triffid113
Day of the Square Peg
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I am a terribly allergic person and totally unschooled about all of this. But one thing jumps out...your mentioning that blah blah raises IgE. Did you know that ZINC lowers IgG?Re H2 receptors -- when they DO work in regulating histamine overload/sensitivity is mainly when they are used in combination with H1 antagonists. I cannot find my notes now but remember a couple of studies describing raised IgE levels when H2 (even H1 from what I can remember) blockers were used on their own. This effects was not present when a H1+H2 antagonists where used in combination.
These could hopefully give you more clues:
Improved outcomes in patients with acute allergic syndromes who are treated with combined H1 and H2 antagonists http://www.ncbi.nlm.nih.gov/pubmed/11054200
Treatment of chronic idiopathic urticaria with combined H1 and H2 blockers http://www.ncbi.nlm.nih.gov/pubmed/30546
Greater inhibition of dermographia with a combination of H1 and H2 antagonists http://www.ncbi.nlm.nih.gov/pubmed/6132569
H1- and H2-receptor antagonists prevent histamine release in allergic patients after the administration of midazolam-ketamine. http://www.ncbi.nlm.nih.gov/pubmed/10219654
Histamine 2 blocker potentiates the effects of histamine 1 blocker in suppressing histamine-induced wheal http://www.ncbi.nlm.nih.gov/pubmed/19052407
Conjunctival eosinophil infiltration evoked by histamine and immediate hypersensitivity. Modification by H1- and H2-receptor blockade http://www.iovs.org/content/27/10/1495.long
… neither cimetidine nor pyrilamine alone produced an inhibitory effect, but a cimetidine-pyrilamine combination caused a significant reduction in the number of infiltrating eosinophils and prevented epithelial damage and goblet cell depletion
Another very interesting thing I was coming across when looking into antihistamines was histaminergic involvement in various areas that are often problematic in CFS/ME like modulation of glutamate release, central cholinergic system, even cardiac systolic function …
A histamine H₂ receptor blocker ameliorates development of heart failure in dogs independently of β-adrenergic receptor blockade http://www.ncbi.nlm.nih.gov/pubmed/20852875
These beneficial effects of famotidine were associated with a decrease of the myocardial cAMP level. Histamine H₂ receptor blockade preserves cardiac systolic function in dogs with pacing-induced heart failure, even in the presence of β-adrenergic receptor blockade. This finding strengthens the rationale for using histamine H₂ blockers in the treatment of heart failure.
http://www.springerlink.com/content/dhn3804v156563r8/
Biomedical and Life Sciences
BioMetals
Volume 22, Number 6 (2009), 1031-1040, DOI: 10.1007/s10534-009-9254-z
Comparison of inhibitory activities of zinc oxide ultrafine and fine particulates on IgE-induced mast cell activation
Kouya Yamaki and Shin Yoshino
Abstract
The effects of ultrafine and fine particles of zinc oxide (ZnO) on IgE-dependent mast cell activation were investigated. The rat mast cell line RBL2H3 sensitized with monoclonal anti-ovalbumin (OVA) IgE was challenged with OVA in the presence or absence of ZnO particles and zinc sulfate (ZnSO4). Degranulation of RBL2H3 was examined by the release of β-hexosaminidase. To understand the mechanisms responsible for regulating mast cell functions, the effects of ZnO particles on the levels of intracellular Zn2+, Ca2+, phosphorylated-Akt, and global tyrosine phosphorylation were also measured. IgE-induced release of β-hexosaminidase was obviously attenuated by ultrafine ZnO particles and ZnSO4, whereas it was very weakly inhibited by fine ZnO particles. The intracellular Zn2+ concentration was higher in the cells incubated with ultrafine ZnO particles than in those with fine ZnO particles. Consistent with inhibitory effect on release of β-hexosaminidase, ultrafine ZnO particles and ZnSO4, but not fine ZnO particle, strongly attenuated the IgE-mediated increase of phosphorylated-Akt and tyrosine phosphorylations of 100 and 70 kDa proteins in RBL2H3 cells. These findings indicate that ultrafine ZnO particles, with a small diameter and a large total surface area/mass, could release Zn2+ easily and increase intracellular Zn2+ concentration efficiently, thus decreasing FcεRI-mediated mast cell degranulation through inhibitions of PI3K and protein tyrosine kinase activation. Exposure to ZnO particles might affect immune responses, especially in allergic diseases.
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The reason I can't relate to the H1 H2 receptor discussion is that I refuse to take drugs (ESPECIALLY PPI inhibitors which I am convinced are the real reason my father passed on). I am extremely sensitive to drugs and so I cannot take them. But turning off your stomach acid production IMHO is ALWAYS a mistake. And fyi I have NEVER SEEN these things prescribed after ACTUALLY testing stomach ph...it is always ASSUMED that if the stomach hurts, then it is too much HCL (when in fact it may be too LITTLE). DO you know that PPI inhibitors have been proven to cause contraction of CDIFFs if the germs are present (whereas people with sufficient HCL do not get CDIFFs). HCL is the body's main defense against pathogens entering through the digestive tract.