What is LPR?
Most people have experienced acid reflux before. Eating a pizza with a beer is enough to trigger those uncomfortable symptoms of chest pain, heartburn, and nausea. While these symptoms clearly indicate gastroesophageal reflux disease (GERD), some people may not develop any obvious signs of GERD. In this case, we call it silent reflux. Laryngopharyngeal reflux (LPR), also known as silent reflux, respiratory reflux, or extra-esophageal reflux, doesn’t typically cause symptoms. Simply, the contents of your stomach go up the esophagus, then find their way to your throat, nasal passages, and voice box. In medicine, we refer to these structures as the larynx and pharynx, hence the name laryngopharyngeal reflux.
The unusual thing about LPR is that you may have the condition without ever noticing it. This is, of course, until some serious complications begin to emerge. From a prevalence point of view, GERD is extremely common. According to studies, GERD affects 20% of all Americans. LPR, on the other hand, is less prominent. Still, millions of people have it. LPR is often underdiagnosed because its symptoms are less obvious than those of GERD, with many people not realizing that their symptoms, like chronic cough, hoarseness, or throat clearing, are related to laryngopharyngeal reflux. Note that infants and children are more likely to develop LPR due to the weak esophageal muscles and the prolonged time in the supine position.
In this article, we will cover everything there is to know about laryngopharyngeal reflux, including LPR reflux treatment. We will also discuss a very important topic – Why proton pump inhibitors may be harmful in the long-term.
What are the signs and symptoms of LPR?
As just mentioned, LPR patients may not experience the classic reflux symptoms of GERD. In some cases, the symptoms of LPR may be confused for GERD, and vice versa. Sometimes GERD is confused for a heart attack. We wrote an article going over this so be sure to check that out.
With that said, LPR has a unique clinical presentation, which includes:
· Chronic cough
· Sore throat
· Vocal hoarseness (i.e, dysphonia)
· Difficulty swallowing (i.e., dysphagia)
· Swollen and sore larynx aka “voice box”
· Chronic clearing of the throat
· Feeling thick mucus at the back of the throat
LPR vs. GERD – Similarities and Differences. Natural sodium alginate for LPR silent reflux therapy?
An abnormally relaxed lower esophageal sphincter (LES) can lead to the regurgitation of your stomach content to the esophagus. The function of the LES is to keep gastric content in the stomach. When it doesn’t work properly, both GERD and LPR develop. While LPR and GERD are quite different from one another, they have a few similarities. For instance, both conditions may affect healthy individuals.
They also share the same risk factors, including:
· Obesity
· Smoking
· Excessive drinking of alcohol
· Binge-eating
· Pregnancy
Moreover, you can have LPR and GERD at the same time. In fact, many healthcare professionals consider LPR to be a symptom of GERD. On the other hand, others find it beneficial to treat the two conditions separately. Still, LPR and GERD do not always occur simultaneously. Some patients may have GERD without LPR and vice versa. What’s concerning, however, is having asymptomatic LPR. Your larynx and pharynx will be inflicted with chronic damage without you even knowing about it. Also, the mucosa lining the larynx is more delicate compared to that of the esophagus and can be damaged by fewer reflux episodes.
Note that researchers found a solid connection between high pepsin levels in the throat and airways and LPR. This enzyme is responsible for breaking down protein. Therefore, it may play an important role in the pathogenesis of LPR. With that said, the activity of pepsin significantly drops in areas with high pH. It is thought that gaseous pepsin is deposited in the throat and is activated when either acid reflux or acidic food or drink contacts the pepsin. Activated pepsin can break down the proteins in the mucous membranes of the throat causing the inflammation and pain of LPR.
How to diagnose LPR and GERD
The diagnosis of LPR and GERD follows the usual routine of medicine:
Taking your medical history
Your doctor will ask you about the symptoms you’ve been experiencing. He/she will also ask about your symptoms duration, dietary habits, triggering factors, and relieving factors. The information gathered at this step is the most important to make an accurate diagnosis. Therefore, do your best to be transparent with your doctor.
Conducting a physical examination
A physical examination to diagnose LPR and GERD is typically normal. However, it could reveal complications of GERD, including pneumonia. In this case, your doctor will listen to your lungs using a stethoscope.
