Koufman, Jamie. JAMA Neurol. Hvid-Jensen, F. Ranjitkar, S. Roesch-Ramos, Laura; Dental erosion, an extraesophageal manifestation of gastroesophageal reflux disease. Vincent W. She worked in her own dental practice in Toronto until when she retired due to health issues.
As part of her healing, she became a Holistic Nutritionist in Alban now works in association with the Spark Institute in Vaughan, Ontario — a clinic devoted to preventive medicine and the natural treatment of digestive disorders, eating disorders, anxiety and depression. In her free time, she volunteers as a grief and crisis counselor with the Toronto Distress Centre and enjoys yoga, hiking and cooking for her family. What you have experienced Gloria is vary mild in comparison to many.
Elevating the head of your bed by 4 inches, and sleeping on your left side will stop liquid refluxates from progressing to your esophagus , but will not stop the fumes from causing perpetual histamines from dripping from your oral cavities. It is even worse when they extend to the whole side of your face into your ears. Using Sensodyne, and constantly drinking green tea without sugar protects my teeth, and helps with clearing the mucus which I frequently choke on. When not drinking tea or water I perpetually sniffle to the point of distraction to anyone I meet.
Night guard eliminates nighttime reflux. My dentist was lecturing me about my tiny teeth from grinding. About 3 months ago I started using my mouthguard. After 20 years of painful acid reflux I no longer have any nighttime symptoms. Younger patients and those with heartburn as a primary symptom were more likely to fail step-down therapy and require maintenance PPI therapy. Although these studies of step therapy reached different conclusions, and although the Howden et al. This not an unreasonable strategy, as many patients with nonerosive GERD or mild erosive esophagitis have adequate symptom relief with H2RA therapy alone.
Patients with more severe disease who require a PPI may experience a delay in achieving symptom relief, and this needs to be balanced against the cost savings of any "step therapy" regimen. The overwhelming majority of studies evaluating the treatment of GERD have included subjects with either documented erosive esophagitis or severe and frequent episodes of heartburn. Most individuals with GERD , however, have nonerosive disease and experience infrequent symptoms up to three episodes per week. The majority of patients, therefore, are treated on the basis of their symptom complex, rather than on endoscopic findings.
Moreover, the presence or absence of esophagitis cannot be accurately predicted from a patient's symptom complex or from the response to therapy. Gastroesophageal reflux is divided into discrete stages based on symptom frequency and severity, as well as the presence of esophageal complications or extraesophageal manifestations of GERD. Stage II disease is characterized by more frequent symptoms more than three times per week.
Full dose therapy with an H2 blocker may be used initially, but PPI therapy is more effective in providing symptom relief and healing esophagitis, which may be present in this group of patients. Patients with GERD complications, including strictures and Barrett's esophagus, should be classified as stage III, as should patients with extraesophageal manifestations of GERD , such as asthma, laryngitis, or chest pain.
These patients typically require PPI therapy either daily or twice daily to relieve symptoms and prevent complications. This staging system is widely applicable in clinical practice as it is based on presenting symptoms rather than the endoscopic finding of esophagitis; it also promotes graded therapy rather than an inflexible regimen of PPIs. A suggested approach to the use of antisecretory therapy in the treatment of GERD , based on symptoms at presentation.
Nighttime symptoms are common in patients with GERD , affecting a majority of those who report frequent daytime reflux symptoms. The importance of nighttime reflux has been underestimated, and a recent Gallup study reported significant morbidity related to nocturnal acid reflux. This study clearly demonstrates that nighttime symptoms of GERD are common and are often difficult to treat with current medical therapy. Additional concern has been raised over the possibility that nocturnal reflux may be associated with a higher frequency of erosive esophagitis and GERD -related complications.
Patients with frequent nighttime symptoms had an even greater relative risk approximately The same authors also demonstrated that a single dose of an H2RA taken at bedtime reduced nocturnal gastric acid breakthrough in a study of normal volunteers.
Further studies of nocturnal acid breakthrough, however, have had inconsistent results. Fackler and colleagues 44 prospectively studied 40 subjects and found that the addition of an H2RA to twice daily PPI therapy was effective only during the first 24 hours after initiation of the H2 blocker. At 1 and 4 weeks, however, ambulatory pH monitoring demonstrated no difference in acid suppression between the two study arms.
