Irritable Bowel Syndrome Message Boards | Why IBS Is NOT caused by Candida

Hopefully this post will help explain it and the actual diagnoses of IBS itself. There are some major misunderstanding about diagnosing IBS, the term IBS- a distint enity- A lower GI disorder of function. And people's frustration and looking for all the things that could cause it. However, some have already been ruled out, some important ones are being researched and some DON"T apply to begin with.

You can read it or not. But I hope it really helps some people. I will continue to add information to it, so its not all at once.

First its important to go over IBS itself. There are some 28 GI disorders of function, some examples are IBS, functional dyspepsisa, functional D, functional c, functional analrectal disorders ect..

The diagnoses of IBS is based on a specific cluster of symptoms. It is NOT a catch all diagnoses.
"What Patients Know About Irritable Bowel Syndrome (IBS) and What They Would Like to Know. National Survey on Patient Educational Needs in IBS and Development and Validation of the Patient Educational
Posted 09/18/2007

"The most prevalent IBS misconceptions included (% of subjects agreeing with the statement): IBS is caused by lack of digestive enzymes (52%), is a form of colitis (42.8%), will worsen with age (47.9%), and can develop into colitis (43%) or malnutrition (37.7%) or cancer (21.4%). IBS patients were interested in learning about (% of subjects choosing an item): (1) foods to avoid (63.3%), (2) causes of IBS (62%), (3) coping strategies (59.4%), (4) medications (55.2%), (5) will they have to live with IBS for life (51.6%), and (6) research studies (48.6%). Patients using the Web were better informed about IBS.
Conclusion: (1) Many patients hold misconceptions about IBS being caused by dietary habits, developing into cancer, colitis, causing malnutrition, or worsening with age; (2) patients most often seek information about dietary changes; and (3) educational needs may be different for persons using the internet for medical information."

"The emerging research typifies IBS as a brain-gut disorder where psychosocial factors (e.g., stress, cognitions, coping, etc.) can alter the symptoms and illness experience for better or worse. Due to these and other disease specific characteristics, that are amenable to education, we believe effective educational interventions may significantly impact the management of this common disorder."

Patients Consider IBS a Diagnosis of Exclusion: Over 50% of the patients considered IBS to be a "catch all" diagnosis and another 22% were unsure. While this could reflect the information provided by their physicians (thus highlighting the need to also educate physicians about IBS), this misconception may motivate patients to seek more and more diagnostic studies to find "the cause." The use of the Rome criteria[17] permits the patient to have a positive diagnosis. With confidence in knowing that IBS is a specific entity , such behaviors are minimized. Thus it is important for the physician to provide proper education about the level of confidence in the diagnosis.

http://www3.interscience.wiley.com/journal/117956426/abstract?CRETRY=1&SRETRY=0

Hopefully also it will help when talking to your doctor.

NEVER self diagnose. The leading cause of misdiagnoses is self diagnoses. Some conditions that mimick some IBS symptoms are also very serious and even potentially deadly.

First though is the change in diagnosing IBS that has been made.

"In the past two decades, medical opinion has changed regarding how to diagnose IBS. The older view emphasized that IBS should be regarded primarily as a "diagnosis of exclusion;" that is, diagnosed only after diagnostic testing excludes many disorders that could possibly cause the symptoms. Because many medical disorders can produce the cardinal IBS features of abdominal discomfort or pain and disturbed bowel habit as well as other symptoms caused by IBS, this approach often led to extensive diagnostic testing in many patients. Since the era when such thinking about IBS was common, laboratory, motility, radiologic, and endoscopic tests have proliferated. Although each of these tests is useful in evaluating certain problems, their routine or indiscriminate use can cause unnecessary inconvenience and cost for patients, and complications even occur infrequently from some of the tests. Fortunately, physicians can now diagnose IBS in most patients by recognizing certain symptom details, performing a physical examination, and undertaking limited diagnostic testing. This simpler approach is grounded on recent knowledge of the typical symptoms of IBS, and it leads to a reliable diagnosis in most cases. Extensive testing is usually reserved for special situations."

