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Showing results for tags 'albicans'.
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Celiac.com 08/28/2024 - Celiac disease is an immune-mediated disorder triggered by gluten consumption, leading to damage in the small intestine of genetically predisposed individuals. Despite its rising prevalence, many aspects of celiac disease remain unclear. One area of interest is the relationship between Candida albicans, a common yeast in the human gut, and celiac disease. This study explores how Candida can shift from a harmless presence to a potential pathogen, influenced by various factors within the body, and its implications for celiac disease. Mast Cells and Their Role in Inflammation Mast cells are part of the body's innate immune system and are abundant in the gastrointestinal tract. They act as sentinels, responding to environmental changes and helping to regulate immune responses. In the context of celiac disease, mast cells can contribute to inflammation and increased intestinal permeability. When mast cells are activated improperly, they release substances that disrupt the intestinal barrier, leading to inflammation. Studies have shown that individuals with celiac disease often have an increased number of mast cells in their intestines, which correlates with the severity of their condition. Candida Albicans: Commensal or Pathogen? Candida albicans is typically a harmless resident of the gut, coexisting with the host's immune system and gut microbiota. However, under certain conditions, Candida can become pathogenic. Research suggests that Candida's transition from a commensal organism to a pathogen may be influenced by similarities between its components and gluten-related proteins that trigger celiac disease. This mimicry can activate the immune system inappropriately, leading to inflammation and tissue damage. Candida has been found in higher levels in individuals with celiac disease compared to healthy controls. This increased presence can exacerbate immune responses, potentially contributing to the intestinal damage seen in celiac patients. The ability of Candida to adhere to the intestinal lining and disrupt the barrier further complicates the situation, as it can promote a cycle of inflammation and increased gut permeability. The Role of IL-9 in Candida and Celiac Disease Interleukin-9 (IL-9) is a cytokine involved in regulating the immune system and maintaining the integrity of the intestinal barrier. In celiac disease, IL-9 levels are often elevated, which can lead to increased intestinal permeability and inflammation. IL-9 also influences the behavior of Candida, promoting its transition to a pathogenic state. This creates a feedback loop where increased IL-9 levels lead to more inflammation and Candida-related damage, worsening the symptoms of celiac disease. Tryptophan Metabolism and Immune Regulation Tryptophan is an essential amino acid that plays a crucial role in maintaining immune balance in the gut. It can be metabolized by the host and gut microbiota into various bioactive molecules, including kynurenines and serotonin, which help regulate immune responses and maintain gut homeostasis. In celiac disease, disruptions in tryptophan metabolism can contribute to inflammation and impaired immune tolerance. Research has shown that individuals with celiac disease often have altered gut microbiota, leading to changes in tryptophan metabolism. This can result in a reduced ability to control immune responses, further exacerbating the condition. Additionally, tryptophan metabolites like kynurenines can promote regulatory T cells, which help maintain immune tolerance. However, in celiac disease, the function of these regulatory cells may be impaired, contributing to ongoing inflammation. Conclusion: Implications for Celiac Disease Patients The study highlights the complex interplay between Candida albicans, the immune system, and tryptophan metabolism in the context of celiac disease. Understanding these relationships can provide new insights into potential therapeutic approaches for managing celiac disease. For individuals with celiac disease, maintaining a strict gluten-free diet is crucial, but addressing underlying factors such as Candida colonization and immune regulation may offer additional benefits. This research is meaningful for celiac patients as it underscores the importance of a comprehensive approach to managing the disease. By targeting factors like mast cell activation, IL-9 levels, and tryptophan metabolism, new treatments could be developed to reduce inflammation and improve gut health, potentially leading to better outcomes for those with celiac disease. Read more at: ncbi.nlm.nih.gov
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Lancet. 2003 Jun 21;361(9375):2152-4. Celiac.com 08/25/2003 – This interesting study compares a specific amino acid sequence found in Candida cell wall protein to a the gliadin amino acid sequence that triggers the immune response in celiac disease. The researchers found that the sequences are "identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes," and propose that Candida is the trigger for the onset of celiac disease. Below is the abstract for this study. Is Candida albicans a trigger in the onset of coeliac disease? Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ. Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains amino acid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.
