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steveb8189
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Quote steveb8189 Replybullet Topic: Bile reflux
    Posted: 19 Apr 2017 at 10:20am
My understanding of current research is that it probably takes both bile and stomach acid to cause Barrett's. It seems that potentially what differentiates people who have reflux esophagitis for years compared with those who go on to develop Barretts is the presence of bile.

Question: Is there any way of knowing if you have bile reflux? I have experienced vomiting of bile a couple of times due to bad stomach bugs and you really know the difference between it and normal stomach contents.

Question 2: Is there any possibility diet could provide a substitute for bile required to develop Barretts? For example, additives in cola contain similar compounds to those found in bile - is there any chance that could be enough, when combined with acid damage to trigger the changes required for development of Barretts? I can't find any research to suggest it has been investigated whether consuming substances can lead to the same outcome as refluxing them. It makes logical sense to me that if you drank bile and stomach acid (probably not recommended) you could also develop Barretts. Is there anything to suggest any food stuff consumed on a regular basis could have the same effect? I mean cola has pH of around 2.5 which is in the ball park for stomach acid.

Thoughts?
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chrisrob
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Quote chrisrob Replybullet Posted: 19 Apr 2017 at 11:04am
Hi Steve,
You're right. Bile does play an important role in the development of Barrett's (and its reflux is also implicated in the production of laryngeal cancers and pulmonary fibrosis).

As described in this genesis of Barrett's Oesophagus, bile acts as a detergent to permit acid to break down fats - including stomach acid breaking down the epithelial layer of the oesophagus.

And there are many research papers that have shown this. Here are just a few from BW archives:
Bile – not Acid – is Bad Guy in Triggering Precancerous Condition Associated with Reflux Disease (April 2012)

The Role of Acid and Bile Reflux in Esophagitis and Barrett’s Metaplasia "data in vitro have begun to explore mechanisms whereby acid and bile salts can regulate expression of CDX2. In HET-1A immortalized human esophageal squamous cells, the bile salts deoxycholic acid and chenodeoxycholic acid have been found to increase CDX2 mRNA expression, and when bile salts are combined with acid, demethylation of the CDX2 promoter can be detected" (April 2010)

Bile acid at low pH reduces squamous differentiation and activates EGFR signaling in esophageal squamous cells in 3-D culture "These results suggest that bile at low pH, but not bile or low pH alone, promotes loss of differentiation status of stratified squamous esophageal epithelium in vitro" (October 2013)

Bile acids induce activation of alveolar epithelial cells and lung fibroblasts through farnesoid X receptor-dependent and independent pathways. "Bile acid microaspiration may promote the development of pulmonary fibrosis by inducing activation of AECs and lung fibroblasts via FXR-dependent and independent pathways." (May 2016)

Bile is not usually found in the stomach but, as was first observed by William Beaumont (the 'father of gastroenterology') in 1833 in his book Experiments and Observations on the Gastric Juice, and the Physiology of Digestion: “I have observed that when the use of fat or oily food has been persevered in for some time, there is generally the presence of bile in the gastric fluids.”
It is permitted to backflow into the stomach from the duodenum when required to help break down animal fats.

Bile has a distinctive taste which is more noticeable in the absence of acid. (So you're more likely to be aware of it if using PPIs.)
In quantity, you may observe it as a thick green liquid.

To reduce bile in the stomach, some suggest reducing the consumption of animal fats. However, some fats are required by the body. It is better to ensure when eating fats, they are consumed in small mouthfuls, well chewed and eaten slowly. This means less bile may be needed.

The cola hypothesis may not work. Foods, and in particular drinks, consumed usually pass through the oesophagus to the stomach too quickly to have any lasting impact on the mucosa - except, perhaps, in achalasia patients.
When refluxed, liquids are not prone to peristaltic pressure, the epithelium is not protected by increased mucous and the upward pressure keeps them in situ longer.
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Saz10
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Quote Saz10 Replybullet Posted: 19 Apr 2017 at 2:49pm
I'm seeing a professor at Cambridge hospital who has told me bile gastritis does not exist. I was diagnosed with bile gastritis and Barrett's without intestinal metaplasia in Jan 2016 by my original consultant at my local hospital as I was continually feeling sick. He prescriped a PPI, but they did not help the sickness/gnawing pain in my stomach. He referred me to the Professor at Cambridge who is a specialist is Barretts because I had a complete melt down by the Barrett's diagnosis. I had another endoscope at Cambridge who concluded it wasn't Barrett's but could not explain why I still felt sick. The Professor said that it can not be bile gastritis because it doesn't exist. I have been prescribed 20mg of amitriptyline which has helped a bit but I am really cautious that these tablets are just masking the irritation to my stomach, but how do you disagree with the Professor. I have had a pH/mobility test but I have not had the full results yet but the dr who performed the test said she did not see any pathological acid reflux when she downloaded my data after my 24hours with the monitor on. However, the dr did say I had poor mobility in my oesophagus at times.
Where do I go from here? Any questions you think are worth putting to the Professor when I next see her in June?
Thanks
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chrisrob
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Quote chrisrob Replybullet Posted: 19 Apr 2017 at 3:16pm
Hi Saz,

