But in recent years, the Food and Drug Administration has issued numerous warnings about P.P.I.’s, saying long-term use and high doses have been associated with an increased risk of bone fractures and infection with a bacterium called Clostridium difficile that can be especially dangerous to elderly patients. In a recent paper, experts recommended that older adults use the drugs only “for the shortest duration possible.”
Studies have shown long-term P.P.I. use may reduce the absorption of important nutrients, vitamins and minerals, including magnesium, calcium and vitamin B12, and might reduce the effectiveness of other medications, with the F.D.A. warning that taking Prilosec together with the anticlotting agent clopidogrel (Plavix) can weaken the protective effect (of clopidogrel) for heart patients.
Other research has found that people taking P.P.I.’s are at increased risk of developing pneumonia; one study even linked use of the drug to weight gain.
More warnings about PPI's
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
More warnings about PPI's
http://well.blogs.nytimes.com/2012/06/2 ... ef=general
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MBombardier
- Rockhopper Penguin
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- Joined: Thu Oct 14, 2010 10:44 am
- Location: Vancouver, WA
But they work sort of the same, just at different stages. I pulled this from about.com: "Histamine blockers block one of the first stimuli for acid production, proton pump inhibitors block the final step in the pathway of acid secretion in the stomach, resulting in greater suppression of acid. PPIs shut down the proton pumps in the stomach, H2 blockers work by blocking the histamine receptors in acid producing cells in the stomach. PPIs have a delayed onset of action, while H2 Blockers begin working within an hour. PPIs work for a longer period of time; most up to 24 hours and the effects may last up to three days. H2 Blockers, however, usually only work up to 12 hours."
When I took Zantac and went off it, I had the same temporary increase in heartburn that I had after going off Prilosec (omeprazole).
When I took Zantac and went off it, I had the same temporary increase in heartburn that I had after going off Prilosec (omeprazole).
Marliss Bombardier
Dum spiro, spero -- While I breathe, I hope
Psoriasis - the dark ages
Hashimoto's Thyroiditis - Dec 2001
Collagenous Colitis - Sept 2010
Granuloma Annulare - June 2011
Dum spiro, spero -- While I breathe, I hope
Psoriasis - the dark ages
Hashimoto's Thyroiditis - Dec 2001
Collagenous Colitis - Sept 2010
Granuloma Annulare - June 2011
To explore this a little further, consider that the parietal cells in the stomach produce the gastric acid needed for digestion, and they also produce the intrinsic factor needed for B-12 absorption in the small intestine (specifically in the terminal ileum). The parietal cells are stimulated to produce acid by several mechanisms; histamine (through H2 receptors), acetylcholine (through M3 receptors) and gastrin (through CCK2 receptors). H2-receptor antagonists reduce stomach acidity by blocking the H2-receptors, thereby preventing histamines from attaching and triggering the production of additional acid. PPIs work by partially disabling the proton pumps in parietal cells in the stomach so that they are unable to produce normal amounts of gastric acid.
Note that by interfering with the ability of the proton pumps in the parietal cells to function normally, this almost certainly introduces a negative influence on the production of intrinsic factor, as well, which probably explains why the use of PPIs tends to cause a B-12 deficiency.
Also note the fact that histamine is produced by enteroendocrine cells in the stomach and is at least partially responsible for triggering the production of gastric acid. IOW, histamine is a normal and necessary element in the digestive process, and eliminating it completely would be counterproductive. The process by which normal digestion proceeds implies that it is normal for histamine levels to increase upon the ingestion of food. Obviously, if a mast cell issue is present (such as MACD) this would almost surely have an adverse effect on the digestive process, beginning with the effects of the increased histamine level on the production of gastric acid.
Tex
Note that by interfering with the ability of the proton pumps in the parietal cells to function normally, this almost certainly introduces a negative influence on the production of intrinsic factor, as well, which probably explains why the use of PPIs tends to cause a B-12 deficiency.
Also note the fact that histamine is produced by enteroendocrine cells in the stomach and is at least partially responsible for triggering the production of gastric acid. IOW, histamine is a normal and necessary element in the digestive process, and eliminating it completely would be counterproductive. The process by which normal digestion proceeds implies that it is normal for histamine levels to increase upon the ingestion of food. Obviously, if a mast cell issue is present (such as MACD) this would almost surely have an adverse effect on the digestive process, beginning with the effects of the increased histamine level on the production of gastric acid.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
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fatbuster205
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Further (silly) questions ...
PPIs are meant to reduce the over-production of stomach acid down to normal amounts rather than reduce it further? Or have I got that wrong? I have always thought that is why I take Lanzoprazole because I over-produce acid causing intense heartburn almost constantly. Give what Marliss says above, is Zantac a reasonable and safe alternative? The reason I ask is because my Mother, who suffers with the acid problem and who has also had duodenal ulcers, takes Zantac and not PPIs.
PPIs are meant to reduce the over-production of stomach acid down to normal amounts rather than reduce it further? Or have I got that wrong? I have always thought that is why I take Lanzoprazole because I over-produce acid causing intense heartburn almost constantly. Give what Marliss says above, is Zantac a reasonable and safe alternative? The reason I ask is because my Mother, who suffers with the acid problem and who has also had duodenal ulcers, takes Zantac and not PPIs.