Ordering some follow-up tests
Follow-up tests are important to diagnose both conditions. However, they are not always necessary. Tests become indispensable when your symptoms have been going on for too long. For example, Barrett’s esophagus is one key complication of GERD. Unfortunately, it is a precancerous state. In other words, if not treated swiftly, it may develop into esophageal cancer. To assess the damage inflicted on your esophagus, your doctor will order an upper endoscopy (i.e., fibroscopy).
We have written an article on Barrett’s esophagus. Learn more about Barrett’s esophagus and the tests used to diagnose it by clicking here.
Another test that your doctor may order is an ambulatory acid (pH) probe test. To conduct this test, a monitor probe is placed in your esophagus. To attach the monitor, your doctor will use an endoscope.
This test provides the following data:
· The frequency of acid reflux episodes (i.e., when the acid leaks back to the esophagus)
· The quantity of acid that reaches the esophagus
· The duration that the acid remains in your esophagus
If a diagnosis of LPR is determined, you may need to see a specialist. The expert in this field is an otolaryngologist. We colloquially refer to these specialists as ear, nose, and throat (ENT) doctors. The current standard of care for LPR is empiric trial of a PPI, but is that truly the best way to treat LPR?
The dangers of long-term PPI use
Proton pump inhibitors (PPIs) are drugs that interfere with the release of acid in the stomach. This increases the pH of stomach content (makes it more basic), which lowers the risk of having symptoms. Common PPIs include omeprazole (Prilosec), lansoprazole (Prevacid), dexlansoprazole (Dexilant), esomeprazole (Nexium), and pantoprazole (Protonix). Before the invention of PPIs, people who experienced severe GERD, gastritis, and other acid-related disorders had to undergo a procedure where the stomach was surgically removed. Therefore, when PPIs became available for public use it was like a revolutionary drug.
For many years, PPIs were considered safe and well-tolerated. However, recent research suggests there is more to the story.
PPIs and C. difficile infection
One study found that using PPIs in the long term disrupts the normal flora of the gut. As a result, your risk of infections, nutritional deficiencies, and osteoporosis increases dramatically. The bacteria in your gut have many roles, including the digestion of food, mood stabilization, and production of certain nutrients. Remove them from the equation, and a whole bunch of disorders emerge.
Another study noted a relationship between PPIs and the proliferation of Clostridioides difficile (formerly known as Clostridium difficile) spores, increasing the risk of severe infection. What’s more, PPIs disrupt the function of leukocytes (i.e., white blood cells) by preventing them from phagocytosing germs. This also increases the risk of C. difficile infection.
Symptoms of C. difficile infection include:
· Dehydration
· Fever
· Nausea
· Watery diarrhea
· Abdominal cramping
· Tachycardia (i.e., rapid heart rate)
· Increased white blood cell count
· Kidney failure
PPIs and magnesium deficiency
The United States Food and Drug Administration (FDA) even released a public safety announcement, warning people of the long-term use of PPIs. Agents at the FDA found that this drug lowers magnesium (Mg) levels, which is a severe complication that disrupts:
· Cardiac function
· Muscle contraction and relaxation
· Electrical heart rhythms
· Brain signaling pathways
According to the FDA, a quarter of cases related to PPIs and magnesium deficiency did not improve after Mg supplementation. As a result, doctors had to discontinue PPIs in these patients. For transparency’s sake, the FDA noted that the risks associated with PPIs are more likely to occur with prescription drugs. This is because over-the-counter (OTC) PPIs usually come in lower doses. With that said, abusing the intake of OTC PPIs can still cause magnesium deficiency and other side effects. PPIs were originally intended only to be used for a two week treatment period up to three times per year, not indefinitely.
PPIs and community-acquired pneumonia
In a 2018 study, scientists attempted to analyze the risk of community-acquired pneumonia after long-term use of PPI. The study included more than 75,000 individuals aged 60 years and more. These participants had a medical reason to take prescription PPIs for one year or longer. During the second year of treatment, the risk of community-acquired pneumonia increased significantly. The results were contrasted with pretreatment pneumonia incidence.
The mechanism behind this predisposition is multifactorial. However, researchers think that PPIs lower the acidity of the stomach, allowing bacteria that usually wouldn’t survive in an acidic environment to grow and reach the lungs via aspiration.
