What is Acid Reflux and GERD?
About sixty million people in the US report that they suffer from painful symptoms of acid reflux at least once a week. Heartburn, abdominal pain, cough, regurgitation, sour taste in the mouth, sore throat, hoarseness, laryngitis, asthma-like symptoms and sinus irritation are the typical symptoms. Smoking, pregnancy, obesity, hiatal hernia and even tight-fitting clothes can make these symptoms worse.
Acid reflux occurs when acid and other contents of the stomach escape into the esophagus and beyond. Chronic acid reflux is often associated with damage because the esophagus and other affected tissues are not protected by the thick mucus layer that coats the inside of the stomach. And, the result is painful irritation which can lead to esophagitis, and Barrett’s esophagus, even esophageal cancer.
Persistent damaging reflux is referred to as gastroesophageal reflux disease (GERD). Acid reflux may also cause severe irritation of the vocal cords, a condition referred to as laryngopharyngeal reflux (LPR).
For me this subject is personal. I am one of the sixty million people. I suffered with acid reflux for a good part of my adult life. I never understood what caused it. I only knew that my constant heartburn and regurgitation symptoms interfered with my work, my sleep and my general wellbeing. My condition continued to get worse leading to anyone’s nightmare.
I awoke in the middle of the night and leapt out of bed still half dreaming, thinking “Oh my god, I’m dying. This is what it feels like to die.” I couldn’t breathe; I was choking for air and my lungs felt like they were filled with burning liquid. I ran to the bathroom coughing up something from my lungs that simply did not register. It felt like acid was filling my lungs. I soon realized that I had suffered severe acid reflux; stomach acid that traveled up my esophagus until I aspirated it into my lungs. I will never forget that moment. It defined the kind of fear and suffering that is possible with GERD.
Like many people with this condition, I recognized that my situation was becoming serious. But the recommended medicines – antacids, H2 blockers and even PPI drugs did not give me adequate relief and I never noticed any dietary pattern that improved my symptoms. But that all changed in 2004.
On the advice of my older son, a personal fitness trainer, I decided to go on a low carb, high fat diet (LCHFD) to lose a few pounds. What happened next made me forget about weight loss, because my reflux symptoms vanished the very next day. I couldn’t believe it! Why had no one ever told me about this? It turns out that most people didn’t know or were just finding out themselves. But thanks to Google, I soon realized that this was no fluke. Many others were saying the same thing and Drs. Mike and Mary Dan Eades had written about this in their bestselling book, Protein Power. I also found out that some doctors at Duke University had done a small clinical study confirming that cutting carbs can relieve symptoms.
While the revelation was a great reward in and of itself, for the first time in my life I could control my symptoms, I was far from satisfied. I really wanted to know why. If removing most carbs stops heartburn, did that mean that carbs caused heartburn? I decided to get to the bottom of things and started doing research on how each type of food (fats, proteins and carbohydrates) is digested. I read about and thought about the digestive process – chewing, salivary amylase for starch, stomach acid and pepsin for protein breakdown, lipase for fats, etc. And, as I started reading about digestion in the small intestine, a light bulb went off involving gut bacteria.
As a microbiologist, I had grown and studied a wide variety of bacteria for years in graduate school. I also worked with intestinal bacteria during a postdoc. at Tufts. While my focus was genetics, we constantly needed to grow enough bacteria to work with. And, I recalled two important traits of intestinal bacteria:
- They get the bulk of their energy from carbohydrates
- Most of them produce lots of gas
Depending on the strain, bacteria produce copious amounts of hydrogen and carbon dioxide gas. Also, intestinal Archaea, which look like bacteria under the microscope, but are actually a separate branch of life, produce a third intestinal gas, methane. Carbohydrates are the best fuel source for gas formation. 30 g of unabsorbed carbohydrate can allow bacteria to produce more than ten liters of hydrogen gas.  Imagine how much pressure this amount of gas would create in the intestines and this is only about one ounce of carbs. Intestinal bacteria produce so much gas that there have been well documented cases of explosions during intestinal surgery., This gave me an idea:
“What if some of the carbs I had been eating were not being efficiently digested and absorbed into my blood steam, and instead they were persisting in my small intestine? Wouldn’t there be a chance that my acid reflux was the result of intestinal gas pressure from a bloom of gas-producing bacteria fed by carbohydrates? I.e. mentos in a coke bottle”
Could the answer be that simple? I needed to learn more and find out if this idea was full of holes. And, I set out to destroy my own theory : )
What we can agree on
The first thing I did was learn all I could about what other scientists thought. One thing everyone seemed to agree on was that acid reflux occurs because the group of muscles at the top of the stomach are unable to keep the stomach’s contents from entering the esophagus. This group of muscles is called the lower esophageal sphincter (LES). The stomach’s contents include hydrochloric acid, bile and digestive enzymes. But why does acid reflux occur? According to the NIH:
“GERD results when the lower esophageal sphincter or LES becomes weak or relaxes when it should not, causing stomach contents to rise up into the esophagus.”
