Heartburn Asthma Link - Explained - Digestive Health InstituteDigestive Health Institute
Management of dietary carbohydrates improves reflux symptoms and reduces esophageal acid exposure. (6,7,8). I believe reducing carbs is an effective treatment because intestinal bacteria are denied fuel which limits their growth and ability to produce gas.
Treatment of GERD patients with the antibiotic erythromycin decreases gastro esophageal reflux and increases apparent LES pressure (9,10). The authors suggested that erythromycin had increased the lower esophageal sphincter (LES) pressure in the these patients. But how can an antibiotic tighten these muscles? LES pressure is measured by inserting a tube through the LES that detects how tightly the LES closes. In this case the LES appeared be closing more tightly after treatment with erythromycin. Possibly, the authors failed to recognize the growth inhibiting effect of erythromycin on intestinal bacteria and how that would limit reflux causing gas. What appears to the authors as “strengthening the defective LES in GERD patients” is, in my opinion, a decrease in intragastric (stomach) gas pressure because erythromycin is inhibiting the intestinal microbes that were producing the gas in the first place. The LES appears to exhibit increased pressure but the effect is actually caused by a decrease in intragastric pressure that no longer pushes as hard on the LES.
Consumption of the carbohydrate fructose oligosaccharide (FOS), which is indigestible by humans, but fermented by gut bacteria produces intestinal gas and increases the number of reflux episodes and symptoms of relfux (11). The authors noted an increase in something called transient lower esophageal sphincter relaxations (TLESRs). In other words, the LES opened more as if it was relaxing. I believe these “Lower esophageal sphincter relaxations” described by the authors actually represent the LES being “forced” open by gas pressure. Consuming FOS ensures 100% malabsorption. The fermentation of FOS by gut microbes makes enough gas to pressurize the small intestine and stomach and force open the LES causing reflux and heartburn in susceptible people.
In GERD patients, reflux was associated with an increase in intra-abdominal (gas) pressure and belching (12,13). The increase in intra-abdominal gas pressure and belching is consistent with the idea that gas produced in the small intestine from carbohydrate fermentation can create gas pressure in the stomach and cause belching as the gas escapes into the esophagus. The only difference between belching and acid reflux is that the gas pushes stomach contents into the esophagus in the later case and escapes on its own in the former.
Cystic fibrosis (CF) patients have a very high (up to 80%) prevalence for GERD and exhibit well documented carbohydrate malabsorption and bacterial overgrowth associated with pancreatic digestive enzyme deficiency due to blockage of pancreatic ducts with thick mucus (14,15,16). After studying the connection between GERD and CF as well as the details of carbohydrate malabsorption in CF, I am convinced that pancreatic enzyme insufficiency leads to malabsorption, SIBO and the reflux-related symptoms so prevalent in cystic patients.
The prevalence of GERD in IBS patients (39%) and IBS in GERD patients (49%) is much higher than the prevalence of GERD (19%) or IBS (12%) in the general population indicating a relationship between the two conditions (17). IBS has been clearly linked to small intestinal bacterial overgrowth via hydrogen breath testing and, like GERD, has been treated successfully with carbohydrate restriction as well as antibiotics (18,19,20,21,22). This evidence is consistent with SIBO playing a role in both conditions.
Half of GERD patients taking PPI drugs showed evidence of SIBO by glucose breath testing compared to only 25% of IBS patients not taking PPIs. Eighty-seven to ninety percent of SIBO-positive patients (with GERD or IBS) showed improvement after antibiotic treatment (23). I believe the SIBO-positive results in both groups would have been higher if the study employed the lactulose breath test instead of the glucose breath test. Lactulose is not digested or absorbed in the small intestine and can detect bacteria (fermenting the lactulose and producing hydrogen) throughout the entire length of the small intestine. Glucose is rapidly absorbed in the first part of the small intestine and will only detect bacteria if they are present in this region. Dr. Pimentel found that 78 percent of IBS patients tested at the Cedars-Sinai Medical Center had SIBO as indicated by a positive lactulose breath test (18).
GERD is associated with obesity and carbohydrate restriction improved symptoms and reduced esophageal acid exposure in obese patients regardless of weight loss (24,25,26). Obese people consume more food, especially carbohydrates, which I believe can lead to “volume based” malabsorption causing SIBO and reflux.
A significant number of GERD patients report new symptoms following fundoplication surgery that include excessive gas (abdominal gas and flatulence), bloating, diarrhea and abdominal pain (27, 28,29). The procedure is aimed at preventing reflux, but the side effects are indicative of trapped stomach and intestinal gas as would be expected with malabsorption and SIBO.
The connection between gut and lungs
Normally, stomach acid forms a barrier between bacteria in your intestines and your esophagus, lungs and sinuses because bacteria are killed by stomach acid. Acid reflux can surpass this protective mechanism, especially if stomach acid is neutralized. When acid neutralizing drugs are used (PPIs, H2 blockers and even antacids), bacteria from the intestines are more likely to overgrow and survive in the small intestine and stomach. Reflux can cause these bacteria to enter the esophagus and potentially the lungs and sinuses. People on acid blocking meds are more susceptible to respiratory infections most likely from bacteria originating in their own intestines.