PPIs and dementia
Another complication of long-term use of PPIs is the increased risk of dementia. This primarily occurs in elderly people. One prospective study followed participants who took PPIs for at least 3 months in an 18-month window. Not all participants used PPIs. Some were used as a control group. After the 8th-year follow-up, researchers found that people who used PPIs had a 44% increase in the risk of developing dementia compared to the control group. The PPIs in question were omeprazole (Prilosec), pantoprazole (Protonix), and esomeprazole (Nexium). The researchers concluded that the avoidance of PPI medication may prevent the development of dementia. This finding was supported by recent epidemiological analyses on primary data and is in line with mouse models in which the use of PPIs increased the levels of β-amyloid in the brains of mice.
PPIs and the risk of kidney disease
Shortly after the introduction of PPIs, case reports emerged suggesting an association between PPI use and damage to kidneys, specifically the development of acute interstitial nephritis (AIN). The first large-scale study examining the relationship between PPI use and Chronic Kidney Disease (CKD) included two individual patient cohorts intended to represent the general population. In each group both the adjusted and unadjusted analysis found a significant positive relationship between PPI use and the development of CKD. A 2016 study found that PPI use was associated with a higher incidence of CKD, kidney disease progression, and end-stage renal disease (ESRD). The mechanism responsible for the association between PPI use and CKD is not well understood. It is postulated that acute interstitial nephritis (AIN) caused by PPI use can lead to the development of CKD.
Summary of the current research on PPIs
We have touched on just some of the major risks associated with PPI use. The American Gastroenterology Association (AGA) reviewed the risks and benefits of PPI therapy in 2017 and its review indicated several conditions that have been associated with PPI usage, including acute kidney injury and chronic kidney disease, dementia, bone fractures, myocardial infarction, small intestinal bacterial overgrowth (SIBO), spontaneous bacterial peritonitis, Clostridium difficile infection, pneumonia, micronutrient deficiencies, and gastrointestinal malignancies. A 2019 literature review showed an association with PPI usage and an increase in gastric cancer risk. Two large studies in 2023 showed an increased risk in dementia with prolonged usage of PPI (>4.4 years) in one, and with an increased rate ratio with longer usage in another. Finally, the U.S. Food and Drug Administration (FDA) has several class warnings on possible effects of PPI usage, including interstitial nephritis, B12 deficiency, and hypomagnesemia.
Why are PPIs not the best option for LPR?
Conventionally, general practitioners treat LPR / respiratory reflux with PPIs or sometimes H2 blockers to relieve persistent throat symptoms. The logic is lowering the acidity of the stomach to minimize throat damage. While this treatment may provide temporary relief, it is not a long-term LPR reflux treatment solution. As we detailed above, the chronic intake of PPIs may cause severe complications. To make things worse, there is little evidence to support the effectiveness of PPIs in the treatment of LPR.
One study attempted to study the effects of lansoprazole on LPR. This study recruited 346 participants who had unexplained throat symptoms. These symptoms were present for 6 months or more at the time of the study.
The authors of the study divided participants into two groups:
The first group – They took lansoprazole.
The second group – They took an identical-looking pill without any effects (a placebo).
Of course, participants from both groups didn’t know whether they were taking the real pill or a placebo. The frequency of pill intake was two pills per day for 16 weeks.
The study found that PPI doesn’t improve throat symptoms. The authors emphasized that routine prescription of lansoprazole and other PPIs for unexplained throat symptoms is not evidence-based and should stop. They also insisted on the benefits of finding alternative therapies for throat symptoms. Analyzing the questionnaires revealed that both groups reported the same symptom improvements. Therefore, there was no evidence that lansoprazole was effective.
Also, new research shows that alkaline and weakly acidic LPR are more prevalent than previously presumed because they concern more than 50% of patients. These patients often do not respond at all to PPI therapy and require alginate therapy to control the alkaline component of reflux.
How alginate therapy works
Alginate is an anionic polysaccharide occurring naturally in brown seaweed, aka kelp. Alginate therapy works by creating a low-density viscous gel raft, that can last up to four hours, when alginate and bicarbonate contact stomach acid. This raft acts as a physical barrier at the opening of the stomach to prevent the leakage of acid as well as gaseous pepsin. Since it is a physical barrier even a gas can’t get through!
