Asthma: The $50 Billion Dollar Medical Mistake
According to the Centers for Disease Control, 8% of all Americans and 17% of poor, non-white children in the U.S. have asthma. The asthma-related costs of doctors, hospitals, and medication add up to $56 billion per year. But what if doctors had it wrong? What if asthma was one of the most common misdiagnoses in America? What if the real problem was actually silent acid reflux and not asthma at all? We spend billions of dollars on asthma treatment each year, and most of it is a waste!
If you or someone you know has a diagnosis of asthma, you must ask this very important question: When you have trouble breathing during an “asthma” attack, do you have more difficulty getting air IN or OUT? Trouble getting air IN (during inhalation) is NOT ever asthma, trouble getting air OUT (during exhalation) is.
How does this work? The difference between breathing IN and OUT is explained by the anatomy and physiology of the airway. With acid reflux, airway obstruction occurs at the level of the larynx (voice box). The upper part of the larynx contains acid receptors, which act like electrical switches. When triggered by exposure to acid, these receptors close the vocal chords. That results in trouble breathing IN. This type of airway obstruction is similar to that seen in children with croup or whooping cough, who may make loud, crowing sounds when breathing IN.
The mechanism of airway obstruction in asthma is completely different. People with asthma have trouble getting air OUT, because breathing tubes in the lungs (inside the chest cavity) become narrower. This narrowing is usually due to an allergy. Then, during exhalation (breathing OUT), the full lungs exert additional pressure on the already narrowed bronchial tubes, resulting in prolonged expiration, also known as wheezing.
For thirty years, my medical practice has focused on patients with acid reflux, and during that time I have made three observations: (1) Approximately 80% of patients with asthma don’t have it; (2) Silent reflux (acid reflux occurring without the obvious symptoms of heartburn or indigestion) is usually the correct diagnosis; and (3) A problem breathing IN is never asthma. Indeed, people with wrongfully-diagnosed asthma, the INs, don’t respond to asthma treatments, but they do get well when their reflux is adequately controlled.
Everyone with asthma should know this: Reflux affects the throat and causes trouble breathing IN. Asthma affects the lungs and causes trouble breathing OUT.Unfortunately, this important clinical point is not understood by most doctors. Therefore, only when everyone is aware of this will the over-diagnosis of asthma cease. And that will result in better health for millions of people, along with healthcare cost savings in the billions of dollars. – Jamie Koufman, M.D.
Dr. Jamie Koufman is the Director of the Voice Institute of New York and is the New York Times best selling author of The Chronic Cough Enigma and Dropping Acid: The Reflux Diet Cookbook & Cure.
Contact information: Dr. Jamie Koufman, Director, Voice Institute of New York, 200 West 57th St., Suite 1203, New York, NY 10019, Tel: (212) 463-8014, firstname.lastname@example.org
Last year, I saw a reflux patient with airway reflux who had completed reflux testing and when I was describing the induction (detox) diet, she interrupted to tell me that was gluten-free. At the time, I did not know enough about this topic to say anything useful and so I just asked her to adapt as best she could to a “reflux-friendly gluten-free” diet. Since that time, I have learned a more about food additives and about gluten, and some from personal experience.
Not long ago I went to see my doctor about my psoriasis. (I have psoriasis on my elbows knees hands and face and I’ve had it for many years; unfortunately, it has gotten worse in the last year.) I also have mild hypothyroidism. My doctor pointed out that certain thyroid conditions and psoriasis are probably autoimmune disorders that they sometimes respond to a gluten-free diet. So, I went on a gluten-free, dairy-free, sugar-free diet; and a week later, I noticed some improvement in my psoriasis.
This, of course, is a preliminary anecdotal report, and the court is still out. In fact, the relationship between gluten and autoimmune disease is unproven. As of this writing, there is no hard scientific evidence directly linking gluten consumption with different kinds of autoimmune disease (other than celiac disease); however, there are clinical data that suggest that there may be a link with thyroid, rheumatologic, and dermatologic disease. Here is a link to a nice review article.
A gluten-free diet is a diet that excludes the protein gluten. Gluten is found in grains such as wheat, barley, and rye. While a gluten-free diet is usually used to treat celiac disease, an inflammatory disease of the small intestines, it may play a role in other autoimmune diseases, e.g., psoriasis, arthritis, scleroderma, thyroid disease. It also is believed to be related to some cases of acid reflux. Eating a gluten-free diet may help some people with the above conditions improve their symptoms.
I am providing here for my readers a hybrid diet that takes into account elements of my reflux diet, that is, a low-fat, low-acid, pH-balanced diet with a gluten-free, dairy-free, sugar-free diet. This is, crude as it is, my reflux friendly gluten-free diet. Caveat emptor and good luck!
Switching to a gluten-free diet is a big change and, like anything new, it takes some getting used to. You may also be surprised to realize how many gluten-free products, such as bread, pasta, frozen foods are now available. Specialty grocery stores like Whole Foods sell lots of different gluten-free foods.
Note: This diet also restricts acidic or high-fat foods as well as dairy and sugars. Why restrict dairy and sugars? Because of possible cross-reactivity.
