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    Does Candida Albicans Trigger the Onset of Celiac Disease?


    Scott Adams

    Lancet. 2003 Jun 21;361(9375):2152-4.


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    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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    Very interesting to know, why do the doctors not make the connection?

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    Guest Trina

    Posted

    Very interesting to know, why do the doctors not make the connection?

    Before being recently diagnosed with celiac disease, I spent quite a few years with symptoms of Candida which I had to research myself and try to convince doctors that my symptoms were not anxiety or depression related. I did not need therapy or more drugs to fix it. My symptoms were real, and I usually got very laid back, vague responses. I couldn't get anyone to take it serious and felt like a hypochondriac. It wasn't until my symptoms got progressively worse in the last 4 years to the point where I had to request a celiac (from a new doctor) test as a last resort did I finally get help. I would say the whole process took ten to fifteen years from the time I noticed the first symptoms. A few weeks ago I actually mentioned this to my nutritionist if there was a connection. So this proves my theory! It was not something she was aware of for sure.

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    Guest Beauty and the Yeaast

    Posted

    Before being recently diagnosed with celiac disease, I spent quite a few years with symptoms of Candida which I had to research myself and try to convince doctors that my symptoms were not anxiety or depression related. I did not need therapy or more drugs to fix it. My symptoms were real, and I usually got very laid back, vague responses. I couldn't get anyone to take it serious and felt like a hypochondriac. It wasn't until my symptoms got progressively worse in the last 4 years to the point where I had to request a celiac (from a new doctor) test as a last resort did I finally get help. I would say the whole process took ten to fifteen years from the time I noticed the first symptoms. A few weeks ago I actually mentioned this to my nutritionist if there was a connection. So this proves my theory! It was not something she was aware of for sure.

    I too have suffered for YEARS with Candida and Celiac. Here's my full story, and I'm so thankful to see that the connection has been made by others as well.

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    This is 100% accurate, and if you clean the candida the gluten sensitivity is gone.

     

    The reason the medical industry doesn't tell you about it, is because people will wonder what caused the naturally occuring candida, to overgrow. Then they would see it's the antibiotics, or meat and dairy products (filled with antibiotics). Once you ingest any of these 3 forms of antibiotic, even just one time, your good bacteria all dies from your gut, and candida then overgrows.

     

    So of course they wouldn't want a similar reaction to antibiotics. Once people catch on just like they did with the autism vaccine link.

     

    They feel it doesn't matter if you know this truth or not, because the benefits (their fattening pockets) outweigh the risks (your death or ill health)

     

    Also candida cleanses won't work because they only clear the candida in the gut and wont address the candida that became fungus and spread along the body. Only Jeff McCombs cleanse is proven to clear the entire body. It is a difficult cleanse I know, but it is worth it. Do it and feel better than you have in years!

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    Guest Teresa

    Posted

    Before being recently diagnosed with celiac disease, I spent quite a few years with symptoms of Candida which I had to research myself and try to convince doctors that my symptoms were not anxiety or depression related. I did not need therapy or more drugs to fix it. My symptoms were real, and I usually got very laid back, vague responses. I couldn't get anyone to take it serious and felt like a hypochondriac. It wasn't until my symptoms got progressively worse in the last 4 years to the point where I had to request a celiac (from a new doctor) test as a last resort did I finally get help. I would say the whole process took ten to fifteen years from the time I noticed the first symptoms. A few weeks ago I actually mentioned this to my nutritionist if there was a connection. So this proves my theory! It was not something she was aware of for sure.

    I too have for many years suffered and been told that I have Candida Albicans in my body. Meaning stomach, blood stream, intestines etc..

    All the doctors that I saw waved off the condition as not possible unless I had been deathly sick like with Cancer and such. I read "The Yeast Syndrome" many years ago and stopped handing over my money to doctors who would give me no reason accept for depression.

    Now that I am older the condition had worsened so that I went to a G.I. who ran tests and concluded that I had Irritable Bowel Syndrome.

    Finally, He began, after almost a year, to consider the possibilities of celiac disease. I have not yet been diagnosed, still in the testing stages, but since my cousins all have it I am thinking I am a prime candidate. I totally understand people's frustration about getting so many tests and then diagnosis is a guess at best.

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  • Related Articles

    Scott Adams
    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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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
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    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
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    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
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    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023