Personally, I believe gluten causes my digestive symptoms, reactions and fatigue in People Without Coeliac Disease as gluten and symptoms in people without coeliac disease as gluten is a trigger of digestive symptoms and fatigue “non-coeliac gluten intolerance”. As a sufferer of what the doctors have resigned to say is IBS in whom coeliac disease had been excluded whose symptoms were controlled on a gluten-free diet.
I eat a daily gluten-free diet, rarely eating gluten free bread or baked goods as I do not find them comfortable in the digestive transit, although small amounts are the key eaten proportionally with fruit, vegetables and proteins, as excess gluten-free could also cause discomfort. My symptoms are worse within thirty minutes of gluten ingestion and had significantly worse bloating, abdominal pain, altered bowel pattern and fatigue, sleeplessness due to the food going through the system causing pain en route.
Gluten is a trigger of inflammation and/or gut dysfunction in IBS and gluten sensitivity the next is to determine whether it is the/or one of the causes of functional symptoms in patients with a positive anti-gliadin antibodies, and gluten restriction.
Mast cells have been implicated showing increased activated mast cells present in the duodenum, ileum and/or colon of individuals with IBS symptoms,these are:
• found resident in tissues throughout the body, particularly in association with structures such as blood vessels and nerves, and in proximity to surfaces that interface the external environment
• are bone marrow-derived and particularly depend upon stem cell factor for their survival
• express a variety of phenotypic features within tissues as determined by the local environment
• withdrawal of required growth factors results in mast cell apoptosis
• appear to be highly engineered cells with multiple critical biological functions
• may be activated by a number of stimuli that are both Fc epsilon RI dependent and Fc epsilon RI independent.
• through various receptors leads to distinct signaling pathways
• may immediately extrude granule-associated mediators and generate lipid-derived substances that induce immediate allergic inflammation
• may also be by the synthesis of chemokines and cytokines as secretion, occurs hours later, may contribute to chronic inflammation.
Biological functions appear to include:
• a role in natural immunity,
• involvement in host defence mechanisms against parasitic infestations,
• immunomodulation of the immune system,
• tissue repair and angiogenesis.
The trigger in these individuals is believed to be a type of immune stimulating event such as:
• an intestinal infection , as in the post-infectious form of IBS
• proteins in the gut such as foods and/or microbes that are sensed by the body as being foreign attackers.
The role of microbes is getting a lot of scientific and research attention whereas food proteins as a cause of IBS, has generally been doubted by research scientists and previously ignored
The presence of genetic markers as for Coeliac disease predicted responsiveness to a gluten-free diet in people with IBS, supporting with my personal experiences. In following a gluten free diet individuals with at risk genetics but who are without proven Coeliac disease, though many had positive testsm with a higher occurrence of these genetics in individuals with augmented mast cells in their intestinal lining, known as Mastocytic Enterocolitis (MCE) or also Mastocytic Inflammatory Bowel Disease (MIBD).
Therefore, it is of the utmost importance that MCE or MIBD are recognised as an inflammatory process in some IBS sufferers as it narrows down the affected area rather than only dietary causes and implications.
• a gluten-free
• low fruit, vegetables, dried legumes,
• no dairy.
The diet results are in a very positive response when I have been similarily diagnosed and treated.
The role of mast cells and gluten in IBS requires research but that costs money, I wish I was Bill Gates and could fund this area of research on the link and affect between mast cells in gastrointestinal disease.