If it's the Cambridge Professor I'm thinking of, I have disagreed with her on a couple of notable occasions.

1. In 2008 when I expressed concern about continual high dose PPIs reducing stomach acid and preventing absorption of essential minerals. She said minerals are absorbed in duodenum.
She now acknowledges low stomach acid can mean minerals are not converted to chlorides for absorption in the duodenum.
2. A few weeks ago, when discussing priorities for research spending, she said surgery was only for when PPIs don't work. I suggested to her surgery was for when the problem was mainly reflux and PPIs were for when symptoms were mainly acid.
This seemed to come as something of a revelation to her to muse on, despite her having been instrumental in producing
this option grid for NHS.

I guess she means bile (per se) doesn't cause reflux? (But neither does acid.)
Whether "bile gastritis" exists may be questionable depending upon terminology. Gastritis is inflammation of the stomach lining usually caused by excess acid. Bile may or may not be a constituent but cannot be the cause by itself.

As described so often, when bile refluxes alongside acid, it can cause problems - such as Barrett's oesophagus etc.

But she is doing a good job getting cytosponge progressed (and getting her name linked with it).
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nanafran
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Quote nanafran Replybullet Posted: 19 Apr 2017 at 3:49pm
probably im completly wrong . but when i saw,my consultant he also did an ultra scan as well as endoscopy. the ultra,scan shiwed a very small polop on my gallblader. The consultant wasnt concerned and said he would order another ultrascan with my endoscopy next January.would the gallblader polop cause bile .
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steveb8189
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Quote steveb8189 Replybullet Posted: 19 Apr 2017 at 7:45pm
Thanks Chris for your extensive feedback. I have read those arrivals so and many more on the subject - I'm lucky as a student to have access to most papers in full :) I have no doubt bile is a strong factorbin progression.

I would challenge you on your comments on my "cola" theory ;) i hadn't considered the rapid transit of food and drink when going down the right way as we are pretty much all refluxers on here so I presumed it would come back up again and then have the potential to sit in the eosophagus. This is why I wonder if food could have a part to play and wonder if any analysis has been done on long term exposure of different foods to the eosophagus.
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jcombs99
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Quote jcombs99 Replybullet Posted: 19 Apr 2017 at 9:48pm
If u think ur having trouble with food laying in O take a SIP of water flushing it back down and not a liter.
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chrisrob
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Quote chrisrob Replybullet Posted: 19 Apr 2017 at 11:02pm
Steve,

There have been many studies about foods.

Here are some which may or may not address your issues:

Diet and Gastroesophageal Reflux Disease: Role in Pathogenesis and Management: "Although anecdotal evidence has suggested associations with certain foods (fats, nonvegetarian, fried foods, and beverages) with reflux symptoms, objective evidence based data in this field remain unclear. Recent evidence points to the increasing importance of lifestyle in disease development as well."

Dietary Intake and Risk for Reflux Esophagitis: A Case-Control Study: "Although there are conflicting data regarding the role of dietary nutrients in GERD, there is no direct evidence that some nutrients promote or protect against GERD."

Are Lifestyle Measures Effective in Patients With Gastroesophageal Reflux Disease? "Despite articles in the literature emphasizing the insufficient evidence to support an association between lifestyle and dietary behaviors and GERD, such interventions continue to be recommended as first-line therapy."

since I may add a small extra segment on diet in the revisions I am making for the second edition of the Down with Acid book, I'd welcome notification of anything you find that may be relevant. (Peer-reviewed research.)

N.B. I do keep an archive of research links which may be visited on the BW website here.

Cheers,
Chris
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