GERD AND THE FEEDLOT FOURTEEN
That substernal burning sensation you get as your goose broils from acid reflux is called aptly enough gastroesophageal reflux disease (GERD). Your Doc in the Box (DIB) will tell you otherwise but the most common cause is from the overconsumption of cereals and sugars which leads to form of dysbiosis. Do you know what I am referring to? What I like to call The Feedlot Fourteen? It’s the 14 USDA recommended servings of heart healthy grains per day that fattens you up like a feedlot animal and potentiates GERD. At least that’s when potatoes were considered a vegetable. As you know the recommended treatment for your cooked goose is through acid suppression. These materials come in three forms: oral antacids like Rolaids, histamine receptor blockers (H2 blockers) like Pepcid and Tagamet, or proton pump inhibitors (PPI) like Prilosec (the old purple pill) and Nexium the new purple pill & a top ten cash cow.
Here’s the problem: the treatment can become the cause. In effect the chronic use of acid suppression therapy allows bacteria to proliferate in the stomach and small bowel where they are not supposed to be. Eating simple carbohydrates and starches provides ample food for bacteria and may promote small intestinal bacterial overgrowth (SIBO, see below for definition) which causes GERD. PPI’s also cause a type of addiction: when stopped abruptly there is theorized to be a type of rebound hyperacidity which potentiates symptoms of GERD. Another study out of Denmark showed that PPI’s generate GERD-like symptoms even in normal, healthy patients without GERD upon discontinuing their PPI after 8 weeks of daily use. The authors suggest that a phenomenon called drug-induced “rebound acid hyper-secretion” (RAHS) may be responsible. In other words, these researchers believe that taking PPI drugs cause you to hyper-secrete stomach acid when the drug is removed.
A detailed explanation offered by Dr Robillard author of Fast Tract Digestion Heartburn is that PPI’s create the perfect environment for SIBO which in turn exacerbates GERD. In other words PPI’s cause GERD but through a novel mechanism. If PPI’s make SIBO worse wouldn’t stopping the medication, which then decreases stomach pH, which in turn decreases the proliferation of bacteria in SIBO, cause relief of symptoms? My personal communication with Dr Robillard answered some of my questions. For example how does his theory explain this rebound phenomenon? Dr. R. explains: once SIBO is established through numerous mechanisms shown below keeping the gastric pH high with PPI drugs favors the conditions for SIBO which in turn accentuates GERD even though the patient is not aware of it. He is not aware of the burning feeling of “regurge” because the gastric pH is high and therefore less “erosive” to the goose. This way Chad can eat two entire hot pepper-meatball subs with extra bun and an order of chili-cheese fries and still operate his front end loader without belching the festering contents all over his new Carhartt’s knockoffs.
Now when you stop the PPI abruptly the pH of the stomach drops within a day or two as the medication wears off. Recall that the lower the pH the higher the acid content. Those pesky SIBO critters aren’t dead yet (from the new lower pH) and now their presence is better known to Chad who feels his goose broiling from the lower pH and a still incompetent GE sphincter due to SIBO. He now has the worst possible conditions of reflux and burning hot stomach acid. This usually prompts Chad or Billy or anyone else for that matter to run for the Tums and Prilosec thus returning the pH to proper, pathologic SIBO conditions and maintaining the disease called GERD.
I asked Dr Robillard if he could explain why patients get heartburn relief from drinking apple cider vinegar or taking an HCL tablet. He explained to me that this might be where the theory of hypersecretion is incorrect. Here we may be adding in much needed acid after PPI therapy is stopped and gastric pH is still high. The extra acid inhibits SIBO and you feel better. I can vouch for that since I have had GERD in the past and gulping down a little vinegar really feels good. Just the opposite of what you might expect. Add in some DGL licorice root to coat the injured epithelium and you are good to go. Just don’t start eating a plate of tamale long johns and funnel cakes with the hope that your heartburn remains at bay.
As you can see we do not have all the answers since there have been no studies to date (Jan. 2013 personal correspondence with Dr R.) that have measured gastric pH after PPI therapy is discontinued. Until then we won’t be able to fully know what is happening in the gut during this time. Even before we learn more about this strange world of the goose if you are on a PPI or your doctor suggests that you try a course consider doing Dr Robillard’s dietary intervention first since PPI’s are not without sometimes bad consequences as shown below.
CHRONIC PPI EXPOSURE
A life-threatening disease caused by the overgrowth of Clostridium difficile has been linked to chronic use of PPI and H2 blockers. Scientists have also demonstrated a link to increased pneumonia caused by reflux of their own stomach bacteria.Dr Laheij at the University Medical Center at St. Radboud in Nijmegen, the Netherlands, found that the risk of pneumonia almost doubled in people taking proton-pump inhibitors for prolonged periods of time.
But wait there’s more. It appears that that chronic use of PPI’s leads to osteoporosis and increased rates of hip fracture. Subjects taking PPIs in high doses for long periods of time increased their risk of hip fracture by 245 percent. Note that as many as 50% of people taking a PPI suffer from bacterial overgrowth.
