Does H. pylori cause GERD?
Based on my review, H. pylori is not a common cause of acid reflux, but may contribute to atypical non-acid reflux symptoms in some people.
I wrote about my own struggles with GERD in my first article and how I was able to control symptoms by modulating dietary carbohydrates. Some years later, I learned that I was infected with H. pylori. I was treated for the infection, but there was no change in my susceptibility to acid reflux following treatment. My symptoms, though completely under dietary control, gradually reemerge when I consume too many carbohydrates over a period of 3-5 days, particularly those that are difficult to digest and absorb. Of course, my experience may not be typical of others with acid reflux and H. pylori. So, let’s take a closer look at this connection.
H. Pylori is a type of bacteria that has adapted through evolution to life in the stomach of approximately two thirds of all humans, though eradication efforts are making progress against this bacteria at least in developed countries. To survive in the stomach, the bacteria swims through mucous that lines the stomach by using multiple flagella, rotating hair-like appendages that provide locomotion. When H. pylori bacteria reach the stomach wall, they attach and begin secreting an enzyme called urease which converts urea to ammonia. The ammonia reduces the stomach acidity where the H. pylori is attached allowing this bacteria to survive and multiply. The biggest risks for people infected with H. pylori are stomach ulcers, duodenal ulcers, and stomach (gastric) cancer.
Studies on H. pylori and GERD
One study found that GERD patients were more likely to harbor H. pylori than non-GERD patients. However, they did not find the same correlation in people with GERD who also had IBS. This makes little sense to me and casts some doubt on the validity of the findings.
On the other hand, numerous other studies have found that people harboring H. pylori are actually less likely to have GERD including esophagitis and Barrett’s esophagus, two serious conditions arising from severe and chronic GERD. I will break down the studies into:
- GERD patients who had H. pylori but were treated for the infection.
- GERD patients with H. pylori infection compared to the same population without.
Studies on GERD patients where H. pylori was eradicated with antibiotics:
- H. pylori eradication had no impact on esophageal acid exposure or LES (lower esophageal sphincter) pressure.
- H. pylori eradication resulted in no consistent change in gastroesophageal acid reflux.
- No differences were detected in acid reflux before and after H. pylori eradication.
- Eradicating H. pylori increased (not decreased) esophageal acid exposure and in some cases, worsened reflux symptoms.
Successful treatment of H. pylori infection does not improve GERD symptoms, esophageal acid exposure, LES pressure changes, or acid reflux. In some cases eradication actually made things worse.
Studies on GERD patients with H. pylori infection compared to the same population without:
- The rate of H. pylori infection is lower in GERD patients compared to the general population. The absence of H. pylori is associated with more severe GERD. The results indicate a protective role of H. pylori against GERD.
- H. pylori infection is inversely associated (protective) with GERD and GERD symptoms.
- The H. pylori infection rate was lower in individuals with acid reflux compared to controls.
- H. pylori infection was inversely associated with the risk and severity of reflux esophagitis, suggesting the organism may have a protective role against GERD.
- H. pylori infection is associated with a lower risk of GERD.
- H. pylori-negative patients had more severe esophagitis and were more likely to have Barrett’s esophagus.
- H. pylori infection was inversely associated (protective) with Barrett’s esophagus and GERD symptoms were not associated with H. pylori infection.
H. pylori infection is less common in patients with GERD, esophagitis and Barrett’s esophagus. H. pylori infection is associated with less severe GERD symptoms and may have a protective role in GERD.
If H. pylori was a causative agent in GERD, one would expect that any decrease in H. pylori infection rates would also reduce the incidence of GERD, but the opposite is actually the case. As the worldwide incidence of GERD is increasing, infection rates of H. pylori are decreasing. And as hospitalization rates have decreased for gastric and duodenal ulcers and gastric cancer, presumably due to H. pylori infection, hospitalization rates due to GERD and esophageal cancer, have risen significantly.