http://www.aboutibs.org/Publications/diagnosis.html

Diagnosis
Patients with IBS can be confidently and correctly diagnosed using the Rome criteria in conjunction with a complete history and thorough physical examination (reviewed by Lacy and De Lee The utility of routine laboratory testing is widely debated, however, especially in those presumed IBS patients with diarrhea predominance, because of concern regarding the possibility of missing the diagnosis of celiac disease or inflammatory bowel disease (IBD). During ACG 2006, studies were presented that evaluated the utility of tests commonly ordered in the evaluation of some IBS patients. Two separate studies[27,28] reported on the diagnostic accuracy of serologic markers for celiac disease and IBD in a prospective, multicenter, observational trial involving 323 patients with IBS symptoms (mean age = 39 years; 68% women) and 241 controls referred for routine colon cancer screening (mean age = 54 years; 43% women). Routine laboratory tests (complete blood count, thyroid-stimulating hormone, and electrolytes), testing for specialized IBD serologic markers (antineutrophil cytoplasmic antibodies, IgA, and IgG anti-Saccharomyces cerevisae antibodies, and anti-OmpC antibodies [outer membrane porin to Escherichia coli]), serologic tests for celiac disease (anti-gliadin, anti-endomysial, anti-tissue transglutaminase antibodies), and colonoscopy were performed in all patients. Patients with serologic evidence of celiac disease also underwent upper endoscopy with biopsies of the small intestine. In this large group of subjects, only 2 patients with IBS symptoms were diagnosed with IBD. In fact, IBD serologic markers had a false-positive rate of 30%, and this finding was similar in both control and IBS patients. Tests for celiac disease were more frequently positive in IBS patients (7.4%) than in controls (2.9%); however, biopsies confirmed the diagnosis of celiac disease in just 1.24% of IBS patients and 0.8% of controls. No single antibody test for celiac disease identified all patients with biopsy-proven celiac disease. This large, ongoing prospective study demonstrates that celiac disease is uncommon in patients with IBS, that no single antibody test can accurately diagnose all patients with celiac disease, and that serologic tests for IBD have a high false-positive rate. Testing for these disorders should thus be limited to those IBS patients with persistent symptoms who fail to respond to standard therapy and should not be routinely performed in all IBS patients.Two other studies presented during this meeting that discussed testing in IBS patients warrant mention. In the first of these studies, Whitlock and colleagues[29] measured lactoferrin, a marker of activated neutrophils, in stool specimens from 94 IBD patients, 22 IBS patients, and 27 healthy controls (mean age, race, and sex breakdown not provided). Although raw data were not included, the study authors reported that fecal lactoferrin differentiated active IBD from IBS patients and healthy controls with 100% sensitivity and specificity. In addition, the test appeared to be highly accurate in differentiating active IBD patients from inactive IBD patients. These preliminary results are very interesting and warrant confirmation in a multicenter, prospective trial. In the second study,

http://www.medscape.com/viewarticle/547772

Celiac disease is one of the conditions they are looking at in regards to a misdiagnoses.

However Celiac is NOT IBS and it has symptoms such as weight loss and other symptoms that can differentiate for IBS, by a knowledeable doctor.

Celiac does not always cause pain either. It is estimated in about 2 % percent of the population and is still some what underdiagnosed. It also has a close genetic relationship, so if family members have it is could be a very good idea to be screened.

If your looking for very accurate Celiac information this is one of the Doctors.

Dr Green is the Director of The Celiac Disease Center at Columbia University

http://www.celiacdiseasecenter.columbia.ed...3-StaffBios.htm

Further research showed a slightly higher celiac population.

So they are saying now that certain people should be tested for celiac.

Next I will post about the rome criteria hopefully used to diagnosed IBS. Als a little on researchers and the rome criteria and local gi doctors and the rome criteria.

