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Barrett's oesophagus - what is it and is it dangerous?

In 2008, after a life-time of reflux, I was diagnosed with Barrett's oesophagus. This is a summary of what I have learned about the condition.

In this page the link =LoP= will take you to my page of references to learned papers relevant to the point. It will open in a new window.

Contents, this page

What is Barrett's oesophagus?

Barrett's oesophagus is a change in the cell type which lines the oesophagus. The change is a response to gastric fluid splashing up into the oesophagus - the cells change from the normal type to a type that is more resistant to the fluid. Most commonly the cells change from the normal type (called squamous cells) to cells similar to the type found in the intestine (called columnar cells), but there are in fact three different types of cell which may occur.

The change is done by the cells switching off certain genes by a process called methylation. As it happens many of these genes are the same as those switched off in cancerous cells. So yes, Barrett's oesophagus can progress to cancer. But so, too, can normal cells: the oesophageal cells do not necessarily have to become Barrett's before developing to cancer.

The main point is that the Barrett's cells are more resistant to normal gastric fluid (acid) than are the unchanged cells.

How dangerous is Barrett's oesophagus?

Your doctor will have intimated that it is indeed dangerous simply by giving it a name and calling it pre-cancerous! If you have done any internet search on it, you will find that it is said to be pre-cancerous - and that is very scary!

However there are several studies =LoP= which put the risk more in perspective. The likelihood of progression seems to be as low as 0.22% per year

But let us look at a few facts about acid and digestion. Maybe the data I have found can help you navigate the least dangerous path as you live with Barrett's, for it's a condition which cannot be cured and may not be as dangerous as you think.

What causes Barrett's oesophagus?

The real snake in the grass is not the Barrett's oesophagus but reflux of gastric fluid into the oesophagus. So what might cause such reflux? None of these conditions are new - but neither is Barrett's oesophagus!

How common is Barrett's oesophagus?

I do not think any one knows the correct answer to this. Barrett's oesophagus (BO) is commonly said to have been first described by one Dr Norman Barrett in 1950 =LoP= but in fact the condition was described some 150 years earlier than that =LoP=

Oesophageal adenocarcinoma (OAC) has been on the rise since about 1985 =LoP=. I find that too closely dated to the release of omeprazole in 1988 =LoP= to be mere coincidence.

Because of this rise in OAC, monitoring for BO has increased, and it seems that the more you look, the more you find. Barrett's Oesophagus has no symptoms itself so until a person is given an endoscopy because of symptoms that may be due to reflux, there is no easy way of detecting BO (though this is changing - search for cytosponge). The only conclusion is that Barrett's Oesophagus is very common and its incidence may be increasing, causes by whatever is triggering the alarming rate of rise in oesophageal adenocarcinoma.

It is interesting that cats and dogs get Barrett's oesophagus. =LoP=It has also been induced with ease in rats. I suspect it can occur is almost any mammal with a digestive system similar to ours (so not in ruminants).

It is interesting that this columnar cell lining of Barrett's oesophagus also appears to be the normal type that occurs in the reptilian oesophagus and in fish. I also suspect in birds. So Barrett's oesophagus is almost certainly a mammalian condition and it is in fact an atavism to a more primitive cell structure found in non-mammals, that can better stand the acid reflux.

We humans (and other mammals) have clearly evolved Barrett's as a protective measure against this acid reflux. It's nothing new and must have been common throughout history!

How necessary is stomach acid?

All animals with backbones appear to have acid stomachs. =LoP= This includes fish, reptiles and birds as well as mammals. So stomach acid evolved many, many millions of years ago. It an evolutionary sense, is beneficial and not dangerous.

But is it necessary? PPIs (Proton Pump Inhibitors) can, if used properly, completely suppress acid production, and there are relatively few adverse effects. The common adverse side effects are almost all only caused by long term use and are listed on sites such as the British National Formulary. But there are other not-so-common side effects which are more serious: =LoP=

However stomach acid is part of a very complicated hormonal system which regulates acidity, controls bile release from the gall bladder, affects appetite and maybe does even more. Switching off acid production (which is what PPIs do) is like throwing a large spanner into a complicated machine. What is amazing is how few unintended effects this actually has - but it can have an effect on the gall-bladder and this is surely the mechanism that causes bile reflux. Bile reflux seems to be ignored by the doctors as they cannot control it. As my consultant endoscopist said I'm surprised you think you can tell whether it's acid or bile. More on this later!

Should bile be a common ingredient in gastric fluid?

Surely the answer to this is NO. It would be extremely simple for the doctors to answer this, simply by sampling gastric fluid - very easily done during an endoscopy! But they do not routinely do this so there are few references. =LoP=

At this point I must add that my opinions are strongly influenced by my own experience with bile when I was experimenting with PPI dosage. Such happenings need explanation!

Is bile necessary for Barrett's oesophagus?

There has been recent work that has been taken to indicate that bile is necessary for Barrett's Oesophagus to form. However all of these studies have either been in vitro or in animals. In science it is extremely difficult to prove a negative - so these experiments do not prove that Barrett's cannot form without the presence of bile.

What these experiments do prove is that acid reflux tainted by bile is far more damaging to the oesophagus than is plain acid reflux. This is strong evidence that bile should not be present in a healthy stomach!

It is also strong evidence that anything that causes abnormal bile reflux is likely to cause BO and to facilitate the progression of BO to OAC (Oesophageal adenoCarcinoma). One such thing is the family of PPIs, if not taken correctly - as I shall hopefully pro ve to your satisfaction.

Should bile be a common ingredient in gastric fluid?

You might think this question would be simply answered. But it seems that, since the medics cannot do anything about bile, they do not want to find out the answer. when I was first diagnosed a sample of gastric fluid was taken. I enquired about whether there was bile present? "We don't test for bile." was the reply.

