Hi Barbara (lil zincer),
Didn't I read on here that you were put on some form of zinc?
I was just reading that zinc deficiency has the potential of causing the following health problems:
weak immunity
poor wound healing
poor sense of smell/taste
sexual dysfunction
Not much fun, in other words!
Take care.
Yours, Luce
Barbara/ ZINC
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Here is a study I found interesting:
Eur J Intern Med. 2008 Mar;19(2):83-91. Epub 2007 Nov 26
Transglutaminase and the pathogenesis of coeliac disease.
Stenberg P, Roth EB, Sjöberg K.Hospital Pharmacy, Malmö University Hospital, S-205 02 Malmö, Sweden. pal.stenberg@apoteket.se
In 1997, a German group demonstrated that the antigen of the biomarker EMA (endomysial antibodies) in coeliac disease is a calcium-dependent thiol enzyme, transglutaminase type 2 (TG2). This most important discovery opened up an exciting field of research aimed at a better understanding of the pathogenesis of coeliac disease, a T-cell-driven autoimmune disorder with a prevalence of about 1%. The accidental activation of TG2, possibly caused by a stress-induced local deficiency of zinc in the intestinal wall, might play a key role where the enzyme catalyzes an atypical deamidation of specific glutamine residues of food gliadins. The genetic contribution is HLA DQ2 or DQ8, which can form a complex with the TG2-modified gliadin residues, resulting in an immune response with the formation of antibodies against both gliadin and the enzyme. Indeed, the immunopathogenesis of coeliac disease can now be recognized partly at the molecular level. Progress has already improved the opportunities for laboratory diagnostics and, hopefully, new ways of treating and preventing coeliac disease will become available. These exciting developments might stimulate research within other fields of autoimmune disorders. With its focus on TG2, this review highlights some of the intriguing mechanisms of the pathogenesis of coeliac disease, such as the structure of the neo-antigen, the involvement of calcium and zinc, and the effects of coeliac antibodies on TG2 activity. Moreover, the many pitfalls due to dubious laboratory practice are addressed, as is the potential when a fundamental biological mechanism is understood at the molecular level.
PMID: 18249302 2008
There is also a lot of information on zinc deficiency and leaky gut / intestinal permeability....you may all know that ... but if not... google it!
Eur J Intern Med. 2008 Mar;19(2):83-91. Epub 2007 Nov 26
Transglutaminase and the pathogenesis of coeliac disease.
Stenberg P, Roth EB, Sjöberg K.Hospital Pharmacy, Malmö University Hospital, S-205 02 Malmö, Sweden. pal.stenberg@apoteket.se
In 1997, a German group demonstrated that the antigen of the biomarker EMA (endomysial antibodies) in coeliac disease is a calcium-dependent thiol enzyme, transglutaminase type 2 (TG2). This most important discovery opened up an exciting field of research aimed at a better understanding of the pathogenesis of coeliac disease, a T-cell-driven autoimmune disorder with a prevalence of about 1%. The accidental activation of TG2, possibly caused by a stress-induced local deficiency of zinc in the intestinal wall, might play a key role where the enzyme catalyzes an atypical deamidation of specific glutamine residues of food gliadins. The genetic contribution is HLA DQ2 or DQ8, which can form a complex with the TG2-modified gliadin residues, resulting in an immune response with the formation of antibodies against both gliadin and the enzyme. Indeed, the immunopathogenesis of coeliac disease can now be recognized partly at the molecular level. Progress has already improved the opportunities for laboratory diagnostics and, hopefully, new ways of treating and preventing coeliac disease will become available. These exciting developments might stimulate research within other fields of autoimmune disorders. With its focus on TG2, this review highlights some of the intriguing mechanisms of the pathogenesis of coeliac disease, such as the structure of the neo-antigen, the involvement of calcium and zinc, and the effects of coeliac antibodies on TG2 activity. Moreover, the many pitfalls due to dubious laboratory practice are addressed, as is the potential when a fundamental biological mechanism is understood at the molecular level.
PMID: 18249302 2008
There is also a lot of information on zinc deficiency and leaky gut / intestinal permeability....you may all know that ... but if not... google it!
Zinc deficiency – Zinc is necessary in maintaining intestinal wall integrity. Supplementing
with zinc could contribute significantly to healing a leaky gut in about eight weeks (Sturniolo
2001). Zinc is also instrumental in a maintaining a healthy immune system (Prasad 2002).
The synthesis of serotonin involves zinc. Since serotonin is also necessary for melatonin
synthesis, a zinc deficiency may result in low levels of both of these compounds, causing
problems with the sleep cycle, calming, and hyperness.
http://j.b5z.net/i/u/2049569/f/conditio ... ndrome.pdf
Zinc supplementation tightens Leaky Gut in Crohn's disease
http://www3.interscience.wiley.com/jour ... 1&SRETRY=0
Zinc Deficiency Induces Membrane Barrier Damage and Increases Neutrophil Transmigration in Caco-2 Cells1,2
Alberto Finamore3, Mara Massimi4, Laura Conti Devirgiliis4 and Elena Mengheri3,*
3 Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione, 00178 Rome, Italy and 4 Dipartimento Biologia di Base ed Applicata, Università de L'Aquila, 67100 Italy
Zinc may contribute to the host defense by maintaining the membrane barrier. In this study, we questioned whether zinc deficiency affects the membrane function and junctional structure of intestinal epithelial cells, causing increased neutrophil migration. We used the Caco-2 cell line grown in control (C), zinc-deficient, or zinc-replete medium until differentiation. Zinc deprivation induced a decrease of transepithelial electrical resistance and alterations to tight and adherens junctions, with delocalization of zonula occludens (ZO-1), occludin, β-catenin, and E-cadherin. Disorganization of F-actin and β-tubulin was also found in zinc deficiency. These changes were associated with a loss of the amounts of ZO-1, occluding, and β-tubulin. In addition, zinc deficiency caused a dephosphorylation of occludin and hyperphosphorylation of β-catenin and ZO-1. Disruption of membrane barrier integrity led to increased migration of neutrophils. In addition, zinc deficiency induced an increase in the secretion of interleukin-8, epithelial neutrophil activating peptide-78, and growth-regulated oncogene-, alterations that were not found when culture medium was replete with zinc. These results provide new information on the critical role played by dietary zinc in the maintenance of membrane barrier integrity and in controlling inflammatory cell infiltration. http://jn.nutrition.org/cgi/content/abstract/138/9/1664
My daughter tested postitive for pyroluria, which causes B6 and zinc deficiency. Many with pyroluria have food sensitivity... so... this relationship between zinc and intestinal barrier function caught my attention. Along with zonulin info, of course.