In contrast, Xue et al. Esophageal acid exposure time was also decreased in the combination therapy group. Importantly, these pH studies were performed at least 4 weeks after initiation of H2RA therapy in a subset of patients, and the response to nighttime H2RA therapy was sustained. A recent study prospectively compared four antisecretory regimens in a cohort of 22 subjects 13 with symptomatic GERD and nine normal volunteers. This difference was not statistically significant, but the number of subjects in the study was small.
Larger prospective studies are needed to confirm this concept, but it remains a reasonable option for patients with seemingly refractory nocturnal GERD. However, caution must be exercised when recommending an H2RA to patients on PPIs because concomitant administration of these two agents abolishes the acid inhibitory effect of PPIs.
Patients should accordingly be instructed never to take both agents together, and to take only small or modest doses of the H2RA at bedtime; higher doses of ranitidine mg or any dose of the longer acting famotidine 20 mg will impair activation of a morning dose of any PPI. Proton pump inhibitor therapy for GERD is typically administered continuously, with either once-daily or twice-daily dosing. Such regimens have been conclusively demonstrated to control symptoms and heal erosive esophagitis. Maintenance PPI therapy has been proven effective in controlling symptoms over a 5- to year period.
Recent studies have examined the possibility of intermittent therapy with PPIs, also known as "on-demand" therapy, in patients with nonerosive reflux disease or mild esophageal mucosal inflammation. Lind and colleagues 48 performed a large randomized controlled trial of on-demand therapy in patients with nonerosive GERD. Patients with typical heartburn symptoms were treated for 4 to 8 weeks; those in whom symptoms resolved were randomized to receive omeprazole 20 mg, omeprazole 10 mg, or placebo. These medications were to be taken "on demand," such that if heartburn recurred, patients would use the study drug daily until symptoms resolved.
The primary end point of this study was discontinuation of the protocol owing to poorly controlled heartburn. The authors concluded that on-demand therapy may be effective in a substantial number of patients. It must be emphasized that this study assessed the effect of PPI therapy given on demand for periods of days to weeks; the use of PPIs on an "as-needed" basis i.
These two trials demonstrate that on-demand PPI therapy is well tolerated by patients who experience recurrent heartburn after discontinuing GERD therapy. This approach is less costly in terms of medication expenditures, but it remains to be determined whether patients outside of clinical trials will prefer interrupted symptom control to the complete relief obtained with daily maintenance therapy.
A recent review by Bardhan 50 summarized the data from several randomized controlled trials and uncontrolled studies. Daily maintenance PPI therapy is preferred for patients with more severe esophagitis and those with a delayed response to PPI therapy. It should be noted, however, that on-demand therapy as defined in these trials is not in keeping with patients' conception of as-needed therapy.
The goal of having rapid-onset long-lasting symptom control with a PPI taken for a single day is unrealistic given the pharmacokinetics of PPIs. In general, at least 4 to 5 days of continuous PPI therapy are required to maximally inhibit gastric acid secretion and ensure symptomatic benefit.
Current research is focused both on improving antisecretory medications and in modifying gastrointestinal motility. More interesting, however, is the ongoing research into non—acid-inhibiting agents that would improve pH restoration or esophageal clearance, enhance gastric accommodation or emptying, or perhaps reverse the disordered neuromuscular function underlying GERD. The role of serotonin in the modulation of gastrointestinal motility is the subject of considerable research, and tegaserod, a selective 5HT 4 receptor agonist, has been demonstrated to be effective in irritable bowel syndrome.
Gut Health: My Experience with SIBO, Gut Inflammation, GERD and Stress
Serotonin stimulates peristaltic contractions and increases gastric motility, and the use of serotonin agonists has the potential to ameliorate GERD symptoms by promoting gastric emptying and enhancing esophageal acid clearance. Early studies with tegaserod demonstrated a decrease in reflux episodes in treated patients, 53 and larger controlled studies with this agent and other 5HT 4 agonists are ongoing. Other approaches to the treatment of GERD include inhibition of gastrin-mediated acid secretion with cholecystokinin antagonists, inhibition of histamine-mediated acid secretion via histamine-3 receptor blockade, and enhancement of esophageal mucosal protection with agents such as prostaglandin E 2 , epidermal growth factor, and transforming growth factor-.