What You Can’t Eat
Barley (NB: malt, malt flavoring, and malt vinegar are usually made from barley)
Triticale (a cross between wheat and rye)
Wheat (avoid all unless labeled gluten-free)
Breads (unless they are labeled gluten-free, dairy-free, and sugar-free)
Cakes and pies (unless they are labeled gluten-free, dairy-free, and sugar-free)
Candies (unless they are labeled gluten-free, dairy-free, and sugar-free)
Cereals (unless they are labeled gluten-free, dairy-free, and sugar-free)
Cookies and crackers (unless they are labeled gluten-free, dairy-free, and sugar-free)
Imitation meat or seafood
Oats (unless labeled gluten-free)
Processed luncheon meats
Salad dressings (unless labeled gluten-free)
Sauces, including soy sauce
Seasoned rice mixes
Seasoned snack foods, such as potato and tortilla chips
Soups and soup bases (unless labeled gluten-free, dairy-free, and sugar-free)
Vegetables in sauce
Avoid food additives, such as malts, starches and medications and vitamins that use gluten as a binding agent
What You Can Eat
Fruit is free of gluten but some fruits are better than others when it comes to reflux. (Acid fruits are best consumed with alkaline water (pH>8.5) or low-fat almond or soy milk)
Apples (red, not green, in moderation, and only after induction)
Apricot (in moderation, and only after induction)
Blueberries (in moderation, and only after induction)
Peaches (in moderation, and only after induction)
Pears (in moderation, and only after induction)
Plums (in moderation, and only after induction)
Raspberries (in moderation, and only after induction)
Strawberries (in moderation, and only after induction)
Zest, the outside of lemon, lime, or orange (not the juice or the fruit)
Vegetables are also naturally free of gluten (fresh or frozen vegetables, that is, not canned)
Onions (cooked, in moderation, and only after induction)
Potatoes (white and sweet)
Meats are always gluten free unless processed, breaded, or fried with breadcrumbs; also avoid gravy as most gravy does have gluten in it. Fish is included here in the meat category.
Beef (in moderation, and only after induction)
Fish (including shellfish, broiled, baked, grilled, but not breaded or fried)
Pork (white pork, pork tenderloin only, in moderation, and only after induction)
Flours and Grains
Brown rice flour
Popcorn (without any coating)
Other Gluten-Free Foods
Almonds (in moderation, and only after induction)
Honey (Manuka honey preferred)
Pistachios (in moderation, and only after induction)
Wine (in moderation; one glass only and only after induction)
INTEGRATED AERODIGESTIVE MEDICINE:
A HEALTHCARE MODEL FOR THE FUTURE
From THE CHRONIC COUGH ENIGMA by Jamie Koufman
Any person with an enigmatic chronic cough will tell you that the specialist model of American medicine has failed. In truth, it has failed for a large number of patients and at many different levels. Not only do we have too many specialists, but too many practice so narrow a specialty that often patients receive incorrect, expensive and wasteful medical care.
An illustration of the chronic cough patient’s predicament with the specialist model of American medicine is the elephant in the fable of the three blind men and the elephant:
The first blind man, feeling the leg of the elephant, exclaims, “I can see it clearly; the elephant is like a big tree.” The second blind man holds the trunk and says, “No, the elephant is like a very large snake.” The third blind man grasps an ear. “You are both wrong,” he proclaims, “The elephant is really like a gigantic leaf.” Each blind man embraces a part of the truth, but none understands its entirety.
In the case of chronic cough, the three blind men are the three medical specialties: (1) the otolaryngologist (ENT, the ear, nose, and throat physician); (2) the gastroenterologist (GI physician); and (3) the pulmonologist (PUL, chest and lung specialist).
The problem is not just ignorance. Today, many doctors behave more like entrepreneurs than healers. Each “profit center” attempts to maximize income by manipulating the medical billing and coding system. Indeed, most medical professional societies offer their physicians advanced training in coding so that they can effectively maximize income.
It is worse than you think. Today in most hospitals, coding specialists routinely make patient-care rounds with the doctors to insure that no code goes unbilled. The idea is that hospitals want to absolutely maximize possible income. And yes, they stretch the truth a lot every day to do so.
Conflicts of Interest and Corruption Are Why Healthcare Is So Expensive
The needs of patients have been lost in a healthcare system dominated by for-profit corporate medicine characterized by conflicts of interest, price fixing, and corruption.
In 2012, I had back surgery, a L3-L4-L5 fusion. I now have two titanium plates and six screws in my back. The hospital billed $111,000 for the hardware alone; unbelievably, it actually was $15,000 per screw. (I know for a fact that you can purchase an excellent quality titanium screw at Home Depot for under a dollar.)
The punch line is not that hospital billed so outrageously, but that my insurance company (United) paid them $146,000 for my surgery ($99,000 for the hardware) and that didn’t cover professional fees. My surgeon charged $117,000, and I believe that he received $104,000. Meanwhile, I am still being billed by the hospital and the surgeon; both want more money.
The total bill for the surgery was $260,000. In Sweden comparable surgery costs about $10,000. One might reasonably ask where the other $250,000 went.