LES relaxation events are called transient lower esophageal sphincter relaxations (TLESRs). The LES appears to undergo these relaxation events, even when we are not swallowing. Both LES pressure and TLESRs can be measured by a technique called manometry, where a pressure-sensitive tube is passed down the esophagus through the LES. This technique has been used for many studies,, and clearly shows that GERD patients exhibit:
- More episodes of reflux
- Less LES pressure
- More frequent episodes of TLESRs
- More extensive reflux during TLESRs, particularly after meals
- More pressure in the stomach (intragastric pressure) and more belching
I wondered if some of these ideas might disprove my theory or were they somehow consistent with my own observations. I thought about each observation to see if there was some common thread. Though increased pressure in the stomach had been well documented in GERD patients, no one had a good explanation about where the pressure was coming from. But, my theory clearly explained a potential source: copious amounts of gas and pressure from bacterial fermentation in our intestines.
As for less LES pressure, you might be able to imagine intragrastric pressure “forcing” the LES to open as a possible mechanism of acid reflux. Clearly if this were to occur, the LES pressure measurement would be reduced by the intragastric gas pressure. In other words reduced LES pressure in GERD patients can be explained by my theory.
The same analogy can be applied to explain TLERs as well as increased reflux during TLESRs. The gas pressure forcing the LES to open would be measured as reduced LES pressure or relaxation events by manometry and be expected to increase the amount of refluxate in each event. This would be particularly true after meals if malabsorbed carbohydrates in each meal were driving the bacterial growth and gas production as I suspected. Thus, my theory also explains the increase in TLERs in GERD patients, particularly after meals.
While on the subject of gas pressure, there is one more important prediction my theory makes. If you were to stop the process of reflux and belching without resolving bacterial overgrowth, you might expect a buildup in gas pressure in the stomach and small intestine. One way to look at this question is to study people who have had fundoplication surgery, where the LES is surgically tightened, thus preventing reflux and belching. Reports on GERD patients who have undergone this procedure show that they suffer from new symptoms including excessive gas, flatulence and bloating., The procedure is aimed at preventing reflux by tightening the LES muscles surgically, but the side effects are indicative of trapped stomach and intestinal gas as would be expected with uncontrolled malabsorption, and excessive bacterial fermentation.
Essentially, I was proposing that excess dietary carbs could promote a kind of gut dysbiosis (unbalanced gut microbiota with too many gas producing strains), possibly small intestinal bacterial overgrowth (SIBO). According to this idea, acid reflux occurs due to microbe-induced gas pressure. As I continued my research, I wondered what the world might look like if my theory was correct. The first thing I focused on was bacterial overgrowth itself. I reasoned that you should see a reduction in GERD symptoms whenever you reduced bacterial growth in the intestine.
One way to control excessive bacterial growth in the intestine is to go on a low carb diet, because this type of diet limits carbohydrate fuel that bacteria need for growth. As I mentioned, low carb diets reduce the symptoms of GERD as well as esophageal acid exposure., These results support my theory.
Similar to a low carb diet, antibiotics can also reduce GERD symptoms, reduce esophageal acid exposure and even prevent reflux into the lungs. ,, One plausible explanation for this effect is that the antibiotics help GERD by inhibiting the growth of gas-producing gut bacteria. Interestingly, antibiotics have been shown to increase LES pressure which is consistent with this idea.
