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? 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. --- 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.