Kim, yes candida overgrowth syndrome has nothing to do with IBS and I personally think it shouldn't be posted along with IBS. People think IBS is a "catch all diagnoses it is NOT."
"If you could clarify something I heard on one of the videos you posted just to make sure I understand it correctly... I heard some of the doctors say that bacterial flora, mucosal inflammation, changes in the mucosal barrier which could allow bacteria through the wall into the gut, gene mutations are things that can play a role in IBS, among other things. Is this recent speculation?"
No its around five or more years old.
This has to do with people who develop IBS from an enteric infection, food poisoning, both viruses and bacterial infections and the infections resolve and a person is left with and dysregulation between the communication brain and ther gut.
Lots of people are studying bacteria and IBS, no SInGLE pathogen has been found, in fact mulitple ones leading to PI IBS have been found and so far altered gut bacteria may play some roles in contributing to IBS synmptoms, but the only bacteria problem found so far, are low counts of certain ones.
Bacteria in the gut changes all the time from diet and stressors. A person in florida, doesn't have the same as a person in Oregon say, because it helps protect you from pathogens around your own enviromenment and in your own house. Only 30 percent of the 500 species have been culture so far.
Candida is one of the most studied organisms in the gut. I will post something soon on this, but the actual gut-permeablity which is NOT the same as "leaky gut" or Dysbiosis, is for one the way the body absorbs nutrients to begin with.
Mucousal inflammation is MACROSCOPIC of specific cells embedded in the gut wall mainly seen in these IBS Post infectious IBSers. About 30% or more of people develop IBS froma previous gut infection that resides and leaves a person with celluar changes to the gut that are used for gut functioning. Also importantly psychological stressors can activate or reativate the inflammation. Bu this CONTRIBUTES to pain and the symptoms, but does not cause them.
You also need to know and this is very very important. Inflammation cannot be a diagnostic marker in IBS, because it does not always cause pain, which is a must for an IBS diagnoses.
Most pathogens in the gut cause D and really bad ones vomting, the two methods for the body to rid itself of a pathogen.
One of the top expert doctors in Inflammation and post infectious IBS is DR Spiller who has done a ton of work and looks at the gut cells with microscopes or sometimes by dissection of cadavers.
The neurotranmitter serotonin is INVOLVED in this as well. Almost all IBSers if not all show serotonin dyregulation between the gut brain and the brain and back. This is the transmitter that signals pain/discomfort to the brain from the gut. The gut can trigger the brain and the brain can trigger the gut, they are both operational top cause the symptoms.
Approximately 1 in ten patients with irritable bowel syndrome (IBS) believe their IBS began with an infectious illness. Prospective studies have shown that 3% to 36% of enteric infections lead to persistent new IBS symptoms; the precise incidence depends on the infecting organism. Whereas viral gastroenteritis seems to have only short-term effects, bacterial enteritis and protozoan and helminth infections are followed by prolonged postinfective IBS (PI-IBS). Risk factors for developing PI-IBS include, in order of importance, prolonged duration of initial illness, toxicity of infecting bacterial strain, smoking, mucosal markers of inflammation, female gender, depression, hypochondriasis, and adverse life events in the preceding 3 months. Age older than 60 years might protect against PI-IBS, whereas treatment with antibiotics has been associated with increased risk. The mechanisms that cause PI-IBS are unknown but could include residual inflammation or persistent changes in mucosal immunocytes, enterochromaffin and mast cells, enteric nerves, and the gastrointestinal microbiota. Adverse psychological factors contribute to persistent low-grade inflammation. The prognosis for patients with PI-IBS is somewhat better than for those with unselected IBS, but PI-IBS can still take years to resolve. There are no specific treatments for PI-IBS; these should be tailored to the predominant bowel disturbance, which is most frequently diarrhea.
Serotonin and GI clinical disorders. Spiller R.
Wolfson Digestive Diseases Centre, C Floor South Block, University Hospital, Clifton Boulevard, Nottingham, NG7 2UH, United Kingdom. robin.spiller@nottingham.ac.uk
Serotonin is widely distributed throughout the gut within both the enteric nerves and enterochromaffin (EC) cells. EC cells are located in the gut mucosa with maximal numbers in the duodenum and rectum where they act as signal transducers, responding to pressure and luminal substances both bacterial and dietary. Activation leads to serotonin release which acts on a range of receptors on mucosal afferent and myenteric interneurones to initiate secretomotor reflexes. These cause nausea and vomiting as well as intestinal secretion, propulsion and if pronounced, diarrhoea. Inflammation in animal models acts via T lymphocytes to increase EC cell numbers and mucosal serotonin (5-HT) content while inflammatory cytokines decrease serotonin transporter (SERT) function. Inflammation due to coeliac disease and following gastrointestinal infection increases mucosal 5-HT availability by a combination of increased EC cells and depressed SERT. Irritable bowel syndrome (IBS) developing after gastrointestinal infection and IBS with diarrhoea is associated with excess 5-HT. The associated diarrhoeal symptoms respond well to 5-HT(3) receptor antagonists. These drugs also inhibit the nausea and vomiting occurring in patients undergoing chemotherapy which cause a marked increase in release of 5-HT as well as other mediators. Other conditions including IBS-C and constipation may have inadequate 5-HT release and benefit from both 5-HT(3) and 5-HT(4) receptor agonists.
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Re: Shawneric