My theory predicts that “overfeeding” gut microbes with hard-to-digest carbs in particular, will make GERD symptoms worse. Prebiotics represent a way to test this idea, because prebiotics are carbohydrates that are not digested or absorbed. They are designed to feed the gut microbiota. But a study that looked at one prebiotic, fructose oligosaccharide (FOS), in GERD patients found that it caused more intestinal gas, increased GERD symptoms and increases in TLESRs. A logical explanation is that the fermentation of FOS by gut bacteria creates excess gas pressure that drives (even more) reflux symptoms.
Lastly, I reasoned that if GERD involved SIBO, there would be an overlap in patient populations between GERD and other conditions known to involve SIBO including cystic fibrosis (CF), irritable bowel syndrome (IBS), obesity and asthma.
GERD, IBS and CF:
Approximately 80% of people with cystic fibrosis (CF) also have GERD compared to about 15% percent in the general population.,,, But that’s not all. CF patients also exhibit less LES pressure and more reflux episodes during TLESRs. Why is that? I think it has everything to do with SIBO.
People with CF exhibit well-documented carbohydrate malabsorption and SIBO. The reason is that CF patients often have blockage of the pancreatic ducts by thick mucus, which blocks the release of the enzyme known as pancreatic amylase. Without this amylase, carbohydrate (starch) digestion and absorption does not occur in small intestine. The lack of amylase results in more carbohydrates available for fermentation by gut bacteria, which leads to reflux.
In GERD sufferers without CF, amylase release may not be blocked. But, for a variety of other reasons covered in the Fast Tract Digestion books (i.e. excess hard-to-digest dietary carbs, slowed motility, lactose intolerance, intestinal damage, etc.) I believe there also exists an oversupply of malabsorbed dietary carbohydrates. These excess carbs likely fuel excessive fermentation and induce reflux.
Approximately 50% of the people who have IBS also suffer from GERD and almost as many GERD patients suffer from IBS. This percentage is about three times higher than what is seen in the general population. IBS has been clearly linked to SIBO, and like GERD, has been treated successfully with carbohydrate restriction as well as antibiotics.,,,, This evidence is consistent with SIBO playing a role in both conditions.
GERD, Obesity and Asthma:
Obesity is tightly linked to GERD. Obese individuals generally consume more food, especially carbohydrates. You might predict that the increase in dietary carbohydrates would increase malabsorption leading to SIBO and reflux. Interestingly, carbohydrate restriction improves GERD symptoms and reduces esophageal acid exposure in obese patients whether or not they lose weight!
Asthma is connected to SIBO by way of IBS. A study of people with asthma showed that they had IBS twice as often as non-asthmatics. And, asthma is even more tightly linked to GERD. As many as 80% of asthmatics suffer from abnormal gastroesophageal reflux compared to about 20% of non-asthmatics.,  Several large studies showed that acid reducing drugs don’t improve asthma symptoms, but stopping reflux itself with fundoplication operations dramatically improves asthma symptoms. And, this results in a significant reduction in medicine usage., This suggests to me that something in reflux other than acid exacerbates asthma. Perhaps bile, bacteria and/or enzymes could be responsible. Leaky gut, another condition linked to SIBO, may be a factor in asthma as well, but the fundoplication data leads me to favor acid reflux as the most significant trigger in the exacerbation of asthma. It could even be an etiological cause of asthma. For more info, check out my blog on the Heartburn-Asthma link.
More recently, SIBO has actually been detected in GERD patients. Half of the GERD patients showed evidence of SIBO by glucose breath testing. Eighty-seven to ninety percent of SIBO-positive patients showed improvement after antibiotic treatment. The study design makes it difficult to draw final conclusions regarding SIBO and GERD however. The study included IBS patients and everyone in the study was taking PPI drugs, known to exacerbate SIBO. Also, the less sensitive “glucose” breath test method used.
I believe the number of SIBO-positive results in both IBS and GERD patients would have been higher if the study employed the more sensitive lactulose breath test instead of the glucose. Because lactulose is not digested or absorbed in the small intestine, it can detect bacteria throughout the entire length of the small intestine. Glucose on the other hand, is rapidly absorbed in the first part of the small intestine and will only detect bacteria if they are present in this region.