Unlike PPIs and other conventional treatments of LPR, alginate antacid therapy takes action immediately. Therefore, once you take an alginate-bicarbonate preparation, the damage that’s being done to your throat and voice box will stop at that moment. Unlike PPIs, alginate therapy is non-systemic. This means that alginate therapy works by forming a physical foam barrier at the lower esophageal junction and its effect is limited to that location. As we have seen, the PPI mechanism of action of cutting off acid production has side effects that affect multiple body systems (stomach, brain, kidneys) with long-term use. Alginate therapy is also safe for use while pregnant.
The good news is that alginate therapy as an LPR reflux treatment protocol has been extensively tested by researchers. The vast majority of studies in this field confirmed the positive effects of natural sodium alginate for LPR as silent reflux therapy without any known side effects. Unfortunately, most physicians are unaware of the benefits of alginate therapy for silent reflux, even though alginates for GERD have been used in Europe since the 1970s.
We covered some evidence-based findings regarding alginate therapy in this article.
Why is Nutritist’s Refluxter the best alginate for LPR?
A systematic review done on the role of pepsin in reflux stated that PPIs generally give little benefit when symptoms arise from reflux damaged organs further away from the esophagus, indicating that unlike in the esophagus, acid may not be the damaging agent. In LPR the damaging agent is pepsin. Pepsin is an enzyme made in the stomach, but its presence within the larynx epithelium, in saliva, and in the breath of those with airway and lung disease suggest that reflux has played a part. Older randomized controlled trials indicated that pepsin becomes inactive at pH≥4 and hence PPIs were thought effective in also treating refluxed pepsin by elevating gastric pH. However, new research indicates that pepsin is still active at ph≥4 and can be reactivated with exposure to acid. Pepsin can also damage cells even in the absence of acid because it can be taken up within epithelial cells by endocytosis ("cellular swallowing") and activated from within. Based on these findings, it seems unlikely that profound acid suppression with PPIs as the sole treatment strategy will give those people with LPR results comparable to those with just acid reflux.
A 2009 study found that an alginate and bicarbonate solution given to those with LPR significantly improved symptoms and clinical findings compared to the control group given nothing. A recent 2021 study enrolled 100 outpatients with LPR. Alginate treatment was administered for two months. Patients underwent four visits (at baseline and 15, 30, and 60 days after treatment). A visual analog scale assessed the perception of dysphonia, dysphagia, and cough. Alginate significantly (p<0.0001) reduced all parameters. Therefore, the study demonstrated that alginate was effective and safe in LPR treatment. Another 2021 study enrolled 50 patients with LPR and split them into two groups of 25 patients. The study compared the efficacy of alginate treatment versus PPI in reducing symptoms and signs of LPR. After 2 months of treatment, LPR symptoms and signs were significantly reduced irrespective of the treatment. Therefore, the study researchers concluded that alginate was non-inferior to PPI and may represent an alternative treatment to PPI for the treatment of LPR. Current sentiment is leaning away from PPI and towards alginate. For example, a 2021 research review recommends alginates as a first-line treatment for individuals newly diagnosed with LPR.
Nutritist Refluxter is the best alginate supplement on the market today.
Because alginate products are sold in the form of supplements, there are no regulations that instruct manufacturers on how to develop these products. Many manufacturers use a random assortment of ingredients that are not equal or similar to the ingredients used in the clinical studies on sodium alginate therapy. Sometimes manufacturers include ingredients that you don’t want like glycerine, aluminum, paraben, or "natural flavor". Other times they include sugars like dextrose or sugar substitutes like stevia, xylitol, or saccharin. Some manufacturers don't even include calcium carbonate and instead use calcium pantothenate, which was not an ingredient used in the clinical studies. In fact, calcium pantothenate is the calcium salt of Vitamin B5! Nutritist’s founder is an M.D. who studied clinical research papers such as the ones mentioned in this article and used the ingredients mentioned in the papers in their correct effective dosages when he created Refluxter. Indeed, a landmark 2019 paper on the current state of alginate therapy in treating acid reflux stated that "the three active ingredients of the most effective products are sodium alginate, sodium bicarbonate, and calcium carbonate". We recommend that when looking at any alginate product, make sure it contains these three key ingredients with sodium alginate being the predominant ingredient.