Additional studies suggest that certain strains of H. pylori (cagA+) may actually be protective for people with more severe forms of GERD.,
Based on my review of the published literature and my own observations lead me to believe that H. pylori is not a causative factor in GERD in most people, and some strains of H. pylori may actually be protective for GERD. I will address H pylori’s role in non-acid reflux below.
Does low stomach acid cause GERD?
Based on my review, low stomach acid is not a cause of acid reflux, but can lead to atypical non-acid reflux symptoms in some people.
Another notion popularized in the book “Why Stomach Acid Is Good For You” by Jonathan Wright suggests that that GERD might actually be caused by too little stomach acid. Hypochlorhydria and achlorhydria refer to having low stomach acid, or no stomach acid respectively.
The most common cause of low stomach acid is acid reducing drugs including antacids, H2 blockers and proton pump inhibitors. The second most common cause of low (or no) stomach acid is chronic inflammation of the stomach referred to as chronic atrophic gastritis (CAG). CAG is often due to long term infection with H. pylori, especially when PPI drugs are taken at the same time. Much less frequently, CAG results from an autoimmune condition where our immune system attacks acid producing stomach parietal cells. Low (or no) stomach acid can also be caused by surgery affecting acid or gastrin-producing cells, other (non H2 blocker or PPI) drugs that affect stomach acid production, stomach cancer, or hormonal disorders.
Low stomach acid – especially if caused by CAG can have profound negative health effects including:
- Increased long term risk of stomach cancer and Hashimoto’s thyroiditis.
- Diminished vitamin B12 absorption (risk of anemia) and likely other vitamins.
- Diminished mineral absorption including calcium (risk of bone fractures), magnesium (risk of serious cardiovascular, neurological problems and also bone health) and iron (risk of anemia)
- Increased risk of bacterial overgrowth in the small intestine and stomach since stomach acid is part of our bacterial control system
- Increased risk of C diff and other GI infections likely because our acid barrier to outside pathogens is missing
While low stomach acid has many harmful health effects, can this condition cause symptomatic GERD? I had the opportunity to put this question to Dr. John Pandolfino, Chief of Gastroenterology and Hepatology at Northwestern Memorial Hospital in Chicago. His answer encompassed the role of H. pylori in the loss of stomach acid:
“The rule of thumb has been that H. pylori is protective of GERD if it is body predominant and reduces acid (Infection with H. pylori in other parts of the stomach, the antrum, for example, can lead to increased stomach acid, but this is less common)[i]. This has been shown in regard to risk of esophageal cancer, Barrett’s esophagus and esophagitis – all are lower in patients with H. pylori and low acid. You certainly would not increase acid production to improve GERD.”
Dr. Pandolfino’s explanation is consistent with studies I have reviewed including one well controlled study that looked at 155 patients with esophagitis, where acid reflux is severe enough to inflame the esophagus. The authors found no differences in gastric acid or pepsin secretion and concluded that “factors other than amount or composition of gastric juice per se must be responsible for susceptibility to esophagitis.”
Another study found that subjects with a particular type of gastritis called “corpus (or body) gastritis”, a form of chronic atrophic gastritis or CAG known to result in reduced stomach acid, had a 54% reduced risk for reflux esophagitis. Two Japanese studies support the conclusion that CAG is protective for GERD., , Finally, two large German studies that looked at 9444 and 8936 older adults respectively, found a strong inverse association of CAG with heartburn., 
I found additional information on stomach acid levels in GERD patients in a study done to support the new drug application (NDA) for the PPI, lansoprazole, with 60 juvenile GERD patients. They conducted 24-hr intragastric pH levels (stomach acidity) and found GERD patients had the same pH levels as healthy adults meaning they did not have low acid levels.
A study where increasingly acidic solutions were infused directly into people’s esophagus showed that more acidic solutions (less than pH 4) triggered greater GERD symptoms.