Instead of “destroying my theory”, all the evidence I looked at supported my idea: carbohydrate malabsorption and bacterial overgrowth is the root cause of acid reflux. But, how about other proposed causes? For instance, H. pylori and low stomach acid? My research has led me to some interesting findings. I examined both in my second article, “Is GERD caused by H. pylori & Low Stomach Acid?”.
Read the third article, “GERD – Why standard treatments are ineffective”.
Read the final article, “GERD diet that works without drugs”.
 Suarez F, Levitt M. Textbook of Primary and Acute Care Medicine. Second edition. Edited by Gideon Bosker. Page 1191.
 Dener IA, Demirci C. Explosion during diathermy gastrotomy in a patient with carcinoma of the antrum. Int J Clin Pract. 2003 Oct; 57(8):737-8.
 Bigard M-A, Gaucher P, Lassalle C. Fatal colonic explosion during colonoscopic polypectomy. Gastroenterology 1979; 77: 1307-1310.
 Iwakiri K, Hayashi Y, Kotoyori M, Tanaka Y, Kawakami A, Sakamoto C, Holloway RH. Transient lower esophageal sphincter relaxations (TLESRs) are the major mechanism of gastroesophageal reflux but are not the cause of reflux disease. Dig Dis Sci. 2005 Jun;50(6):1072-7.
 Dodds WJ, Dent J, Hogan WJ, Helm JF, Hauser R, Patel GK, Egide MS. Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. N Engl J Med. 1982 Dec 16;307(25):1547-52.
 Trudgill NJ, Riley SA. Transient lower esophageal sphincter relaxations are no more frequent in patients with gastroesophageal reflux disease than in asymptomatic volunteers. Am J Gastroenterol. 2001 Sep;96(9):2569-74.
 Dodds WJ, Dent J, Hogan WJ, Helm JF, Hauser R, Patel GK, Egide MS. Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. N Engl J Med. 1982 Dec 16;307(25):1547-52.
 Vakil N, Shaw M, Kirby R. Clinical effectiveness of laparoscopic fundoplication in a US community. Am J Med. 2003 Jan;114(1):1-5. Klaus A, Hinder RA, DeVault KR, Achem SR. Bowel dysfunction after laparoscopic anti reflux surgery: incidence, severity, and clinical course. Am J Med. 2003 Jan;114(1):6-9.
 Beldi G, Gláttli A. Long-term gastrointestinal symptoms after laparoscopic Nissen fundoplication. Surg Laparosc Endosc Percutan Tech. 2002 Oct;12(5):316-9.
 Yancy WS Jr, Provenzale D, Westman EC. Improvement of gastroesophageal reflux disease after initiation of a low-carbohydrate diet: five brief cased reports. Altern Ther health med. 2001. Nov-Dec; 7(6):120,116-119.
 Austin GL, Thiny MT, Westman EC, Yancy WS Jr, Shaheen NJ. A very low-carbohydrate diet improves gastroesophageal reflux and its symptoms. Dig Dis Sci. 2006 Aug;51(8):1307-12.
 Pennathur A, Tran A, Cioppi M, Fayad J, Sieren GL, Little AG. Erythromycin strengthens the defective lower esophageal sphincter in patients with gastroesophageal reflux disease. Am J Surg. 1994 Jan;167(1):169-173.
 Pehl C, Pfeiffer A, Wendl B, Stellwag B, Kaess H. Effect of erythromycin on postprandial gastroesophageal reflux in reflux esophagitis. Dis Esophagus. 1997 Jan;10(1):34-37.
 Mertens V, Blondeau K, Pauwels A, Farre R, Vanaudenaerde B, Vos R, Verleden G, Van Raemdonck DE, Dupont LJ, Sifrim D. Azithromycin reduces gastroesophageal reflux and aspiration in lung transplant recipients. Dig Dis Sci. 2009 May;54(5):972-9.
 Piche T, des Varannes SB, Sacher-Huvelin S, Holst JJ, Cuber JC, Galmiche JP. Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease. Gastroenterology. 2003 Apr;124(4):894-902.