This connection has been proven in a large study linking acid reducing medications to pneumonia. A study of more than 364,000 people led by Robert J.F. Laheij at the University Medical Center St. Radboud in Nijmegen , the Netherlands , found that the risk of pneumonia was almost double for people taking proton-pump inhibitors for prolonged periods compared to people not taking such drugs (41). The increased risk of respiratory infection was also seen in children taking acid reducing medication (42).
As further proof of the connection between reflux and lung problems, Belgium researchers found that the potent antibiotic azithromycin reduced gastroesophageal reflux as well as esophageal acid exposure and the concentration of bile acids in fluid removed from the lungs of lung transplant patients (43). Similar to the erythromycin studies cited above, the authors did not consider that the profound effect might be due to the antibiotic treatment inhibiting gut microorganisms. In this case, stomach acid and bile were being refluxed not only into the esophagus, but directly into the lungs. Azithromycin treatment helped prevent reflux into the esophagus and lungs likely via its effect on SIBO inhibition. The results were quite beneficial for the patients.
What should reflux sufferers and asthmatics do?
Clearly GERD and asthma are very different and complex conditions that share a link. People undergoing treatment for either condition should not make any immediate changes before consulting their own health care provider. Your own health care provider may offer diagnostic tests to determine if you suffer from various types of carbohydrate malabsoption such as lactose or fructose intolerance. Some health care providers provide screening for SIBO itself. If you, or someone you know have asthma which is not well controlled, I suggest talking to your doctor about initiating one of my diets that control acid reflux (clinical research studies support both approaches). One approach is an overall low carbohydrate diet described in my book Heartburn Cured. The other approach, documented in my new book Fast Tract Digestion Heartburn, limits only difficult to digest carbohydrates – Fast Tract Digestion Heartburn. If you are taking PPI drugs, I recommend talking to your doctor about tapering off these drugs over a period of two to three weeks. I do not recommend people with SIBO undergo antibiotic treatments without first trying to control the overgrowth of bacteria by the two approaches described above. Based on the rational presented in this article, controlling SIBO and GERD by general or selective carbohydrate restriction should dramatically improve the symptoms and severity of asthma, but only clinical testing can provide the proof.
"One approach is an overall low carbohydrate diet described in my book Heartburn Cured. The other approach, documented in my new book Fast Tract Digestion Heartburn, limits only difficult to digest carbohydrates – Fast Tract Digestion Heartburn"The following nine points of evidence convinced me that carbohydrate malabsorption coupled with SIBO may be the ultimate cause acid reflux and perhaps a factor in asthma:
Management of dietary carbohydrates improves reflux symptoms and reduces esophageal acid exposure. (6,7,8). I believe reducing carbs is an effective treatment because intestinal bacteria are denied fuel which limits their growth and ability to produce gas.
Treatment of GERD patients with the antibiotic erythromycin decreases gastro esophageal reflux and increases apparent LES pressure (9,10). The authors suggested that erythromycin had increased the lower esophageal sphincter (LES) pressure in the these patients. But how can an antibiotic tighten these muscles? LES pressure is measured by inserting a tube through the LES that detects how tightly the LES closes. In this case the LES appeared be closing more tightly after treatment with erythromycin. Possibly, the authors failed to recognize the growth inhibiting effect of erythromycin on intestinal bacteria and how that would limit reflux causing gas. What appears to the authors as “strengthening the defective LES in GERD patients” is, in my opinion, a decrease in intragastric (stomach) gas pressure because erythromycin is inhibiting the intestinal microbes that were producing the gas in the first place. The LES appears to exhibit increased pressure but the effect is actually caused by a decrease in intragastric pressure that no longer pushes as hard on the LES.
Consumption of the carbohydrate fructose oligosaccharide (FOS), which is indigestible by humans, but fermented by gut bacteria produces intestinal gas and increases the number of reflux episodes and symptoms of relfux (11). The authors noted an increase in something called transient lower esophageal sphincter relaxations (TLESRs). In other words, the LES opened more as if it was relaxing. I believe these “Lower esophageal sphincter relaxations” described by the authors actually represent the LES being “forced” open by gas pressure. Consuming FOS ensures 100% malabsorption. The fermentation of FOS by gut microbes makes enough gas to pressurize the small intestine and stomach and force open the LES causing reflux and heartburn in susceptible people.
In GERD patients, reflux was associated with an increase in intra-abdominal (gas) pressure and belching (12,13). The increase in intra-abdominal gas pressure and belching is consistent with the idea that gas produced in the small intestine from carbohydrate fermentation can create gas pressure in the stomach and cause belching as the gas escapes into the esophagus. The only difference between belching and acid reflux is that the gas pushes stomach contents into the esophagus in the later case and escapes on its own in the former.
