I made little search on web. Its difficult to find some info apart from companies promoting their products. But I found two animal studies showing, what I understand:
- Stress is causing greater ulcer extent.
- Acute stress causes inhibition of gastric secretion, but later on there is habituation of secretion as response to this inhibition. So stomach is then “hit” by prolonged acid secretion.
So this “pill” may be important to lower this secretion and shield stomach (as was in my case).
I just realized I know professional gastroenterologist. I will ask her about this stress-acid-treatment problem.
Gastric secretion as a function of acute and chronic stress in the gastric fistula rat.
By Pare, William P.; Isom, Kile E.
Journal of Comparative and Physiological Psychology. Vol 88(1), Jan 1975, 431-435.
Abstract
Conducted 2 experiments using a total of 54 male Long-Evans rats chronically implanted with gastric cannulas. In Exp I Ss exposed to signaled and unsignaled grid shock secreted more gastric acid after shock stress (chronic stress) for 8 days compared to the 1st 12 hrs of shock stress (acute stress). However, Exp II indicated that the higher gastric acid values under chronic stress were not significantly greater than prestress baseline values. Results are interpreted to reflect an inhibition of gastric acid secretion as a function of acute stress. During chronic stress this inhibition was followed by an habituation of gastric secretory processes which was observed as a return of secretion volume to baseline levels. (PsycINFO Database Record © 2009 APA, all rights reserved)
Scandinavian Journal of Gastroenterology
2002, Vol. 37, No. 11, Pages 1259-1264
Long-term Stress and Helicobacter pylori Infection Independently Induce Gastric Mucosal Lesions in C57BL/6 Mice
Y.-H. Kim, J. H. Lee, S. S. Lee, E. Y Cho, K. C. Koh, S. W Paik, J. C. Rhee, K. W. Choi, H. J. Son, P.-L. Rhee, J. J. Kim and Y. L. Oh*
Background: Long-term psychological stresses may have a role in the pathogenesis of peptic ulcer. However, the interaction between stress and Helicobacter pylori infection in the development of peptic ulcer is not established. The aim of this study was to elucidate the roles of long-term stress and H. pylori infection in the development of gastric mucosal lesions in mice. Methods: The Sydney strain (SS1) of H. pylori was inoculated into the stomach of C57BL/6 mice. Twelve weeks later, mice with or without H. pylori infection were exposed to long-term repeated water-immersion-restraint stress (WIRS) for 12 h per day, 3 times per week, for 8 weeks. Gastric mucosal lesions were evaluated both macroscopically (ulcer index) and microscopically (Updated Sydney System). Results: The long-term WIRS induced mild inflammation, oedema, interstitial haemorrhage and superficial erosions in the stomach of mice both with and without H. pylori infection. The degree of mucosal inflammation or atrophy in H. pylori -infected mice was not influenced by the stress. In the mice without H. pylori infection, the ulcer index of the stressed mice was greater than that of non-stressed mice (1.66 ? 0.39 versus 0.17 ? 0.08, P = 0.007). In the mice with H. pylori infection, the ulcer index (mean ? s x ) of the stressed mice was also greater than that of nonstressed mice (2.31 ? 0.59 versus 0.64 ? 0.22, P = 0.027). Conclusions: The present study showed that long-term stress can induce gastric mucosal inflammation and erosions, and this effect may occur independently of H. pylori infection.