 Ledson MJ, Tran J, Walshaw MJ. Prevalence and mechanisms of gastro-oesophageal reflux in adult cystic fibrosis patients. J R Soc Med. 1998 Jan;91(1):7-9.
 Vic P, Tassin E, Turck D, Gottrand F, Launay V, Farriaux JP. Frequency of gastroesophageal reflux in infants and in young children with cystic fibrosis. Arch Pediatr. 1995 Aug;2(8):742-6.
 Fridge JL, Conrad C, Gerson L, Castillo RO, Cox K. Risk factors for small bowel bacterial overgrowth in cystic fibrosis. J Pediatr Gastroenterol Nutr. 2007 Feb;44(2):212-8.
 Pauwels A, Blondeau K, Dupont LJ, Sifrim D. Mechanisms of increased gastroesophageal reflux in patients with cystic fibrosis. Am J Gastroenterol. 2012 Sep;107(9):1346-53.
 Lisowska A, Wójtowicz J, Walkowiak J. Small intestine bacterial overgrowth is frequent in cystic fibrosis: combined hydrogen and methane measurements are required for its detection. Acta Biochim Pol. 2009;56(4):631-4.
 Pimentel M, Chow EJ, Lin HC. Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome. Am J Gastroenterol. 2000;95:3503-6.
 Austin GL, Dalton CB, Hu Y, Morris CB, Hankins J, Weinland SR, Westman EC, Yancy WS Jr, Drossman DA. A very low-carbohydrate diet improves symptoms and quality of life in diarrhea-predominant irritable bowel syndrome. Clin Gastroenterol Hepatol. 2009 Jun;7(6):706-708.
 Majewski M, Reddymasu SC, Sostarich S, Foran P, McCallum RW. Efficacy of rifaximin, a non absorbed oral antibiotic, in the treatment of small intestinal bacterial overgrowth. Am J Med Sci. 2007 May;333(5):266-70.
 Pimentel M. Review of rifaximin as treatment for SIBO and IBS. Expert Opin Investig Drugs. 2009 Mar;18(3):349-58.
 Yang J, Lee HR, Low K, Chatterjee S, Pimentel M. Rifaximin versus other antibiotics in the primary treatment and retreatment of bacterial overgrowth in IBS. Dig Dis Sci. 2008 Jan;53(1):169-74.
Hagen J, Deitel M, Khanna RK, Ilves R. Gastroesophageal reflux in the massively obese. Int. Surg. 1987 Jan-Mar;72(1):1-3. Fisher BL, Pennathur A, Mutnick JL, Little AG. Obesity correlates with gastroesophageal reflux. Dig Dis Sci. 1999 Nov;44(11):2290-4. Austin GL, Thiny MT, Westman EC, Yancy WS Jr, Shaheen NJ. A very low-carbohydrate diet improves gastroesophageal reflux and its symptoms (Obese patients). Dig Dis Sci. 2006 Aug;51(8):1307-12.
Roussos A, Koursarakos P, Patsopoulos D, Gerogianni I, Philippou N. Increased prevalence of irritable bowel syndrome in patients with bronchial asthma. Respir Med. 2003 Jan;97(1):75-9.
Sontag SJ, O’Connell S, Khandelwal S, Miller T, Nemchausky B, Schnell TG, Serlovsky R. Most asthmatics have gastroesophageal reflux with or without bronchodilator therapy. Gastroenterology. 1990 Sep;99(3):613-20.
Leggett JJ, Johnston BT, Mills M, Gamble J, Heaney LG. Prevalence of gastroesophageal reflux in difficult asthma: relationship to asthma outcome. Chest. 2005 Apr;127(4):1227-31.
 Rothenberg S1, Cowles R. The effects of laparoscopic Nissen fundoplication on patients with severe gastroesophageal reflux disease and steroid-dependent asthma. J Pediatr Surg. 2012 Jun;47(6):1101-4.
 Spivak H1, Smith CD, Phichith A, Galloway K, Waring JP, Hunter JG. Asthma and gastroesophageal reflux: fundoplication decreases need for systemic corticosteroids. J Gastrointest Surg. 1999 Sep-Oct;3(5):477-82.
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