Barrett's oesophagus, Omeprazole dosage and bile reflux: links

This is a listing of URLs relevant to Barrett's oesophagus, Omeprazole dosage and bile reflux. The search reveals some interesting pages! But a quote from Robert A. Heinlein's short story Life-Line is relevant here:

"There are but two ways of forming an opinion in science. One is the scientific method, the other the scholastic. One can judge from experiment, or one can blindly accept authority. To the scientific mind, experimental proof is all-important, and theory is merely a convenience in description, to be junked when it no longer fits. To the academic mind, authority is everything, and facts are junked then they do not fit theory laid down by authority.

"It is this point of view - academic minds clinging like oysters to disproved theories - that has blocked every advance of knowledge in history."

Many (most) medical papers are academic! Scientific medical papers are few. I have tried to find scientific papers...

Alternative therapies for acid reflux

PPIs are the conventional cure, but there are other possibilities


I have not tried hypnotherapy myself, but I have noted that, although the oesophagus is in theory insensitive to pain, reflux seems to cause much pain in a lot of people. I am lucky, I suffer little pain, yet have had reflux apparently all my life. Is this due to my relaxed attitude towards reflux? If so, hypnotherapy could be very useful to some sufferers.


Manipulation by a skilled chiropractor or osteopath is claimed to be helpful to some hiatal hernia sufferers. A Google search is informative, including a few YouTube videos. There are also self-help exercises that are claimed to help.

However it seems that, with advancing age, the phrenoesophageal ligament relaxes and allows a sliding hiatal hernia, so manipulation is only likely to have any effect in the young, where reflux tends to resolve naturally as the child ages.

However I went to a chiropractor who did the manipulation. I think it did nothing useful. But she did say that my diaphragm was tense and she manipulated my spine to relax my diaphragm. I believe this did have useful effect. This is backed up by the next alternative therapy.

Abdominal breathing

The Medscape article Can Complementary and Alternative Therapies Relieve GERD Symptoms? says that this is indeed useful.

Conventional antacids

Probably the most important alternative therapy to Proton Pump Inhibitors is to use the old, time proven, traditional antacids. There are so many, it probably deserves a separate page. So watch this site - or use the contact button!

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Barrett's oesophagus sufferers may be more prone to GERD pain than normal

I did a search of Google search which indicated that an inflamed oesophagus is more sensitive than a normal oesophagus, so Barrett's oesophagus sufferers are more prone to GERD pain than normal, at least in the early stages while their is still inflammation. There are other pages in the search that show the same results. I find no information on sensitivity after the inflammation has abated.

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Barrett's oesophagus in animals

Barrett's oesophagus occurs in animals other than humans. In fact many laboratory studies of how Barrett's develops have been done in rats, rabbits and dogs. Columnar epithelial oesophageal cells (as develop in Barret's oesophagus) are apparently normal in fish, reptiles and birds, to judge by the few studies that can be found. So Barrett's appears to be an atavism to a reptilian / piscine (and probably avian) cell structure. As such it seems to be an atavism to a pre-mammalian structure. If so, it is probably possible in nearly all mammals! The following papers discuss the piscine, reptilian or avian oesophagus:: animals are also used in experiments to study OAC and barretts, See Bile - is in necessary for Barrett's to form?

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Bile - is in necessary for Barrett's to form?

To prove bile is necessary for Barrett's to form you would need to prove that Barrett's cannot form without bile. Negatives in science are notoriously difficult to prove. But what the literature surely demonstrates is that bile-tainted gastric juice is much more dangerous than untainted juice. So there's no real argument! See my own experiments with PPI dosage.

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Bile or duodenogastric reflux

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Bile, presence of in the normal gastric fluid

Bile is suspected to be a cause of Barrett's oesophagus. But should bile ever be present in a normal healthy stomach? A search for gastric bile measurement reveals much confusion: most measurements that have been made are on patients with Barrett's oesophagus or other digestive problems. Papers do not say whether PPIs have been taken but it is a safe bet that all of these will have been on PPIs for a significant time. To establish whether PPIs are the cause of such bile, these papers are irrelevant for obvious reasons.

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Bile Reflux caused by PPIs

A Google search for - omeprazole causes bile reflux is of interest. However see also the section below Gall bladder and PPI usage

There is a page describing the regulation of bile release, from the University of Washington. This gives no clues as to how PPIs might affect bile release.

So there seems to be few references to Omeprazole promoting bile reflux - but at more than one paper realises that it probably does. My own experience is that it certainly does!