Rome III Journal Articles: Gastroenterology, April 2006
The Rome III book was published in condensed form in a journal supplement that appeared in Gastroenterology (volume 20, issue 5, May 2006) the official journal of the American Gastroenterological Association. The Rome Foundation obtained permission to post the journal articles on our website for download by the American Gastroenterological Association Institute.

Table of Contents

The Functional Gastrointestinal Disorders and the Rome III Process
D. A. Drossman

Fundamentals of Neurogastroenterology: Basic Science
D. Grundy, E. D. Al�Chaer, Q. Aziz, S. M. Collins, M. Ke, Y. Tach�, and J. D. Wood

Applied Principles of Neurogastroenterology: Physiology/Motility Sensation
J. E. Kellow, F. Azpiroz, M. Delvaux, G. F. Gebhart, H. R. Mertz, E. M. M. Quigley, and A. J. P. M. Smout

Pharmacological and Pharmacokinetic Aspects of Functional Gastrointestinal Disorders
M. Camilleri, L. Bueno, F. de Ponti, J. Fioramonti, R. B. Lydiard, and J. Tack

Gender, Age, Society, Culture, and the Patient's Perspective in the Functional Gastrointestinal Disorders
L. Chang, B. B. Toner, S. Fukudo, E. Guthrie, G. R. Locke, N. J. Norton, and A. D. Sperber

Psychosocial Aspects of the Functional Gastrointestinal Disorders
R. L. Levy, K. W. Olden, B. D. Naliboff, L. A. Bradley, C. Francisconi, D. A. Drossman, and F. Creed

Functional Esophageal Disorders
J. P. Galmiche, R. E. Clouse, A. B�lint, I. J. Cook, P. J. Kahrilas, W. G. Paterson, and A. J. P. M. Smout

Functional Gastroduodenal Disorders
J. Tack, N. J. Talley, M. Camilleri, G. Holtmann, P. Hu, J.-R. Malagelada, and V. Stanghellini

Functional Bowel Disorders
G. F. Longstreth, W. G. Thompson, W. D. Chey, L. A. Houghton, F. Mearin, and R. C. Spiller

Functional Abdominal Pain Syndrome
R. E. Clouse, E. A. Mayer, Q. Aziz, D. A. Drossman, D. L. Dumitrascu, H. M�nnikes, and B. D. Naliboff

Functional Gallbladder and Sphincter of Oddi Disorders
J. Behar, E. Corazziari, M. Guelrud, W. Hogan, S. Sherman, and J. Toouli

Functional Anorectal Disorders
A. E. Bharucha, A. Wald, P. Enck, and S. Rao

Childhood Functional Gastrointestinal Disorders: Neonate/Toddler
P. E. Hyman, P. J. Milla, M. A. Benninga, G. P. Davidson, D. F. Fleisher, and J. Taminiau

Childhood Functional Gastrointestinal Disorders: Child/Adolescent
A. Rasquin, C. Di Lorenzo, D. Forbes, E. Guiraldes, J. S. Hyams, A. Staiano, and L. S. Walker

Design of Treatment Trials for Functional Gastrointestinal Disorders
E. J. Irvine, W. E. Whitehead, W. D. Chey, K. Matsueda, M. Shaw, N. J. Talley, and S. J. O. Veldhuyzen van Zanten

The Road to Rome
W. G. Thompson

http://www.romecriteria.org/rome_III_gastro/

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My website on IBS is www.ibshealth.com

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No problem, I feel it is really needed at this point, because of the recent posts that cause more confusion on the actual diagnoses of IBS and the cause/causes.

People are posting IBS is an infections disease or food allergy, or toxins or bacterial infection, or fungus, or pathogens this is totally inaccurate. Those condition if some exist at all to begin with are not IBS, but there own seperate conditions.

Experts are working very hard to validate functional gi disorders as real seperate entities.

I will get to the candida in a bit here.

Next a history of the funtional Bowel disorders.

This is from the President of the Rome commitee to diagnosed functional disorders.

