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bdr1
Regular Member


Date Joined Aug 2005
Total Posts : 121
   Posted 8/23/2005 3:59 PM (GMT -7)   
Hey Norm, et. al --
 
Norm, I'm going to write more extensively in a response your previous post.  However, I just thought -- has any of your research into the carb "lifestyle" noted results from an endoscopy.
 
I thought of this -- as I spoke to a patient today who complained of mild-GERD symptoms with occassional night-time GERD.  I put her on Nexium = she was symptom free (after 1 day) & referred her for an endoscopy.  I received the results today stating that she actually had a Grade-D erosion (from the LA Classification system).  I was shocked because she came in virtually pain free and only mentioned any symptoms because her daughter brought it up during her visit.
 
Additionally -- I did a quick literature check and found an article by Johnston & Fennerty stating that heartburn symptom drastically underestimated erosive severity in the elderly.
 
That said -- on your diet, I wonder if people are still refluxing (and possibly could be damaging their esophogus) but not feeling symptoms?
 
best,
ckgMD

Teri16
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Date Joined Dec 2003
Total Posts : 5230
   Posted 8/23/2005 4:04 PM (GMT -7)   
Some interesting thoughts.

Best Wishes to you, Teri :)
"Because he is he and I am I."......E. V. Lucas

"I Hope You Dance".............LeeAnn Womack
 
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Norm1
Regular Member


Date Joined Jul 2005
Total Posts : 326
   Posted 8/23/2005 11:22 PM (GMT -7)   
ckg,

Nice to hear from you again. Concerning your question about current endoscopic work for low carb lifestyle, I am aware of work in this area but cannot comment due to a confidentiality agreement. I believe, however, that you have things reversed.

Esophageal damage was once considered a direct result of acid refluxing from the stomach into the esophagus. There is a growing belief emerging that the damage is caused both by acid (associated with heartburn pain) and duodenal enzymes and bile (perhaps not associated with pain) caused by duodenal reflux. My book explores this concept in detail. If gas from microbes consuming unaborbed carbs is the root cause and driver of reflux, as I believe it is, then duodenal reflux will most definately play a role, as the duodenum is the first part of the intestine connected to the stomach via the pyloric sphincter. Gas in the small intestine (and maybe early part of the large intestine) pushes intestinal / duodenal contents into the stomach and then pushes the whole mess into the esophagus. When you limit (significantly limit, at least for two or three days, as mentioned in my other posts) your consumption of excess carbs, much less gas is produced and the driver of both duodenal reflux and acid reflux is removed. The esophagus should not be exposed to either acid or duodenal enzymes and bile. I believe this could be the reason the dramatic increase in the consumption of carbonated beverages containing lots of carbs (and carbs in general) have been correlated with a huge increase in the frequency of esophageal cancer.

Now, you mentioned that your patient, who was on Nexium and pain free, was suffering from significant esophageal damage. We know for certain that the PPIs like Nexium only neutralize stomach acid. If people (on Nexium) continue to consume more carbs than they can absorb via their intestines, the microbes eat these carbs and produce gas. The gas pressure causes cycles of reflux. The acid is gone, due to the Nexium, but the duodenal enzymes and bile are still there and reflux into the stomach and then esophagus. On top of that, stomach acid normally causes floculation of bile entering the stomach. The bile falls out of solution like sand and causes not more damage. But if you are on a PPI, like Nexium, the acid is not there to stop the bile from refluxing intact into the esophagus. That is why people on PPIs like Nexium, but not on my diet plan, may be at a significantly higher risk for esophageal damage, barretts esophagus and even esophageal cancer.

I would like to hear your views on this. As always, nice to converse with you. This debate is greatly needed.

Dr. Norm

bdr1
Regular Member


Date Joined Aug 2005
Total Posts : 121
   Posted 8/26/2005 1:41 PM (GMT -7)   
Hey Norm,

I just got a chance to read your response post ... again ... thank you for your thoughts.

Just a quick point of clarification ... I initiated the PPI therapy only 2 days before the endoscopy. I was quite shocked when I saw the GE report that my patient had such endo-verified damage ... as her symptom severity definately did not correlate to her disease state. My concern with part of your argument arises, though, when you discuss duodenal reflux. I definately conceed that an acidic environment is necessary for daily functioning (thus, PPI therapy only maintains a pH>4 for a certain period of time) and that pH neutralization by PPI therapy neutralizes the acid in the stomach ... I'm not exactly sold, though, on how bile caused by duodenal reflux could not be symptomatic. Especially given that the relaxation at the LES junction.