These remain in early phases of development and are not currently available for clinical use. Acid reflux is responsible for a number of clinical syndromes outside the esophagus, and these extraesophageal manifestations of GERD have been recognized with increasing frequency Table 2. As these symptoms may occur without coincident symptoms of heartburn and regurgitation, a high index of suspicion for GERD is required when patients present with any of these features. The association between GERD and pulmonary symptoms is well established.
El-Serag and colleagues 54 studied a cohort of over , service veterans with erosive esophagitis and demonstrated an increased association with asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis. Kiljander and colleagues 57 performed a randomized controlled trial in 52 patients with asthma and abnormal ambulatory pH studies. Omeprazole 40 mg twice daily for 8 weeks was associated with a significant improvement in nocturnal pulmonary symptoms; similar results were reported in an additional uncontrolled trial.
Otolaryngeal symptoms, including hoarseness, globus sensation, and excessive throat clearing, may be manifestations of GERD. Koufman 60 studied patients presenting suspected GERD -induced otolaryngeal symptoms. Other trials suggest that nearly one third of otolaryngeal symptoms result from unsuspected GERD , and ear, nose, and throat physicians maintain a high index of suspicion for GERD in patients who are referred for hoarseness, chronic cough, or globus sensation.
El-Serag et al. Noordzij and colleagues, 64 in a similar study, demonstrated a significant reduction in hoarseness and throat clearing in patients treated with omeprazole 40 mg twice daily for 8 weeks. Thus, for patients with suspected GERD -induced otolaryngeal symptoms, a trial of PPI therapy twice daily for 8 to 12 weeks is reasonable.
Noncardiac chest pain NCCP is defined as angina-type chest pain substernal pressure or heaviness occurring without demonstrable cardiac disease. Proton pump inhibitor therapy is administered twice daily before breakfast and dinner for 8 to 12 weeks, and patients whose chest pain symptoms resolve are considered to have GERD as a cause of their NCCP. Top of page Key Points Although gastroesophageal reflux disease GERD is a disorder of esophageal motility, the therapy of reflux disease is aimed at reducing gastric acidity in order to decrease the injurious effect of the refluxate to the esophageal mucosa.
Lifestyle modifications may be effective in reducing or eliminating GERD symptoms, but the majority of patients require pharmacologic therapy. This varies with the severity of symptoms, and ranges from intermittent antacid therapy for mild disease to histamine-2 receptor antagonist H2RA therapy for moderate symptoms to daily protein pump inhibitor PPI therapy for severe symptomatic GERD. Continuous maintenance therapy with PPIs is the standard of care for severe GERD , but some patients may respond to intermittent short courses of PPI therapy given "on demand" when symptoms recur.
Patients who are "refractory" to PPI therapy should have pH monitoring performed to confirm acid suppression. Causes of refractory symptoms include "functional" heartburn, bile acid reflux, and a hypersensitive esophageal mucosa that registers symptoms at low levels of acid exposure. Nighttime GERD symptoms and extraesophageal manifestations of GERD , including hoarseness, chest pain, and asthma, are an important source of morbidity, and may respond to the use of twice daily PPI therapy.
Top of page Introduction Gastroesophageal reflux disease GERD affects more than 60 million Americans and remains one of the most common gastrointestinal disorders. Top of page Pathogenesis of Gastroesophageal Reflux Disease Gastroesophageal reflux disease results from continued exposure of the esophageal mucosa to gastric secretions, particularly acid and pepsin. Top of page Principles of Gastroesophageal Reflux Disease Therapy Gastroesophageal reflux disease is primarily a disorder of esophageal motility, as most patients with GERD do not secrete abnormal quantities of gastric acid.
Lifestyle Modifications Although the majority of patients with GERD require pharmacologic therapy, patients should be educated regarding the factors that contribute to gastroesophageal reflux and the nonpharmacologic measures that may improve symptoms Table 1. Antacids Antacids are a class of medications that act by directly neutralizing gastric acid. Prokinetic Agents Gastroesophageal reflux is primarily a motility disorder, and the use of pharmacologic agents that improve esophageal and gastric motility are conceptually attractive as therapies for GERD. Histamine—2 Receptor Antagonists Histamine—2 receptor antagonists H2RAs bind to the histamine—2 receptor on the basolateral membrane of the gastric parietal cell.