History of Functional Disorders

THE PAST
HISTORICAL PRECEDENTS
Historians and physicians have documented the presence of Functional GI disorders throughout
recorded human history. However, until recently, limited attention has been granted to these
disorders due to the lack of identifiable pathology and the absence of a conceptual framework to
understand and categorize them. Systematic investigation of functional GI disorders did not
begin until the middle of the 20th century, and prior to this time, only occasional reports of
functional GI symptoms were published, the first appearing only 200 years ago.
Over the past 25 years, scientific attention to understanding and properly caring for patients with
functional GI disorders has grown progressively. With the understanding comes the rationale for
use of medications directed at intestinal receptors as well as psychopharmacological, behavioral,
and psychological forms of treatment. Additionally, there has been an increase in the rate of
scientific publications and greater media exposure to the public through television, radio, and
Internet.
To understand the historical classification of these disorders, two differing theories relating to the
interaction between the mind and body should be considered."

More explain in the document.

'THE PRESENT
CONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERS
o The recent acceptance of functional GI disorders as legitimate medical entities is
based on the following three developments:
o The concept of the Biopsychosocial model of illness and disease
o The development of new investigative methods for studying disease
o The development of the Rome Criteria
Biopsychosocial Model
In 1977, the publication of the concept of the Biopsychosocial model by George Engel, and its
later demonstration specifically for gastrointestinal disorders, marked an important change in
thinking. A biopsychosocial model of illness and disease provides the needed framework to understand, categorize, and treat common GI symptoms. These symptoms are the integrated
product of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and often
are influenced by psychosocial factors. Figure 1 illustrates the proposed relationship between
psychosocial and physiological factors with functional GI symptoms and the clinical outcome.
Early in life, genetics and environmental influences (family attitudes toward bowel training or
illness in general, major loss or abuse history or exposure to infection) may affect one's
psychosocial development (susceptibility to life stress, psychological state, coping skills, social
support) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity).
Additionally, the presence and nature of a functional GI disorder is determined by the interaction
of psychosocial factors and altered physiology via the brain-gut axis. In other words, one
individual afflicted with a bowel disorder but with no psychosocial disturbances, good coping
skills and adequate social support may have less severe symptoms and not seek medical care.
Another having similar symptoms but with coexistent psychosocial disturbance, high life stress,
or poor coping skills may frequent his physician's office and have generally poor outcome.

DEVELOPMENT OF NEW INVESTIGATIVE METHODS
The second concurrent process has been the expansion and refinement of investigative methods
that allow the study of functional GI disorders in terms of biological, cultural, and psychosocial
(i.e. brain) influences. These developments include:
1. the improvement of motility assessment,
2. the standardization of the barostat to measure visceral sensitivity,
3. the enhancement of psychometric instruments to determine psychosocial
influences,
4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution to
symptoms, and
5. the molecular investigation of brain-gut peptides, which provide insight into how
these symptoms become manifest.
In less than ten years, these methods have produced new knowledge of the underlying
pathophysiological features that characterize the age-old symptoms we now define as functional
GI disorders.

ROME CRITERIA
The Rome Criteria is an international effort to characterize and classify the functional GI
disorders using a symptom-based classification system. This approach that has its precedents
with classification systems in psychiatry and rheumatology. The rationale for such a system is
based on the premise that patients with functional GI complaints consistently report symptoms
that breed true in their clinical features, yet cannot be classified by any existing structural,
physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria,
which was developed from discriminate function analysis of GI patients.
The decision to develop diagnostic criteria by international consensus was introduced as part of a
larger effort to address issues within gastroenterology that are not easily resolved by usual
The UNC Center for Functional GI http://www.med.unc.edu/ibs
& Motility Disorders
4
scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria,
which ultimately resulted in the publishing of many articles in Gastroenterology International
and a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)".
Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in
2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the Rome
Coordinating Committee has met to begin Rome III, expected to be published in 2006. To learn
more about the Rome Committees and to see a summary of the Rome II book: go to
www.romecriteria.com.