Also, recall from our previous discussion that 80% of cystic fibrosis (CF) patients have acid reflux. There is evidence that these patients produce normal amounts of stomach acid. But, we know for a fact that mucus often clogs their pancreatic ducts: therefore, they are unable to release sufficient amounts of digestive enzymes. This results in well documented carbohydrate malabsorption and SIBO,, which I believe without question is the underlying cause of acid reflux in CF.
Finally, the success of carbohydrate-restricted diets for treating GERD symptoms supports the published findings above, simply because carbohydrate-restriction works without any manipulation of stomach acidity.
The quick action of antacids in quelling heartburn symptoms in most people attests to the importance of stomach acid in reflux symptoms. People with heartburn who regularly take bicarbonate understand that they can feel the gas forming from the baking soda and acid reacting, followed by a burp of relief. You can easily test this yourself whenever you have a bout of heartburn.[ii] Just take some Tums or baking soda and see if you feel better. If you do, low acid is likely not your problem!
What about Non-acid or “Bile” Reflux?
But how do the studies cited above jibe with the well- documented connection between low stomach acid and bacterial overgrowth in the stomach and small intestine? My own theory predicts that gas produced from bacterial overgrowth (regardless of the cause) should increase intragastric pressure leading to more reflux episodes – not less.
While low stomach acid may not provoke as many typical GERD symptoms (which are likely more dependent on the acid component), it might be expected to lead to more episodes of “non-acid” reflux. In fact, there are reports of symptomatic reflux in people that lack stomach acid. One case report used something called impedance monitoring, which can tell the difference between acid reflux and non-acid reflux, to document a case of non-acid reflux in an individual with confirmed achlorhydria. In this case the 72 year old woman was H. pylori negative, but was diagnosed with autoimmune atrophic gastritis and had undergone gallbladder removal.
A larger study that examined both “acid” and “non-acid” reflux in GERD patients taking PPI drugs (they have low stomach acid by definition) found that about half of the participants registered positive symptoms scores, of which 11 % were due to acid reflux, while 37% were due to non-acid reflux.
While typical GERD symptoms are more common in people who produce normal levels of stomach acid, people with low stomach acid (mostly, these are people taking PPIs but also some with CAG) can also suffer from symptomatic non-acid reflux. Potential triggers for non-acid reflux include caustic bile salts which are normally produced to help digest fats, and digestive enzymes, particularly pepsin. Bile salts have been linked to heartburn symptoms in at least one study.
From my review, I conclude that classic GERD symptoms are more dependent on the presence, not the absence, of stomach acid, but symptomatic non-acid reflux can occur in people with low stomach acid – most of whom are taking PPI drugs.
Given the number of serious consequences from having insufficient levels of stomach acid, and the observations (though limited) of symptomatic reflux in a subset of people with low stomach acid, anyone who suspects they have low stomach acid should be tested. People who are on acid reducing drugs don’t need to be tested. That’s what these drugs do – reduce stomach acid.
If low stomach acid is confirmed, the underlying cause of the condition (PPIs, H. pylori-mediated or autoimmune-mediated gastritis, etc.) should be addressed where ever possible. Betaine HCl may help, but check with your doctor and proceed with caution because too much stomach acid can irritate or burn your stomach lining or even cause an ulcer over time. The risk is much higher for people taking NSAIDs.
Summing it up
1. H. pylori infection is NOT linked to GERD and some strains of H. pylori may be protective for GERD.
2. People with low stomach acid have fewer GERD symptoms and are less likely to have esophagitis and Barrett’s esophagus.
3. Most people with GERD have normal amounts of stomach acid.
4. Low stomach acid induced by PPIs use, H. pylori or other causes while not a cause of acid reflux, may result in symptomatic non-acid reflux in some people as well as a host of other problems.
Because stomach acid and other components of reflux (i.e., bile and pepsin) can trigger symptoms, it’s critical to stop the reflux itself. The Fast Tract Diet strategy will help control both acid and non-acid reflux by limiting fermentable carbohydrates that allow gut microbes to produce gas, leading to gas pressure and reflux.
