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Histamine intolerance is a presumed set of adverse reactions (such as flush, itching, rhinitis, etc.) to ingested histamine in food. The mainstream theory accepts that there may exist adverse reactions to ingested histamine, but does not recognize histamine intolerance as a separate condition that can be diagnosed.
The manifestations of histamine intolerance, or, adverse reactions to ingested histamine, are not confined to the gastrointestinal system, and are usually systemic, affecting the entire body; still, these symptoms are often sporadic and non-specific: [5] [6] [7] symptoms attributed to histamine intolerance are wide-ranging and may affect various physiological systems, including the skin ...
The antibodies will cause cells in the body to produce histamine. This histamine will act on different areas of the body (eyes, throat, nose, gastrointestinal tract, skin or lungs) to produce symptoms of an allergic reaction. The allergic response is not limited to a certain amount of exposure.
“Histamine is released in the body and enters the gastrointestinal tract, which can cause gas, bloating, nausea, stomach pains and diarrhea.” He notes specific foods that can make seasonal ...
Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve ...
The reaction is caused by the release of histamine and mast cell granule proteins by a process called degranulation, as well as the production of leukotrienes, prostaglandins and cytokines, by mast cells following the cross-linking of allergen specific IgE molecules bound to mast cell FcεRI receptors. [3]
Histamine is a weak base (a compound able to react with a hydrogen ion to form an acid) that can link with acid groups within the granules of the mast cells. [8] The mechanism of the displacement theory. The crux of this theory lies in the assumption that histamine liberators release histamine by displacing it from cells.
Histamine release in the brain triggers secondary release of excitatory neurotransmitters such as glutamate and acetylcholine via stimulation of H 1 receptors in the cerebral cortex. Consequently, unlike the H 1 -antihistamines which are sedating, H 3 -antihistamines have stimulant and cognition-modulating effects.
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