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Celiac.com 05/31/2006 - Most patients, upon reporting their fear to their doctor that they may have chronic candida infection throughout the intestinal tract, are met with a sneer, a frown, and a chuckle. Most physicians scoff when the large bowel is mentioned as an infected site. However, the Merk Manual, commonly found and held in esteem in any doctors office says that Candida is "Usually transmitted sexually, the infection can also spread from the intestine. The increased incidence is partially due to indiscriminate use of broad-spectrum antibiotics and a large number of women taking contraceptive pills." It also includes corticosteroids (Cortisone) as a possible predisposing factor.(1) Further, a paper printed in "The Journal of the American Medical Association" in 1977 stated: "Vaginal Candidiasis does not occur naturally without infection of C. Albicans within the large bowel and that a cure is not likely as long as the vagina remains the only treatment target."(2) To make matters even more interesting, other inhabitants of the gastrointestinal tract can cause a disruption of the ecology of the large bowel, allowing an overgrowth of C. Albicans. These pathogens also produce gastrointestinal distress and allergic reactions similar to Candida. These microbes or pathogens can lead to an incorrect diagnosis of Candida Albicans, if the doctor is using questionnaires or considering symptoms alone! A partial listing of pathogens would include Aeromas and Plasiomonas, Campylobacter je juni, Citrobacter species, Clostridium difficile, Enterobacter species, Mucoid E. coli and Hemolytic E. Coli, Klebsiella, Pseudomonas and Yersinia Enterocolitica.(3) All can produce similar symptoms to that of a patient with true over-colonization of Candida Albicans. So while the research states Candida can occur both vaginally and in the large bowel, then allowing the broad-spectrum of symptoms we hear about to occur, it also needs to be clarified when another possible microbe is causing the Candida-like symptom. You, the reader, must be careful in allowing yourself and your doctor to begin a Candida regimen before it is documented that you have C. Albicans and not some other pathogen. Any disturbance in your intestinal flora can allow the above mentioned pathogens to begin their dirty work. C. Albicans is not the only opportunist who is waiting for you to use broad spectrum antibiotics. Dont go by symptoms alone! Diagnostic Tools Unfortunately, most tests being used by well-meaning practitioners have drawbacks and require more interpretation than might be currently realized. Stool cultures and rectal mucus swabs have been found of no diagnostic value.(4) That is a rather strong statement bound to offend many people. However, consider these facts. "C. Albicans organisms do not distribute homogeneously throughout the G.I. tract, rather they are found on plaques in the mucosal surfaces and streak scattered throughout the fecal material."(4) In application, this datum means consistent contact with the over-colonization of C. Albicans by fecal matter is not guaranteed due to the nature of growth of C. Albicans. It does not evenly spread itself throughout the bowel. This makes it a matter of chance whether the fecal matter or rectal swab will contact an area which contains C. Albicans. It is true that C. Albicans inhabits the mucosal surface, but in plaques. It is a matter of judgement by the practitioner ! whether the fecal or rectal swab reading is indicative of over-colonization, since everyone does have some Candida Albicans in their bowel. Good practitioners knowing this will want several consecutive negative readings before pronouncing the patient clear of Candida. Also, the amount that qualifies as a true overgrowth in the stool can be a controversy. The true value of a stool culture is in determining the amounts of friendly bacteria relative to unfriendly bacteria, and to discover the presence of harmful bacteria which can weaken the friendly flora, allowing yeast to grow and live. The practitioner who takes into account response to therapy, other biochemical tests which would reveal immune response and mineral absorption in addition to the stool or rectal swab stands a better chance of understanding the patients status. A popular test for detection of antibodies against Candida also has drawbacks. First, a decrease in the antibodies may not mean the patient is doing better, it could mean a decreased immune response. Other biochemical tests are needed to interpret this. An increase in the antibodies may indicate an increase in immune response and not a worsening of the patients health. Many times these antibodies will increase when immune status indicators improve, showing an increase in immune response. So this test also needs to be carefully interpreted. A new test that shows great promise, as it has none of the previously mentioned drawbacks, is the Candisphere Enzyme Immuno Assay. The main difference between this test and other blood studies for C. Albicans is that it is not influenced by the "external" antigens of C. Albicans that are harmless, produced constantly by small "normal" colonies of C. Albicans. Only large numbers of colonies producing a hidden cytoplasmic antigen are reported. This hidden antigen must make its presence known to the bodys immune defenses in order to produce many of the typical symptoms. An overgrowth cannot be missed as with stool or mucus swabs. A blind control treatment study for the FDA revealed a 92% correlation between therapeutic response and test response. The test is now available in the New York City area. I hope this data can be used to clear up some of the confusion both holistic and orthodox practitioners have on this subject. Michael Biamonte holds a Doctorate of Nutripathy, a Degree in Natural Healing, and a Masters in Clinical Nutrition. He is affiliated with the International Academy of Clinical Nutritionists and the International Academy of Nutrition and Preventive Medicine. He is listed in "The Directory of Distinguished Americans" for his research in Nutrition and Physiology. For more info also see: Does Candida Albicans Trigger the Onset of Celiac Disease? References: The Merk Manual, 14th Edition, pages 1625-1626. Miles Mr, Olsen L. Roger A. Recurrent Vaginal Candidiasis, JAMA 238, Pages 1836-1837; 1977. Great Smokies Lab Medical Lab Parasite/Pathogen Primer. Progress in diagnosing. Candida related complex. David Bauman, Ph.D. For an appointment, contact our office at: Michael Biamonte, C.C.N. 139 Fulton St. Suite 507 New York, NY 10038 (212) 587-2330
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