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I have read anecdotal accounts of individuals deriving benefit from GERD symptoms by use of Xanax. Anyone have any experience, positive or negative, with this?
Yes, I have seen those websites before. My problem is primarily 'atypicalAtypical pneumonia chest pain' often associated with fattyXanthoma food intake, so am interested in CCK inhibition. Removing gallbladder and sphincterotomy did not help, in spite of gastroenterologist claims.
I would like to see if anything other than Xanax exists to inhibit CCK. I would like to try something with less baggage. No, I have not tried Xanax.
Wombat...what about something like Questran or Colestid (cholesterol lowering meds that remove bile acids). I'm not sure if this is what you're interested in.
My cholesterol is GREAT: 151 last week. (Was in the hospital after ERCP; will do separate post on that someday soon; ALT, AST and bilirubin were high). What I seem to notice is gripping in my chest after eating fatty meals. Nothing in the gut, just gripping in the chest, as if someone were squeezing my esophagus. I noticed the same thing with CCK stimulation. I know the literature which indicates that endogenous CCK can affect LES function and that Xanax is a CCK antagonist. Am wondering if such an approach could benefit me. Or more precisely, if there is something with less risk and baggage than Xanax that could benefit me.
Thank you so much, and I will review,
When I was told to change my diet I did 6 years ago and lost 40 lbs. I am on a bland diet so I know I can't control with diet alone .
I have given up alot and do as directed and find comfort at my MVP support club. Wish me luck at the G.I. appt. today Hope to be eating a little more soon.........
I wasn't suggesting that your cholesterol needed lowering. Those meds just happen to remove bile which is what CCK is all about. CCK or Cholecystokinin is the hormone secreted by the small
intestine that stimulates gallbladder contraction hence the bile which may be culpret in bile reflux. I never read anything about CCK affecting the LES. If you have that information I would be very interested.
The below is a summary of the article "Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors". Clavé P, Gonzales A, Morano A, et. al., Gastroenterology 1998; 115:597-604.
Summary: Previous studies have demonstrated that exogenous cholecystokinin decreases lower esophageal sphincter (LES) pressure and increases transient LES relaxations in humans. In the present study, the authors use cholestyramine to increase endogenous CCK release, and studied the effect of this on postprandial transient LES relaxation in 8 healthy volunteers. Subjects ingested a 181 kcal meal either alone or in combination with 12 grams of cholestyramine while esophageal and LES manometry, esophageal pH and gall bladder emptying were monitored. Cholestyramine ingestion was found to cause a marked increase in endogenous CCK release. This was associated with an increase in gall bladder emptying, reflux episodes, transient LES relaxations and esophageal acid exposure that was reversed by administration of the CCK-A receptor antagonist loxiglumide. Loxiglumide also prevented the decrease in LES pressure induced by cholestyramine. Parallel in vitro studies indicated that CCK-8 contracted human LES muscle strips through a tetrodotoxin-insensitive pathway, without modifying LES relaxations induced by stimulation of intrinsic nerves. The authors conclude that endogenous CCK enhances postprandial gastroesophageal reflux in humans by increasing the rate of transient LES relaxations and reducing postprandial LES pressure. The actions appear to be mediated by extrasphincteric CCK-A receptors that override a direct excitatory effect of CCK on the LES muscle.
I am more interested in this aspect of CCK than bile reflux (for my own case, at least!)
What a informed message board;
I would like to know if xanax could then heal the problem. It is a very addictive drug, I read.
Why does ones LES weaken and how would it strenghthen on its own.
What primary requirements for that study. Do you have a website I could forward to the G.I. nurse ?
Is there a correlation with ones CNS ?
Thank you for the article summary. Is there a URL that I can access this article or the summary? I tried the American Journal of Gastroenterology (1998 issues)but I couldn't find this particular article. I know many people on Heartburn-help.com forum would be interested in seeing it.
It's article #63 under Mental Health / anxiety.
Xanax is alprazolam. It's suppose to indirectly inhibit bile
reflux and some say it helps with transient relaxation of the LES.
It's a tranquilzer and can be addictive.
also....algy.com/pdi/research.html
I would like to see if anything other than Xanax exists to inhibit CCK. I would like to try something with less baggage. No, I have not tried Xanax.
When I was told to change my diet I did 6 years ago and lost 40 lbs. I am on a bland diet so I know I can't control with diet alone .
I have given up alot and do as directed and find comfort at my MVP support club. Wish me luck at the G.I. appt. today Hope to be eating a little more soon.........
intestine that stimulates gallbladder contraction hence the bile which may be culpret in bile reflux. I never read anything about CCK affecting the LES. If you have that information I would be very interested.
The below is a summary of the article "Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors". Clavé P, Gonzales A, Morano A, et. al., Gastroenterology 1998; 115:597-604.
Summary: Previous studies have demonstrated that exogenous cholecystokinin decreases lower esophageal sphincter (LES) pressure and increases transient LES relaxations in humans. In the present study, the authors use cholestyramine to increase endogenous CCK release, and studied the effect of this on postprandial transient LES relaxation in 8 healthy volunteers. Subjects ingested a 181 kcal meal either alone or in combination with 12 grams of cholestyramine while esophageal and LES manometry, esophageal pH and gall bladder emptying were monitored. Cholestyramine ingestion was found to cause a marked increase in endogenous CCK release. This was associated with an increase in gall bladder emptying, reflux episodes, transient LES relaxations and esophageal acid exposure that was reversed by administration of the CCK-A receptor antagonist loxiglumide. Loxiglumide also prevented the decrease in LES pressure induced by cholestyramine. Parallel in vitro studies indicated that CCK-8 contracted human LES muscle strips through a tetrodotoxin-insensitive pathway, without modifying LES relaxations induced by stimulation of intrinsic nerves. The authors conclude that endogenous CCK enhances postprandial gastroesophageal reflux in humans by increasing the rate of transient LES relaxations and reducing postprandial LES pressure. The actions appear to be mediated by extrasphincteric CCK-A receptors that override a direct excitatory effect of CCK on the LES muscle.
I am more interested in this aspect of CCK than bile reflux (for my own case, at least!)
I would like to know if xanax could then heal the problem. It is a very addictive drug, I read.
Why does ones LES weaken and how would it strenghthen on its own.
What primary requirements for that study. Do you have a website I could forward to the G.I. nurse ?
Is there a correlation with ones CNS ?