Additionally -- specifically regarding carbonated drinks -- diet carbonated drinks lacking caffeine & carbohydrates still induce refluxation. How do you account for this?

Further -- one big portion of discussion that I'd like to have is those patients whose anxiety/depression/panic/etc. drives their reflux. As a case example, I've recently had a patient who I diagnosed with GERD and (subsequently) GAD. PPI therapy helped her quite a bit, but she was still having some break-through symptoms particularly in the afternoon. In further discussions with her, she revealed a history of anxiety symptoms. After continuing her PPI therapy, I added a mild anti-anxiety med (BuSpar, if I recall correctly) + Zoloft and her GE distress stopped very shortly thereafter. I did, however, refer her to psych for an eval and they initiated behavioural therapy which I think will help her more in the long run. But, nonetheless, I am intrigued what your thoughts would be on such a phenomenon and it's relation to your methodology.

On a personal note --- you did work with Cipro, eh? Interesting to see such a jump from one of the strongest anti-biotics to naturopathic-type therapy. As a side-note, the Bayer make me mad when they advocate CiproXR for UTI's ... they still can answer me why I would use a quinalone, when I could use something far less strong and comparably as effective. Oh, and i'm in NY-Metro -- not a CA doc, yet.

Norm1
Regular Member


Date Joined Jul 2005
Total Posts : 326
   Posted 8/26/2005 10:57 PM (GMT -7)   
ckg,
I wanted to write a quick note to you while I digest (no pun intended) your points. I agree that duodenal reflux may in fact contribute to symptoms. I am not sure about that as this phenomenon is not easily separated from acid reflux. Bile is basic but reportedly just as corrosive as acid.

Concerning your patient (I really envy your connection with these patients. If you were in LA, I would ask to go on rounds with you one day), I understand now that you were surprised at her condition because her symptoms (even before treatment) had been reported as mild and it relates your your reading on the elderly with less symptoms, worse condition. Could it be that nerve endings become damaged by the reflux and eventually people can't feel the continuing damage. This would be interesting to look into.

You continue to speak of relaxing LES. I am still not on board with this concept and feel that gas pressure is more likely driving reflux. One reason I am less concerned with the carbon dioxide in soda is from my personal experience with diet cola on low carb. I don't get acid reflux but do belch. I think the reasoning might be that soda likel releases its CO2 gas shortly after entering the stomach as it is no longer presurized. The belching right after you consume it is likely inert because it is being released near the top of the stomach and therefore does not tend to push stomach contents through the LES. Gas produced further on in the intestinal tract is much more likely to push intestinal/ duodenal and stomach contents into the esophagus.

I am not knowledgeable about the connection with depression / anxiety and reflux. I have heard this and at times likely experienced it. All I know is that on low carb, I never get reflux, even under max stress. Are you aware of studies that have quantitated this connection? Interesting that you have found some clinical success with anti-axiety drugs. I had not heard of this as a treatment for GERD. You can educate me here.

I see you have stumbled accross some of my early papers on Cipro. In my early days with Bayer, I conducted research on the mechanism of action of quinolone antibiotics. My strategy was to isolate resistant mutants and map or clone the genes responsible, find out what they did and hopefully develop a strategy to make better antibiotics. I know some in the company did not like the fact that I was publishing papers on cipro resistance!

I was never in the marketing end and so can't comment on how Bayer markets cipro. It's off patent now anyway. I agree with you though, that almost anything will cure a UTI, why use cipro. I moved into biotech research after that, making mouse human chimeric antibodies and developing PCR assays for virus detection. Those were some fun days. I am currently with another biotech company. I am not against drugs. But there is a risk / benefit decision that needs to be made. I also feel that when you can treat successfully with diet or other holistic approaches, they tend to make more sense. The only problem is that many homeopathic remedies just don't work and have not been tested very extensively, if at all, for safety. My son and daugher in law lived with me for a time and now that they have moved I have thrown out more GNC products than you can imagine. I would never take that stuff..... Just a personal choice.

Norm1
Regular Member


Date Joined Jul 2005
Total Posts : 326
   Posted 9/2/2005 12:54 AM (GMT -7)   
ckg,
I miss your posts. One question I have about PPIs is that just neutralizing the acid, according to my threory, will not stop resflux caused by consuming too many carbs. If reflux continues and duodenal contents contribute to esophageal damage, will these patients still be at risk for Barretts and esophageal cancer? Has any definitive work been done in this area?

Thanks,
Dr Norm
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