Kim, the leading cause of misdiagnoses is self diagnoses.
IBS is not caused by candida or fungus.
They know some foods trigger IBS and has nothing to do with fungus, but for other chemical reasons.
The second study you posted is from 2005 and there has been an explosion in IBS research since then your leaving out of the picture here. There are almost no candida and IBS references in Pubmed out of 19 million IBS references.
In 20 years of so called "candida syndrome" it has never been found in ANYONE.
"invisibly within the intestinal tract," NOT WITH AN ELECTRON MICROSCOPE it isn't.
Three mechansims contribute to IBS.
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
VISCERAL HYPERSENSITIVITYVisceral 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. http://www.med.unc.edu/ibsThe UNC Center for Functional GI& Motility Disorders5
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. "