The higher pH of the stomach leads to decreased absorption of both calcium and magnesium. The decreased absorption of calcium eventually shows up as weakened bones and fractures. Throw in the current insanity of sun-fear and the consequence of very low vitamin D3 levels and you have yet another reason to break your hip. Keep in mind that as you get older your stomach’s ability to produce acid decreases and an H pylori infection may also decrease stomach acid.
Magnesium levels are already too low in about 75% of the population due to several reasons including soil depletion over the last century. Low magnesium levels can cause serious metabolic disturbances of the heart and brain. Magnesium may the single most important mineral in human health since it is involved in hundreds of metabolic processes and it’s an antidote to excitotoxin induced brain cell damage. Lastly, a nice DADD (Dangerous and Deadly Dysergy) forms when we consider the fact that many Americans do not eat enough fruits and veggies which serve as a nice alkaline balance to the excessive consumption of meats and cheeses which acidify the blood. I know we are told to eat cheese and dairy for strong bones but eating those foods generate acids which require more buffer from-you guessed it-bones leading to a perfect hip fracture storm. If you want strong bones eat more dark, green leafy vegetables.
BACTERIA IN THE SMALL INTESTINE
Much of the following comes from Dr. Robillard’s ebook. 
Lactobacillus acidophilus and several related species present in the small intestine are known as homolactic fermenters. Unlike most other bacteria, homolactic fermenters do not produce gaseous end products which is a good trait right?
Other (heterolactic) bacteria break down starch and sugars to produce a wide variety of end products including lactic, acetic, propionic and butyric acids, but they also produce gases such as carbon dioxide, hydrogen, and sometimes methane. Together these gases may induce reflux along with other fun things.
Fermentation therefore needs to be confined to the large intestine where it normally occurs. Your stomach acid serves several purposes. One it helps to prevent the proliferation of harmful bacteria from your food or drink. Two it keeps the overall cell count in the stomach/small intestine low so that fermentation occurs downstream only. Keeping the cell count low in the stomach prevents reflux of harmful bacteria into your sinuses or lungs. Bile also acts as an antimicrobial in addition to its other functions. This helps to keep small intestine bacteria at bay. A protective mucus is secreted by special cells in the stomach and small intestine that coats and shields the intestinal surface from harmful bacteria and stomach acid.
Peristalsis is the rhythmic contraction of the gut from the stomach to the small intestine (SI) to the large intestine (LI). This motion is normally one way from proximal (SI) to distal (LI). It too helps to keep bacteria from the large intestine from migrating into the small intestine. There exists the ileo-cecal valve at the beginning of the large bowel. It acts as a one way valve to allow SI partially digested material called chyme to be introduced into the LI without allowing bacteria to enter the SI.
When your gut is functioning properly starches and glucose are readily absorbed across the SI lumen thus depriving any bacteria of an excess food supply and allowing proliferation to occur. Special intestinal epithelial cells secrete antimicrobial mucin proteins and certain peptides that help kill foreign bacteria. They also secrete antibodies IgA and IgM produced in response to bacterial cell surface proteins on harmful bacteria. SIBO and GERD get their start when this balance breaks down. We’ll continue our discussion of SIBO next week.
Fossmark R, Johnsen G, Johanessen E, Waldum HL. Rebound acid hypersecretion after long-term inhibition of gastric acid secretion. Aliment Pharmacol Ther. 2005 Jan 15;21( 2): 149-54.
Robillard Ph.D., Norman (2012-04-12). Fast Tract Digestion Heartburn (Kindle Locations 6733-6741). Self Health Publishing. Kindle Edition.
 Reimer C, Søndergaard B, Hilsted L, Bytzer P. Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology. 2009 Jul; 137( 1): 80-7.
Robillard Ph.D., Norman (2012-04-12). Fast Tract Digestion Heartburn (Kindle Locations 6744-6746). Self Health Publishing. Kindle Edition.
 Dial S, et al Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated disease. JAMA. 2005 Dec 21;294( 23): 2989-95. From Robillard Ph.D., Norman (2012-04-12). Fast Tract Digestion Heartburn (Kindle Locations 6533-6535). Self Health Publishing. Kindle Edition.
 Robillard Ph.D., Norman (2012-04-12). Fast Tract Digestion Heartburn (Kindle Locations 6533-6535). Self Health Publishing. Kindle Edition.
 Lombardo L, Foti M, Ruggia O, Chiecchio A. Increased incidence of small intestinal bacterial overgrowth during proton pump inhibitor therapy. Clin Gastroenterol Hepatol. 2010 Jun; 8( 6): 504-8.
Robillard Ph.D., Norman (2012-04-12). Fast Tract Digestion Heartburn (Kindle Locations 6773-6776). Self Health Publishing. Kindle Edition.
 IBID Fast Tract Digestion Heartburn (Kindle Locations 6773-6776). Self Health Publishing. Kindle Edition.
 Robillard Ph.D., Norman (2012-04-12). Fast Tract Digestion Heartburn (Kindle Location 522). Self Health Publishing. Kindle Edition.