Marcia - Here's The Research Data You Were Searching For

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Hi Marcia,

Sorry it took me a while to get back to this, but I finally had time to locate the research data that you asked for. I'm not sure how familiar you are with reading such reports, but if you need some background information on how lower esophageal sphincter, (LES), pressure is measured, the first link below, connects to a reference on that. Your GI doc, (hopefully), should know and understand all this background information. Basically, the pressure of the LES is measured as a tube or catheter is withdrawn through it.

http://www.hon.ch/OESO/books/Vol_5_Eso_ ... rt042.html

Below, is a link to an article that clearly details the information that you need. Note this observation from the preliminary information in the article:

Cannon (1908) observed in cats that the gastric contents were rhythmically regurgitated into the oesophagus after ingestion of a neutral starch meal. The phenomenon was prevented by acidification of the meal. Moreover, he demonstrated that a greater intragastric pressure was required to produce gastrooesophageal reflux when the gastric contents were acid than when they were not.

And here's the "punch line" from the discussion of the results:

The results of this study show, in support of Giles et al. (1969a), that exposure of the cardia and of the distal portion of the gastro-oesophageal junctional zone to solutions of low pH has a significant influence upon the resting pressures recorded from the lower oesophageal sphincter.

IOW, if you look at figure 2, in the article, for example, you can clearly see that higher sphincteric pressure resulted from the perfusion of increasingly greater concentrations of stomach acid solutions. The higher the sphincteric pressure, the less likely the LES is to allow any reflux into the esophagus. Thus, the more acidic the stomach contents, (the lower the pH), the lower the possibility that acid reflux will occur.

http://www.ncbi.nlm.nih.gov/pmc/article ... 56/?page=1

Here's a PDF file of the entire article, that you can print for your doctor:

http://www.ncbi.nlm.nih.gov/pmc/article ... 6-0067.pdf

That article was published in Gut magazine in January, 1979, so one would think that most GI specialists would be aware of it by now.

Here's some more information, including a simplified explanation of how the process works:

http://refluxdefense.com/heartburn_GERD ... -acid.html

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Of course, another problem with taking a PPI, is that after using them for a while, (a month or so), they tend to weaken the LES, so that if they are withdrawn, the reflux symptoms usually become worse, (at least until the LES muscles can slowly rebuild their original strength).

The medical community misunderstands this effect. Researchers determined, (by analyzing survey results from questionnaires sent to patients), that there is a rebound effect following withdrawal of a PPI, which they assumed to be due to increased acid production by the stomach. Well sure there's increased acid production, because the parietal cells in the stomach are no longer being artificially suppressed by a PPI. But that's not the reason for the reflux - the reflex is caused by the fact that PPIs cause the LES to slowly lose muscle tone, (since LES pressures are lower with the use of a PPI - when you use a muscle less, it loses strength), and this weakening of the muscle, causes increased reflux problems, after the drugs are withdrawn, until the LES can slowly build up it's normal strength, again.

http://www.webmd.com/heartburn-gerd/new ... x-symptoms

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