Top of page Maintenance Therapy Gastroesophageal reflux disease is a chronic disorder, and the majority of patients relapse after discontinuation of antisecretory therapy. Top of page An Approach to the Treatment of Gastroesophageal Reflux Disease The overwhelming majority of studies evaluating the treatment of GERD have included subjects with either documented erosive esophagitis or severe and frequent episodes of heartburn. Top of page Nocturnal Gastroesophageal Reflux Disease Symptoms Nighttime symptoms are common in patients with GERD , affecting a majority of those who report frequent daytime reflux symptoms.
Top of page Intermittent Therapy with Proton Pump Inhibitors Proton pump inhibitor therapy for GERD is typically administered continuously, with either once-daily or twice-daily dosing. Top of page The Future of Pharmacological Therapy for Gastroesophageal Reflux Disease Current research is focused both on improving antisecretory medications and in modifying gastrointestinal motility. Top of page Extraesophageal Manifestations of Gastroesophageal Reflux Disease Acid reflux is responsible for a number of clinical syndromes outside the esophagus, and these extraesophageal manifestations of GERD have been recognized with increasing frequency Table 2.
Top of page Ancillary details. Nighttime heartburn is an under-appreciated clinical problem that impacts sleep and daytime function: the results of a Gallup survey conducted on behalf of the American Gastroenterological Association. Am J Gastroenterol ; 98 7 — Katz PO. Optimizing medical therapy for gastroesophageal reflux disease: state of the art. Rev Gastroenterol Disord ; 3 2 — Characteristics and frequency of transient relaxations of the lower esophageal sphincter in patients with reflux esophagitis. Gastroenterology ; 95 3 — Kahrilas PJ.
GERD Pathogenesis, pathophysiology, and clinical manifestations. Cleve Clin J Med ; 70 suppl 5 :S4— Natural history of gastro-oesophageal reflux disease without oesophagitis. Gut ; 32 8 — Double-blind comparison of liquid antacid and placebo in the treatment of symptomatic reflux esophagitis. Dig Dis Sci ; 28 6 — Weberg R, Berstad A. Symptomatic effect of a low-dose antacid regimen in reflux oesophagitis. Scand J Gastroenterol ; 24 4 — Low-dose antacids versus mg cimetidine twice daily for reflux oesophagitis.
A comparative, placebo-controlled, multicentre study. Scand J Gastroenterol ; 25 3 — The medical therapy of reflux oesophagitis. Baillieres Clin Gastroenterol ; 1 4 — Cisapride 20 mg b. Aliment Pharmacol Ther ; 13 6 — Cisapride and ranitidine in the treatment of gastro-oesophageal reflux disease-a comparative randomized double-blind trial.
Aliment Pharmacol Ther ; 7 6 — Treating the symptoms of gastro-oesophageal reflux disease: a double-blind comparison of omeprazole and cisapride. Aliment Pharmacol Ther ; 11 4 — Maton PN. Profile and assessment of GERD pharmacotherapy. Cleve Clin J Med ; 70 suppl 5 :S51— Metoclopramide in gastroesophageal reflux disease: rationale for its use and results of a double-blind trial.
Am J Gastroenterol ; 79 3 — Ranitidine vs metoclopramide in the medical treatment of reflux esophagitis. Hepatogastroenterology ; 30 3 — Ramirez B, Richter JE.
Review article: promotility drugs in the treatment of gastro-oesophageal reflux disease. Aliment Pharmacol Ther ; 7 1 :5— I strongly feel that no grains or high sugar fruits is my answer along with keto. I also do the unthinkable now and make a glass of homemade lemonade with stevia before my two meals to take with digestive enzymes. Life is good and I feel free! Sounds great, Marcella! So glad you've found something that works for you. There is a good deal of faulty information here. I was on a ketogenic diet for years before developing reflux.
For 25 years I avoided carbs and grains as a patient of the real Dr. I was also using apple cider vinegar. I developed reflux while on this ketogenic low carb diet which included using ACV. The most respected doctors working with LPR contradict all of the advice given here. In LPR the reflux goes farther than the esophagus all the way up into the throat. To protect against damage from the stomach acid mucus is formed in the esophagus and larynx. Excessive mucus in the throat which causes voice issues is a symptom of LPR. The most respected New York City doctors treating acid reflux are Jonathan Aviv and Jamie Kouffman who have written books on the subject and have appeared on numerous TV programs including the Dr.