I also have a malabsorbtion of bile acid and have had a duodenal ulcer, I take Omerprazole one 20mg in the morning, if I am late taking it I get a burning in my throat, even taking omerprazole for many years my recent Gastroscopy showed antral gastritis and patchy erythema to the duodenum, and was told to continue the PPI indefinitely, there are many times on occasions I have to take a dose of Gaviscon also later in the day for the heartburn I get, especially after meals,are there any safer alternatives.
Marg.
Marg.
Doctors probably like to think that is the case, but based on their mode of action, I see no reason why PPIs will not indiscriminately reduce stomach acid in every case, usually to far below normal levels.Anne wrote:PPIs are meant to reduce the over-production of stomach acid down to normal amounts rather than reduce it further? Or have I got that wrong?
The problem with this entire concept is that most of us don't produce too much stomach acid -- we're short on it. The older we get, the less gastric acid we produce. The symptoms of too much acid and too little acid are the same, so rather than actually test the patient, if the symptoms are heartburn, acid indigestion or acid reflux, most doctors just reach for a prescription pad and prescribe a PPI. If the doctor is a little more considerate of their patient, they will prescribe an H2 blocker. If the doctor is actually serious about looking out for the patient's health, he or she will do some testing of stomach acidity before deciding on a treatment.
That said, yes, if you actually have a reason to reduce stomach acidity, then virtually anything is safer than a PPI, and H2 blockers (such as Zantac) are usually effective.
Just be aware that for some people, H2 blockers can trigger MC, and for everyone, they reduce the effectiveness of the digestive system, possibly leading to poor digestion of some foods, and an increased risk of infections from food-borne pathogens (stomach acid is the first line of defense against bacteria in food).
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Marg,
Have your doctors ever thoroughly tested you for an H. pylori infection? The reason I say "thoroughly" is because most such infections are very difficult to diagnose, and they're commonly missed. The odds are pretty high that the cause of both your gastritis and your duodenal ulcers and erythema is an H. pylori infection. Your doctors are taking a typical route (a route that doesn't require them to think) and they're treating the symptoms, rather than trying to eliminate the cause of the problem.
Bile acids are normally absorbed and recycled in the terminal ileum. The fact that in your case they are being malabsorbed is clear evidence of a state of inflammation in the terminal ileum (which is quite common with MC). The cause of that inflammation is probably the omeprazole. Omeprazole has been known as a leading cause if MC for many years. PPIs are notorious for causing the very problems for which they are prescribed as a treatment. I can cite plenty of research documentation to back all this up, if you would like to see the research articles.
PPIs are addictive in that they cause a rebound effect that is stronger then the original proton pump response. That's why if you stop taking them, the acid reflux effect is worse than ever. If you discontinue the drug, it takes several weeks to months for the rebound effect to slowly fade away. PPIs cause more health problems "than you can shake a stick at", and yet naive doctors continue to prescribe them.
Yes, once they hook you on the drug, it's tough to get away from it.
Tex
Have your doctors ever thoroughly tested you for an H. pylori infection? The reason I say "thoroughly" is because most such infections are very difficult to diagnose, and they're commonly missed. The odds are pretty high that the cause of both your gastritis and your duodenal ulcers and erythema is an H. pylori infection. Your doctors are taking a typical route (a route that doesn't require them to think) and they're treating the symptoms, rather than trying to eliminate the cause of the problem.
Bile acids are normally absorbed and recycled in the terminal ileum. The fact that in your case they are being malabsorbed is clear evidence of a state of inflammation in the terminal ileum (which is quite common with MC). The cause of that inflammation is probably the omeprazole. Omeprazole has been known as a leading cause if MC for many years. PPIs are notorious for causing the very problems for which they are prescribed as a treatment. I can cite plenty of research documentation to back all this up, if you would like to see the research articles.
PPIs are addictive in that they cause a rebound effect that is stronger then the original proton pump response. That's why if you stop taking them, the acid reflux effect is worse than ever. If you discontinue the drug, it takes several weeks to months for the rebound effect to slowly fade away. PPIs cause more health problems "than you can shake a stick at", and yet naive doctors continue to prescribe them.
Yes, once they hook you on the drug, it's tough to get away from it. Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Thats really interesting Tex,
I did have a SeHCAT test after the ulcer and constant D, the results were - bile acid malabsorption retention only 2%, so in my case I must produce to much bile acid, I will mention the H2 blocker to my GI, as its so worrying about the bad press i've heard of late on PPI, I would prefer not to take them.
Marg.
I did have a SeHCAT test after the ulcer and constant D, the results were - bile acid malabsorption retention only 2%, so in my case I must produce to much bile acid, I will mention the H2 blocker to my GI, as its so worrying about the bad press i've heard of late on PPI, I would prefer not to take them.
Marg.
so looked it up and its a test for H Pylori.It will be very, very difficult to discontinue the omerprazole (because of they way that PPIs cause rebound symptoms) but I agree with you that you might be much better off if you could switch to an H2 antihistamine.
Good luck with this,
Tex
Good luck with this,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.