Maybe a Google search for Barrett's bile or proton pump bile reflux will reveal more?

So, if you are on PPIs you may be replacing acid reflux with bile - or with bile-tainted acid! How can you tell the difference?

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Bile Reflux, effects of PPIs on

The astute reader will have noticed my own belief that Barrett's oesophagus is a protection against acid reflux and is not protective against bile. So to be fair, I quote some papers that disagree. I Googled for Proton pump inhibitor bile

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Bile, effects on the oesophageal lining

Whatever the truth about PPIs causing bile reflux, there is growing evidence that bile is more damaging to the oesophageal (and, presumably the stomach) lining. PPIs cause definite malfunction of the gall bladder in the majority of cases and as this is likely to cause bile release at the wrong time it is likely that PPIs can cause bile reflux: certainly they did so in myself.

Until the medical profession understand this - and bile as a contributory cause of Barrett's is a clouded view - over use of PPIs will continue! I have no doubt that bile is a contributory cause of progression to cancerous oesophageal adenocarcinoma will also increase.

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Biliary dyskinesia

Gall bladder function is normally measured in terms of GallBladder Ejection fraction (GBEF). This is the percentage of bile released when the gall-bladder contracts. It is usually measure by injecting the hormone - CholestoCystoKinin or CCK - that causes it to release bile.

Diskynesia means poor ability to move: in this case it is poor functioning of the gallbladder. Searches for PPI biliary dyskinesia and GallBladder Ejection fraction are revealing:

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Cancer risk?

Barrett's oesophagus is said to be a cancer risk, sometimes leading to oesophageal cancer. However cats and dogs get Barrett's and it has been experimentally induced in rats and rabbits (both of which are used to study the phenomenon!) - with great ease. So it is an evolved response to acid reflux and is probably possible in all mammals. This hardly satisfies me that Barrett's is any real cancer risk!

The actual figure of incidence of cancer developing in Barrett's oesophagus is open to doubt: figures once were quoted as high as 5% of Barrett's sufferers develop cancer per year, but other, more recent, studies have shown the risk to be far smaller than that. 0.5% to 0.9% or even as low as 0.22% per year! In other words, the experts simply do not know!

It seems likely that whatever causes oesophageal adenocarcoinoma also causes Barrett's oesophagus, on its way to full-blown cancer. So Barrett's is a danger sign and the cause of it should be reduced. However - Barrett's seems not necessarily to be the actual cause but more of a symptom.

Cancer risk generally is also linked variously to certain foods: some foods reduce the risk of cancer, others seem to increase it. Whether this affects orsophageal adenocarcinoma, I would not like to guess. See my own thoughts on Cancer.

I found that PPIs caused, in myself, bile reflux - something I never experienced before taking medication. As PPIs are known (but not generally admitted) to cause gall-bladder malfunction in a large number of people, bile reflux seems likely to be a common effect of taking PPIs. It seems likely that this increase in cancer risk is likely to be due to the bile reflux. See PPIs - long term use increases risk of cancers.

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Digestive and Endocrine systems

There is an interesting series of biomedical hyperbooks at Colorado State University. If you are suffering from digestive problems, you should learn about yourself and how things work. This is a very good place to learn. Some that are of particular relevance are:

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Enzyme inhibitors: the way they work

See also how Proton-Pump Inhibitors work.

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Gall bladder and PPI usage

A couple of correspondents emailed me with huge problems with bile reflux and gastritis. Both have had their gall-bladders removed. Both have been on long-term PPIs. So is there a link?

A Google Scholar search for Gall bladder PPI turns up:

If PPIs cause cholestasis, the pair of papers above, which were done by a CholestoCystoKinin-stimulated hepatobiliary acid scan, indicate that there are two possibilities: either PPIs interfere with the CCK hormone receptor of the gallbladder, or else PPIs interfere with the motor ability of the gallbladder. But is seems that some 20% of the population tested may be immune to the effect. Why? For more evidence of bile problems see the links above on:

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Gastric fluid analysis

An article in Pharmacy times says investigators from Duke University Medical Center and Toronto General Research Institute wondered how PPIs affect gastric fluid˜an area few researchers have examined in the past. The article they refer to is below. The analysis looked for bile, gastricsin, trypsin, and pepsin concentrations. Bile and trypsin are not produced in the stomach, but in the liver and pancreas respectively, so should not normally enter the stomach unless the sphincters of Oddi and the pyloric sphincter are incompetent in some way. Gastricsin and pepsin are both produced in the stomach so their percentage may be expected to rise if acid production is reduced.