10 Ways To Cure Your Heartburn (Without Taking Drugs)
Oz show. These doctors state that vinegar is the worst thing one can consume if one has reflux. They say that that vinegar can exacerbate acid reflux, maybe even cause it. They prescribe a bland low fat diet that is high in grains, beans and many foods avoided on the low carb keto diet. Hello Linda, I'm sorry this happened to you but I beg to differ. Keep in mind that there are other factors that play a significant role in developing acid reflux.
A ketogenic diet does not cause acid reflux unless you can point us to the scientific evidence proving the opposite? I'm afraid we really can't take Dr. Oz into consideration because that resource is far from being respectable. As with every dietary approach there are people who would claim anything but what matters is scientific evidence. The claim that "vinegar can exacerbate acid reflux" is based on the assumption that acid reflux sufferers need to suppress their acid production rather than support it and that is fundamentally wrong.
A low-fat diet high in carbs is what makes these poor patients take PPIs for life. After reading this article and another one like it, I decided to stop taking that little pill every day. I have been on antacids since early childhood. I took so many tums as a child that my bones are extremely dense. While that may sound like a good side effect, kidney stones from the excess calcium were defynot. My doctor put me on Zantac and I used antacids in between. The problem is, the prescription kept going up and my acid reflux just got worse. This is a family problem.
Both my sister and I started having problems asphyxiating on our own heartburns in the middle of the night. Even when I was faithfully taking mg of Zantac both am and pm. For my birthday in December, I thought I should give myself the gift of getting rid of my antacid dependence.
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I started taking beteine HCL every time I had a heartburn. I quit the antacids cold turkey to give it a fair shot. What was the worst that could happen? I was already nearly choking to death on stomach acid on a nightly basis. To my amazement, it actually worked!
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Happy rebirth day to me!!! I still have reflux occasionally, at which point I just pop some extra beteine or apple cider vinegar, whichever is closer. It has already changed my life! Do u have hiatal hernia? I'm sure that fermenting carbohydrates is one of the problems in causing acid reflux. And according to Barry Groves, foods like red meat and possibly other animal proteins also cause your body to make more stomach acid.
So a low carb diet may not only help by lowering the carbs, but since people tend to eat more meat on this diet, that may have an added benefit, particularly for those people who have too low stomach acid in the first place. I have also read that a low salt intake can cause low stomach acid, causing acid reflux. I wonder how many people have been ruined by the guidelines to eat as little salt as possible? Considering that half the salt molecule -- sodium chloride NaCl is chloride, which is needed to produce HCl hydrochloric acid, stomach acid , it wouldn't surprise me if a very low salt intake does contribute to low stomach acid, thus exacerbating the issue to begin with.
Great post. I can say that from experience with acid reflux for 30 plus years that since starting a keto regime over 7 months ago that i simply have not suffered from acid reflux from about day two. I am amazed of this outcome as i had researched a lot into reducing carbs and had not come across any mention of this possible positive side effect! So not only have I managed to lose about 30Kg in weight with he diet change and increase in exercise, i no longer have to suffer or worry about that burning feeling and having to rush for my daily dose of antacid tablets.
Excellent post Amy, you really took time out to write this incredible knowledge enhancing post. This is so true. I suffered terribly from acid reflux.
When I started the keto diet, this was the first thing I noticed Reflux had subsided. I also found out from my Dr why. My body doesn't produce enough of the enzyme that breaks down carbs as well as though high in sugar. Eliminating these things from my diet has given me great relief. I experienced a reduction in indigestion following a keto diet but my symptoms were very severe beforehand. I had a fundoplication last year and have been eating carbs recently following recovery. I think there is a message there I was in constant pain and discomfort for a long time and I tried everything to get rid of my reflux.
I am even drinking coffee again!!! I am playing around with fasting and seeing if that flairs it back up again just to test the waters. I will say that I used to take an apple cider vinegar pill daily but cut it out because it did seem to instigate minor feelings of acid reflux. With this said, I am assuming my reflux was mainly associated with diet. Glad to hear it's working for you! I have not found relief from Gerd with my success on the Keto diet.
I am scared to try vinegar. But am going to go for it. I will let you know how it all turns out.
It's possible there's something else going on, Peggy. Is there any chance you have a hiatal hernia? I think there are also other structural issues that can contribute to a weakened LES, and if that's the case, keto probably wouldn't have the same effect on resolving the GERD. Of course, it's possible that some people do have too much acid. It's just a lot more common for people to have too little. Let us know what you think, rate this post! Leave a comment. Required Please choose another name. Invalid email address. Blog optional.
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