PRESENT PATHOPHYSIOLOGICAL OBSERVATIONS
Despite differences among the functional gastrointestinal disorders, in location and symptom
features, common characteristics are shared with regard to:
o motor and sensory physiology,
o central nervous system relationships,
o approach to patient care.
What follows are the general observations and guidelines.

MOTILITY
In healthy subjects, stress can increase motility in the esophagus, stomach, small and large
intestine and colon. Abnormal motility can generate a variety of GI symptoms including
vomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GI
patients have even greater increased motility in response to stressors in comparison to normal
subjects. While abnormal motility plays a vital role in understanding many of the functional GI
disorders and their symptoms, it is not sufficient to explain reports of chronic or recurrent
abdominal pain.

VISCERAL HYPERSENSITIVITY
Visceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain,
which are not well correlated with changes in gastrointestinal motility, and in some cases, where
motility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lower
pain threshold with balloon distension of the bowel or have increased sensitivity to even normal
intestinal function. Additionally, there may be an increased or unusual area of somatic referral of
visceral pain. Recently it has been concluded that visceral hypersensitivity may be induced in
response to rectal or colonic distension in normal subjects, and to a greater degree, in persons
with IBS. Therefore, it is possible that the pain of functional GI disorders may relate to
sensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injury
to the viscera.

BRAIN-GUT AXIS
The concept of brain-gut interactions brings together observations relating to motility and
visceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinal
and CNS central nervous system activity, the brain-gut axis explains the symptoms relating to
functional GI disorders. In other words, senses such as vision and smell, as well as enteroceptive
information (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,
motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect central
pain perception, mood, and behavior. For example, spontaneously induced contractions of the
colon in rats leads to activation of the locus coeruleus in the pons, an area closely connected to
pain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associated
with a decrease in the frequency of MMC activity of the small bowel possibly mediated by stress
hormones in the brain. Based on these observations, it is no longer rational to try to discriminate
whether physiological or psychological factors produce pain or other bowel symptoms. Instead,
the Functional GI disorders are understood in terms of dysregulation of brain-gut function, and
the task is to determine to what degree each is remediable. Therefore, a treatment approach
consistent with the concept of brain-gut dysfunction may focus on the neuropeptides and
receptors that are present in both enteric and central nervous systems.

THE ROLE FOR PSYCHOLOGICAL FACTORS
Although psychological factors do not define these disorders and are not required for diagnosis,
they are important modulators of the patient's experience and ultimately, the clinical outcome.
Research on the psychosocial aspects of patients with functional GI disorders yields three general
observations:
o Psychological stress exacerbates gastrointestinal symptoms in patients with
functional GI disorders and can even produce symptoms in healthy patients (but to
a lesser degree).
o Psychological disturbances modify the experience of illness and illness behaviors
such as health care seeking. For example, a history of major psychological trauma
(e.g. sexual or physical abuse) is more common among patients seen in referral
centers than in primary care and is associated with a more severe disorder and a
poorer clinical outcome. Additionally, psychological trauma may increase painreporting
tendency.
o Having a functional GI disorder has psychological consequences in terms of one's
general well-being, daily functional status, concerns relating to control over
symptoms, and future implications of the illness (e.g. functioning at work and
home).
APPROACH TO TREATMENT
The approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatient
relationship. The basis for implementing a strong physician-patient relationship is
supported by evidence that patients with functional GI disorders have anywhere from a 30 to
80% placebo response rate regardless of treatment.

http://www.med.unc.edu/medicine/fgidc/historyfunctionaldisorders.pdf

This is important to notice and understand also

" functional GI disorders have anywhere from a 30 to
80% placebo response rate regardless of treatment."

This is an excellent new video.

An interview with Douglas A. Drossman, MD, Co-Director, UNC Center for Functional GI & Motility Disorders, University of North Carolina, Chapel Hill, NC. Dr. Drossman is a clinician, a clinical researcher, and an educator. In this video, Dr. Drossman explains continuing advances that help us understand and visualize these conditions.

http://www.youtube.com/watch?v=bm3gboLimvw

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My website on IBS is www.ibshealth.com

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