If you believe you have low stomach acid (based on the “antacid test”) and may be suffering from non-acid reflux, it’s important to identify and address the causes, such as PPI, H2 blocker medicine usage, chronic atrophic gastritis or other causes discussed in this article and my book. Talk to you doctor about the Heidelberg acid test which will confirm if you suffer from this condition before taking betaine supplements.
The third article, “GERD – Why standard treatments are ineffective”, of this blog series reviews the pitfalls of current therapies.
Read the first article, “What Really Causes Acid Reflux and GERD?”
Read the final article, “GERD diet that works without drugs”
[i] The effect of H. pylori on stomach acid is a bit complex, but there are three basic types of H. pylori infection, each affecting stomach acid levels differently:
- Body-predominant (more common) where H. pylori infection occurs in the middle or “body” of the stomach often leads to low stomach acid secretion and a higher risk of stomach (gastric) cancer.
- Antral-predominant (less common) where H. pylori infection occurs in the lower part of the stomach often leads to increased stomach acid secretion and a higher risk of stomach and duodenal ulcers but a lower risk of stomach (gastric) cancer.
- Mixed where (more common) H. pylori infection occurs in both the antral and body portion of the stomach typically resulting in no net change in stomach acid secretion.
[ii] This technique is not applicable for conditions involving more subtle forms of acid (or non-acid) reflux including laryngopharyngeal reflux (LPR).
 Yarandi SS, Nasseri-Moghaddam S, Mostajabi P, Malekzadeh R. Overlapping gastroesophageal reflux disease and irritable bowel syndrome: increased dysfunctional symptoms. World J Gastroenterol. 2010 Mar 14;16(10):1232-8.
 Verma S, Jackson W, Floum S, Giaff er MH. Gastroesophageal refl ux before and after Helicobacter pylori eradication. A prospective study using ambulatory 24-h esophageal pH monitoring. Dis Esophagus 2003;16:273-278.
 Tefera S, Hatlebakk JG, Berstad A. Th e eff ect of Helicobacter pylori eradication on gastro-oesophageal reflux. Aliment Pharmacol Th er 1999;13:915-920.
 Manifold DK, Anggiansah A, Rowe I, Sanderson JD, Chinyama CN, Owen WJ. Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis. Eur J Gastroenterol Hepatol. 2001 May;13(5):535-9.
 Wu JC, Chan FK, Wong SK, Lee YT, Leung WK, Sung JJ. Effect of Helicobacter pylori eradication on oesophageal acid exposure in patients with reflux oesophagitis. Aliment Pharmacol Ther. 2002 Mar;16(3):545-52.
 Garrido Serrano A, Lepe Jiménez JA, Guerrero Igea FJ, and Perianes Hernández C. Helicobacter pylori and gastroesophageal reflux disease. REV ESP ENFERM DIG (Madrid). 2003. Vol. 95. N.° 11, pp. 788-790.
 Corley DA, Kubo A, Levin TR, Block G, Habel L, Rumore G, Quesenberry C, Buffler P, Parsonnet J. Helicobacter pylori and gastroesophageal reflux disease: a case-control study. Helicobacter. 2008 Oct;13(5):352-60.
 Shirota T, Kusano M, Kawamura O, Horikoshi T, Mori M, Sekiguchi T. Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings. J Gastroenterol. 1999;34(5):553.
 Chung SJ, Lim SH, Choi J, Kim D, Kim YS, et.al. Helicobacter pylori Serology Inversely Correlated With the Risk and Severity of Reflux Esophagitis in Helicobacter pylori Endemic Area: A Matched Case-Control Study of 5,616 Health Check-Up Koreans. J Neurogastroenterol Motil. 2011;17(3):267.
 Labenz J, Jaspersen D, Kulig M, Leodolter A, et.al. Risk factors for erosive esophagitis: a multivariate analysis based on the ProGERD study initiative. Am J Gastroenterol. 2004 Sep;99(9):1652-6.
 Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, Eskes SA, Meuwissen SG. Helicobacter pylori and the efficacy of omeprazole therapy for gastroesophageal reflux disease. Am J Gastroenterol. 1999 Apr;94(4):884-7.
 Rubenstein JH, Inadomi JM, Scheiman J, Schoenfeld P, Appelman H, Zhang M, Metko V, Kao JY. Association between Helicobacter pylori and Barrett’s esophagus, erosive esophagitis, and gastroesophageal reflux symptoms. Clin Gastroenterol Hepatol. 2014 Feb;12(2):239-45.
 Chait MM. Gastroesophageal reflux disease: Important considerations for the older patients. World J Gastrointest Endosc. 2010 Dec 16;2(12):388-96.
 el-Serag HB, Sonnenberg A. Opposing time trends of peptic ulcer and reflux disease. Gut. 1998;43(3):327.
 Vicari JJ, Peek RM, Falk GW, Goldblum JR, et.al. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology. 1998;115(1):50.
 Vaezi MF, Falk GW, Peek RM, Vicari JJ, et.al. CagA-positive strains of Helicobacter pylori may protect against Barrett’s esophagus. Am J Gastroenterol. 2000;95(9):2206.
 Kuipers EJ, Lundell L, Klinkenberg-Knol EC, Havu N, et.al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med. 1996;334(16):1018.
 Personal communication, January 16, 2014.
 Hirschowitz BI. A critical analysis, with appropriate controls, of gastric acid and pepsin secretion in clinical esophagitis. Gastroenterology. 1991 Nov;101(5):1149-58.
 El-Serag HB
, Sonnenberg A
, Jamal MM
, Inadomi JM
, Crooks LA
, Feddersen RM
. Corpus gastritis is protective against reflux oesophagitis. Gut.
 Koike T1, Ohara S, Sekine H, Iijima K, Kato K, Shimosegawa T, Toyota T. Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis. Am J Gastroenterol. 1999 Dec;94(12):3468-72.
 Fujiwara Y1, Higuchi K, Shiba M, Watanabe T, Tominaga K, Oshitani N, Matsumoto T, Arakawa T. Association between gastroesophageal flap valve, reflux esophagitis, Barrett’s epithelium, and atrophic gastritis assessed by endoscopy in Japanese patients. J Gastroenterol. 2003;38(6):533-9.
 Weck MN1, Stegmaier C, Rothenbacher D, Brenner H. Epidemiology of chronic atrophic gastritis: population-based study among 9444 older adults from Germany. Aliment Pharmacol Ther. 2007 Sep 15;26(6):879-87.
 Gao L, Weck MN, Rothenbacher D, Brenner H. Body mass index, chronic atrophic gastritis and heartburn: a population-based study among 8936 older adults from Germany. Aliment Pharmacol Ther. 2010 Jul;32(2):296-302.
 Smith JL, Opekun AR, Larkai E, Graham DY. Sensitivity of the esophageal mucosa to pH in gastroesophageal reflux disease. Gastroenterology 1989;96:683-689.
 Hallberg K, Abrahamsson H, Dalenbäck J, Fändriks L, Strandvik B. Gastric secretion in cystic fibrosis in relation to the migrating motor complex. Scand J Gastroenterol. 2001 Feb;36(2):121-7.
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. 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.
 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.
 R C Orlando, E M Bozymski. Heartburn in pernicious anemia–a consequence of bile reflux. New England Journal of Medicine 10/1973; 289(10):522-3.
 Mainie I, Tutuian R, Shay S, Vela M, Zhang X, Sifrim D, Castell DO. Acid and non-acid reflux in patients with persistent symptoms despite acid suppressive therapy: a multicentre study using combined ambulatory impedance-pH monitoring. Gut. 2006 Oct;55(10):1398-402.
 Siddiqui A, Rodriguez-Stanley S, Zubaidi S, et al. Esophageal visceral sensitivity to bile salts in patients with functional heartburn and in healthy control subjects. Dig Dis Sci 2005;50:81-85.