I understand that, but once we have an MC diagnosis, all bets are off, because virtually none of the rules are chiseled in stone, from that point on. Just because a food/hormone/chemical worked fine yesterday, or today, does not guarantee that it will be safe tomorrow, unfortunately. Even if you had been in a flare when you started the HRT, and a few days later you went into remission, that does not guarantee, (or even imply), that HRT cannot cause a flare now. That may seem contrary to logic, but it's not.Pat wrote:Tex, I have had this disease much longer than I have taken progesterone. I never saw a change when I started on HRT.
Essentially, we're down to grasping at straws here, because we're running out of options, due to the fact that the conventional considerations don't appear to be sufficient to resolve your issues. I've included some more "straws" below.
Mary Beth,
You may be on to something, because the function of the goblet cells in the colonic mucosa is to secrete mucus, which in turn compacts the feces.
While we're grasping at straws, another possibility is D caused by impaired function of sodium ion/hydrogen ion exchanger 3.
http://ajpgi.physiology.org/content/295/1/G63.fullNa+/H+ exchanger 3 (NHE3) provides a major route for intestinal Na+ absorption. NHE3 has been considered a target of proinflammatory cytokines and enteropathogenic bacteria, and impaired NHE3 expression and/or activity may be responsible for inflammation-associated diarrhea. However, the possibility of loss of NHE3 function reciprocally affecting gut immune homeostasis has not been investigated. In this report, we describe that NHE3-deficient mice spontaneously develop colitis restricted to distal colonic mucosa. NHE3–/– mice housed in a conventional facility exhibited phenotypic features such as mild diarrhea, occasional rectal prolapse, and reduced body weight. Genomewide microarray analysis identified not only a large group of transport genes that potentially represent an adaptive response, but also a considerable number of genes consistent with an inflammatory response. Histological examination demonstrated changes in the distal colon consistent with active inflammation, including crypt hyperplasia with an increased number of 5-bromo-2'-deoxyuridine-positive cells, diffuse neutrophilic infiltrate with concomitant 15-fold increase in matrix metalloproteinase 8 expression, an increased number of pSer276-RelA-positive cells, and a significant decrease in periodic acid-Schiff-positive goblet cells.
Apparently, an adequate dietary intake of the essential amino acid threonine is also necessary for the production of mucus, so a deficiency of threonine could possibly contribute to an environment that might promote D.
http://ajpgi.physiology.org/content/292/5/G1293.fullOverall, our results suggest that adequate dietary threonine was critical in the production of mucus
Here's some info on threonine:
http://www.springboard4health.com/noteb ... onine.html
The bottom line is, yes, I believe that Pat may well have some sort of complicating factors that might be causing the D, even though she may be eliminating all possible sources of problems in her diet. Her GI system has been under fire for so many years, that we have to consider the possibility of possible unforeseen negative effects, ranging from nutrient deficiencies, to altered chemical processes, hormones, and possibly including damage due to medications that didn't work as planned, (such as antibiotics).
Tex
. Fingers crossed that you both are "out of the woods" for now.