Of importance, Refluxter has the most of the key ingredient sodium alginate in its formula compared to its competitors. By law manufacturers have to list ingredients in order of quantity present. According to FDA regulations, ingredients must be listed in descending order of predominance by weight The first ingredient listed in Refluxter's alginate complex is sodium alginate, and the complex itself weighs 1,400 mg per serving. Competitor product Reflux Gourmet lists calcium pantothenate as the first ingredient in its alginate complex, followed by sodium alginate. The complex itself weighs 425 mg per serving. Therefore, by FDA regulation sodium alginate cannot comprise more than 50% (212.5 mg) of the complex since it is the second ingredient listed. Competitor product Reflux Raft PM lists calcium carbonate as the first ingredient in its alginate complex, followed by sodium alginate. The complex itself weighs 306 mg per serving. Again, by FDA regulation sodium alginate cannot comprise more than 50% (153 mg) of the complex since it is the second ingredient listed. Therefore, Refluxter has approximately 5x the amount of sodium alginate per serving than present in Reflux Gourmet or Reflux Raft! Many people report that taking the recommended serving of 5 ml of those competitor products is not enough to relieve their symptoms. Even if you were to double the dose to 10 ml, you still wouldn't get as much sodium alginate per serving compared to Refluxter. Refluxter also has no sugars or artificial sweeteners and isn't an inconvenient gel that needs to be measured, but a simple to swallow capsule. For these reasons, Refluxter is not not only the best alginate for acid reflux, but also the alginate for LPR one should reach for first.
If you have LPR you should be taking Refluxter by Nutritist.
Why? Because of three reasons:
First, LPR is a chronic condition that requires long-term therapy. Opting for a PPI or H2 blocker for long-term use is not a good choice due to all the factors listed earlier.
Next, LPR is mostly asymptomatic "silent reflux". Hence, you might not know about it even though it is damaging your throat. In this case, would you prefer to take a natural supplement without any reported side effects or a PPI?
Lastly, more than 50% of people with LPR have alkaline LPR or weakly acidic LPR. PPIs will not help much, if at all, for these people. Because alginate works by forming an actual physical barrier when it along with bicarbonate reacts with stomach acid, it doesn’t matter whether the LPR is alkaline or acidic. Either way, its blocked!
These three reasons should be enough to make you choose Refluxter as your LPR reflux treatment tool to solve LPR.
** On dosing Refluxter for LPR: Make sure to take 2 capsules after every meal. Do not skip a dose as LPR is more difficult to treat since pepsin can be a gas. You may need to take an extra capsule at night for severe LPR. Alginate is safe at even high doses, but
monitor calcium and sodium intake if you have kidney or blood pressure issues. **
If you are ready to make the smart choice like many of our readers already have, check out Refluxter by clicking here.
Takeaway message
LPR, or silent reflux, is a mostly asymptomatic condition that wreaks havoc on the larynx and pharynx, causing all sorts of complications. Unfortunately, these complications do not give us any warning signs, meaning we only learn about them when it’s too late. So, how can you treat a condition if you don’t know it’s there? One might think that PPIs are the answer. Unfortunately, the long-term complications of these drugs are just too scary to take the risk. Also, the evidence that they actually work to treat LPR is just not compelling enough.
For this reason, we recommend that people with GERD or suspected LPR should take Refluxter to address their symptoms. It is a safe, natural supplement that uses basic chemical knowledge to protect your esophagus, larynx, and pharynx from damage caused by acid and pepsin. Pregnant women will be glad to hear that Refluxter is safe to take during pregnancy as it does not have artificial sweeteners or other harmful chemicals.
We hope that this article managed to highlight the different aspects of LPR and how it is different from GERD.
If you have any questions, concerns, or personal experiences with LPR, please do not hesitate to share your thoughts in the Comment section below. You can also use the Contact page to reach out for a private conversation.
Disclaimer: This article is not intended to provide medical advice. This article is intended for informational and educational purposes only and is not intended to substitute for professional medical advice, diagnosis, or treatment. This article does not constitute the formation of a patient-physician relationship. The statements in this article have not been evaluated by the Food and Drug Administration. Refluxter is not intended to diagnose, treat, cure or prevent any disease. Please consult your physician for medical advice.
Further readings
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Please help me. Do I start taking this and then stop my PPI's? Been on them for almost 5 years.