from what I have seen that the etiology and its understanding is only separated from revelation by the amount of money that can be raised to complete the work. The smoke and fire are both visible daily to a small number of lab personnel and clinciains using the results. That will change since Dr. B. has agreed to supervise the next level of development, and several other very capable doctors are involved as well as I mentioned.Just some local activity to share.Have a DFDMNL_______________ www.leapallergy.com [This message has been edited by Mike NoLomotil (edited 09-28-2000).]
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