| John Que 2005-01-15, 4:08 am |
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Background on gastrin function.
The elevated gastrin is a result of the PPI meds suppression
of HCL and the resulting high pH in the lower stomach
and duodenum. To shut off gastrin production the pH
has to go lower than 1.5 in the duodenum and 3.0 in
the stomach antrum, both of which block release of gastrin.
Gastrin stimulates the growth of gastric glands and secretion large amounts
of gastric juice. It supposely stimulates the contraction of the lower
esophageal sphincter, increases the motility of the stomach and relaxes
the pylori sphinter. Sounds good except that the text says that "too
much chyme can overwhelm the duodenum." Therefore the gastrin level
needs to be dialed back by the release of hormone secretin as signaled
by the lowering pH. Secretin reduces the gastrin level and decreases
HCl secretion. CCK another hormone which is released at the same
time and the release is apparently by products of digestion. CCK
alters the stomach motility by antagonizing some receptors also influenced
by gastrin. Among it many functions, CCK slows the exit of food
from the stomach and it times the release of bile.
I'll also suggest that either CCK or secretin helps to tighten
the lower esophageal sphinter. It has been claimed by
many some off the mainstream of medical practice that
supplemental acids can lower stomach pH enough enough
to cause the LES to tighten. This presented as a clincal
observation. In the above paragraphs, I've provided
some possible mechanisms by which this takes place.
If you disagree, explain why.
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