Cystic fibrosis (CF) patients have a very high (up to 80%) prevalence for GERD and exhibit well documented carbohydrate malabsorption and bacterial overgrowth associated with pancreatic digestive enzyme deficiency due to blockage of pancreatic ducts with thick mucus (14,15,16). After studying the connection between GERD and CF as well as the details of carbohydrate malabsorption in CF, I am convinced that pancreatic enzyme insufficiency leads to malabsorption, SIBO and the reflux-related symptoms so prevalent in cystic patients.
The prevalence of GERD in IBS patients (39%) and IBS in GERD patients (49%) is much higher than the prevalence of GERD (19%) or IBS (12%) in the general population indicating a relationship between the two conditions (17). IBS has been clearly linked to small intestinal bacterial overgrowth via hydrogen breath testing and, like GERD, has been treated successfully with carbohydrate restriction as well as antibiotics (18,19,20,21,22). This evidence is consistent with SIBO playing a role in both conditions.
Half of GERD patients taking PPI drugs showed evidence of SIBO by glucose breath testing compared to only 25% of IBS patients not taking PPIs. Eighty-seven to ninety percent of SIBO-positive patients (with GERD or IBS) showed improvement after antibiotic treatment (23). I believe the SIBO-positive results in both groups would have been higher if the study employed the lactulose breath test instead of the glucose breath test. Lactulose is not digested or absorbed in the small intestine and can detect bacteria (fermenting the lactulose and producing hydrogen) throughout the entire length of the small intestine. Glucose is rapidly absorbed in the first part of the small intestine and will only detect bacteria if they are present in this region. Dr. Pimentel found that 78 percent of IBS patients tested at the Cedars-Sinai Medical Center had SIBO as indicated by a positive lactulose breath test (18).
GERD is associated with obesity and carbohydrate restriction improved symptoms and reduced esophageal acid exposure in obese patients regardless of weight loss (24,25,26). Obese people consume more food, especially carbohydrates, which I believe can lead to “volume based” malabsorption causing SIBO and reflux.
A significant number of GERD patients report new symptoms following fundoplication surgery that include excessive gas (abdominal gas and flatulence), bloating, diarrhea and abdominal pain (27, 28,29). The procedure is aimed at preventing reflux, but the side effects are indicative of trapped stomach and intestinal gas as would be expected with malabsorption and SIBO.
The connection between gut and lungs
Normally, stomach acid forms a barrier between bacteria in your intestines and your esophagus, lungs and sinuses because bacteria are killed by stomach acid. Acid reflux can surpass this protective mechanism, especially if stomach acid is neutralized. When acid neutralizing drugs are used (PPIs, H2 blockers and even antacids), bacteria from the intestines are more likely to overgrow and survive in the small intestine and stomach. Reflux can cause these bacteria to enter the esophagus and potentially the lungs and sinuses. People on acid blocking meds are more susceptible to respiratory infections most likely from bacteria originating in their own intestines.
This connection has been proven in a large study linking acid reducing medications to pneumonia. A study of more than 364,000 people led by Robert J.F. Laheij at the University Medical Center St. Radboud in Nijmegen , the Netherlands , found that the risk of pneumonia was almost double for people taking proton-pump inhibitors for prolonged periods compared to people not taking such drugs (41). The increased risk of respiratory infection was also seen in children taking acid reducing medication (42).
As further proof of the connection between reflux and lung problems, Belgium researchers found that the potent antibiotic azithromycin reduced gastroesophageal reflux as well as esophageal acid exposure and the concentration of bile acids in fluid removed from the lungs of lung transplant patients (43). Similar to the erythromycin studies cited above, the authors did not consider that the profound effect might be due to the antibiotic treatment inhibiting gut microorganisms. In this case, stomach acid and bile were being refluxed not only into the esophagus, but directly into the lungs. Azithromycin treatment helped prevent reflux into the esophagus and lungs likely via its effect on SIBO inhibition. The results were quite beneficial for the patients.
What should reflux sufferers and asthmatics do?
Clearly GERD and asthma are very different and complex conditions that share a link. People undergoing treatment for either condition should not make any immediate changes before consulting their own health care provider. Your own health care provider may offer diagnostic tests to determine if you suffer from various types of carbohydrate malabsoption such as lactose or fructose intolerance. Some health care providers provide screening for SIBO itself. If you, or someone you know have asthma which is not well controlled, I suggest talking to your doctor about initiating one of my diets that control acid reflux (clinical research studies support both approaches). One approach is an overall low carbohydrate diet described in my book Heartburn Cured. The other approach, documented in my new book Fast Tract Digestion Heartburn, limits only difficult to digest carbohydrates – Fast Tract Digestion Heartburn. If you are taking PPI drugs, I recommend talking to your doctor about tapering off these drugs over a period of two to three weeks. I do not recommend people with SIBO undergo antibiotic treatments without first trying to control the overgrowth of bacteria by the two approaches described above. Based on the rational presented in this article, controlling SIBO and GERD by general or selective carbohydrate restriction should dramatically improve the symptoms and severity of asthma, but only clinical testing can provide the proof.