My own experience is that I did not have bile present before I took PPIs. I did afterwards. See My life with gastro-oesophageal reflux.

While there is plenty of evidence that bile reflux is more dangerous than acid =LoP= there is plenty of evidence which finds that unproven! There is also evidence that PPIs cause upsets with the bile system. There is also evidence that PPIs can suppress bile reflux! This ambivalent attitude to PPIs and bile can, however, be explained. Read on!

Bile has even been implicated in the formation of Barrett's =LoP= so how much more must it be implicated in the progression to adenocarcinoma?

I consider the effect PPIs have on bile to be so important I have written a whole page about bile.

How do PPIs work?

Proton pump inhibitors have a very specific and well-defined chemical action on an enzyme (known as H+/K+ ATPase - or hydrogen-potassium adenosine triphosphatase) which controls the production of acid in special cells (parietal cells, aka oxyntic or delomorphous cells) in the stomach. There are links to technical papers =LoP=.

The point is that, unlike other drugs, the action is incredibly specific. If the concentration of the PPI in the blood is adequate, all of the enzymes in all of the cells will be poisoned and no acid can be produced. =LoP=

Acid will not again be produced until the liver metabolises away enough of the PPI for the blood concentration to fall below the critical level. The higher the concentration of chemical in the blood, the faster can the liver clear away the PPI. So the level does not drop constantly. As a result a 40mG dose is only very slightly better than a 20mG dose! =LoP= It is better to take several smaller doses than one large one!

However the stomach parietal cells are not the only place that Proton Pumps exist: every cell in the body has to maintain its correct acidity level and therefore contains a proton pump. Fortunately the way PPIs work is fairly specific to the parietal cells so there seem to be very few adverse effects on other cells. Nevertheless there are some indications that the story may not be that simple! =LoP=

The main problems with PPIs are that our bodies evolved with acid in our stomachs and our whole digestive hormonal system is geared to the presence of acid. So complete acid suppression throws a massive spanner in the works and this affects the gall bladder and the bile release system. =LoP= As a result bile reflux is common in people taking PPIs. =LoP= Surely this is why oesophageal adenocarcinoma has risen rapidly as the use of PPIs has increased. =LoP=

What are the disadvantages of taking PPIs?

So what are the pros and cons on taking PPIs? Certainly, as the history papers =LoP= prove, life before Omeprazole was discovered was extremely hazardous for some people. Without PPIs, the doctors would have no good solution to the pain acid reflux causes many. As my consultant said in an email One of the problems that we face with Barrett's oesophagus is that we have no good treatment for bile reflux and many of our patients they find the symptoms intolerable without suppressing the acid. PPIs do have several side-effects and potential long term sequelae although their record is pretty good.

But let's look at a few facts:

  1. Oesophageal adenocarcinoma has risen alarmingly since PPIs were introduced. The rise in OAC has been too closely linked to the increasing use of PPIs to be comfortable.
  2. If the rise in OAC has not been caused directly by the use of PPIs, then nobody seems to have established exactly what else is causing it. Things such as modern lifestyle or diet have been blamed, but no study has shown any true cause. Neither acid reflux nor Barrett's oesophagus are new. =LoP=
  3. PPIs cause reduced gall bladder function (biliary dyskinesia). =LoP=. Exactly what the mechanism is, I have not been able to determine, but the two papers I have found =LoP= have established experimentally that this is extremely common, even normal. The doctors noticed that patients gall bladder improved after a fundoplication. This surprised them. They hypothesised that the poor operation of the gall bladders before surgery might be due to the PPIs. So they tested healthy volunteers befor and after taking PPIs. The result was very clear!

    Since the PPIs reduce the efficiency of the gall bladder, there are circumstances undre which it is possible t show that PPIs reduce bile reflux.

  4. Exactly how this biliary dyskinesia causes bile reflux is not known, but apply a bit of logic. If bile builds up too much in the gall bladder, either gall stones will develop - and there are people who have had their gall bladders removed as, they claim, the result of being on PPIs too long. Otherwise the gall bladder will simply leak gall as the pressure gets too high. This will not be at the correct time, not under control of the hormones so may well get into the stomach.

    From my own experience, bile reflux seems to occur as a dose wears off, before new parietal cells can produce significant acid.

  5. Bile in the stomach is harmful. =LoP= It has been shown to cause gastric cancer and it has been shown to be a trigger for Barret's oesophagus. =LoP= It surely is the link between the increasing use of PPIs and the rise in OAC.


The only conclusion I can make from what I have found is that the alarming rise in oesophageal adenocarcinoma since PPIs were introduced is a direct result of the increasing use of PPIs. Statistically PPIs are relatively safe and even when on PPIs there is little chance of any one user developing cancer. However PPIs are so commonly prescribed when there is no real need that such a small chance becomes a huge number. If you have real problems with reflux - you need PPIs. But if you can manage reflux by any other method then that is surely your best option.

Can I stop using PPIs?

Here we hit on a problem. PPI cause a massive imbalance in the body's hormonal system. This system is a feedback loop which controls digestion. If you suddenly free such a system a rebound will occur. My own experience is that this rebound was bile - not acid. But it was extremely unpleasant! I went through it because I knew I had no other choice!

If you are to quit - how else will you handle the problems that originally caused you to go on to PPIs? You need to change your lifestyle - body weight seems to be a huge factor for most people and it's likely you need to be at the low end of what is normally considered healthy. Or maybe even lower than that!

My experiments tell you how I quit. I cannot say whether that will work for you but good luck and please let me know how things go!

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Page first published 15th November 2016.
Last modified: January 09 2020 17:32:52.
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