Returning to chronic cough and reflux, there is corruption in endoscopy. Many doctors have profound conflicts of interest because of ambulatory surgery centers. ASCs are big business. Typically, a doctor negotiates an ownership position in an ASC with the understanding that s/he will perform a certain number of procedures, say 1,000 per year, at that ASC. Conflict of interest? The return on investment is astonishing! One GI from New York happily informed me that his annual income from his ASC was $800,000.
Last year, there were 10 million sedated endoscopies performed in the U.S. at a facilities fee cost of $10 billion, that is, an average of $1,000 per procedure. And that does not include the professional fees of the gastroenterologist, anesthesiologist, and pathologist.
Also questionable, when GIs perform upper endoscopy for reflux, they routinely examine the entire upper GI tract and perform biopsies. Why? Is it because EGD (esophagogastroduodenoscopy) with biopsy pays much more than a lesser procedure or a procedure without biopsies?
When it comes to non-pulmonary chronic cough, pulmonologists also appear to be inefficient and wasteful. When a patient comes to a pulmonologist with any type of reactive airway disease or shortness of breath, the doctor will usually perform pulmonary function tests (PFTs). S/he may also perform bronchoscopy, endoscopy of the airway and lungs, but these doctors are not trained to examine the throat. When it comes to silent airway reflux, the usual result is misdiagnosis and incorrect treatment.
Most pulmonologists diagnose asthma in all cases of reactive airways disease, because they apparently cannot differentiate inspiratory, airway reflux-caused reactive airway disease from true asthma characterized by expiratory wheezing. The misdiagnosis of asthma is costly. No one knows exactly how much; however, asthma medication costs $56 billion annually in the U.S. See Chapter 7: Asthma that Isn’t Asthma.
Otolaryngologists should be able to examine the larynx (voice box) and throat, but they are generally handicapped by outmoded instrumentation and inadequate training. Thus, most ENTs can neither accurately diagnose nor effectively treat airway reflux.
Perhaps the greatest waste due to inaccurate diagnosis in the otolaryngology area is sinusitis. Many patients come to me after having had multiple unsuccessful sinus surgeries, still suffering the same symptoms. Yes, again it’s airway reflux. Nocturnal (nighttime) reflux in particular can cause sinus symptoms, the most common of which is post-nasal drip.
The typical chronic cough patient who comes to see me has been coughing for more than a decade and has already seen more than a dozen physicians (ENTs, GIs, PULs, allergists, etc.). One patient who had been coughing for 20 years reported that he had seen 34 doctors, some from four major medical centers, before seeing me.
Where did this excessive, inefficient, and unnecessarily expensive medical mess come from? The healthcare industry has shown a strong propensity to chase funding. When Medicare agreed to cover renal dialysis, for example, thousarnds of new dialysis centers quickly sprung up. (Remember, U.S. healthcare is private industry, but much of it is paid for by the government, e.g. Medicare, Medicaid). A big part of the problem is lack of accountability. There is little or no objective scrutiny in healthcare. What do we get for our money? Fifteen-thousand dollar a piece screws?
Specialist medicine has proliferated in part because Americans want to have “the best.” They like seeing the best doctors just as they like seeing the best sports teams. The problem, however, is what doctor to see when your self-diagnosis is wrong? The best at what?
Furthermore, while the idea of seeing the “best doctor” is appealing, there is no such doctor when it comes to non-pulmonary chronic cough, silent airway reflux and vagally-mediated neurogenic syndromes.
Today, people are skeptical and cautious, and at this point consumer confidence cannot be restored by the marketing claim, “We are the best.” Patients are rightly mistrustful of the current healthcare system.
People no longer believe that healthcare providers necessarily have their best interests at heart. It is now clear that patients must be their own advocates and that for-profit medicine leads to more attention to gain and less to quality patient care.
We pay almost four times more than any other civilized country for healthcare, and we rank 37th in quality of care. Last year, the price tag for U.S. healthcare was $2.7 trillion. Strip away the excesses and the price would probably have been closer to $700 billion ($0.7 trillion). That’s a lot of excess!
We need a healthcare system that is less fragmented and self-serving. Specialists often do what they do well, but nothing more.
If chronic cough, airway reflux, reactive airway disease, and (vagal) neurogenic syndromes are so prevalent—almost one-out-of-five (18%) Americans has airway reflux3 and falls into one of the above categories—then the current system is wasting massive healthcare dollars on inappropriate diagnostics and ineffective treatments.
Maybe we don’t need so many gastroenterologists, pulmonologists, and otolaryngologists. Maybe we need doctors who take better care of the whole patient with aerodigestive diseases. Reflux is the tip of an appalling iceberg.Integrated Aerodigestive Medicine
I have practiced integrated aerodigestive medicine for thirty years now. What does that mean? I am part otolaryngologist, but I know the parts of otolaryngology that most otolaryngologists don’t know. I am part gastroenterologist, but I know the parts of gastroenterology that most gastroenterologists don’t know. And I am part pulmonologist, but I know the parts of pulmonology that most pulmonologists don’t know.
I don’t practice all aspects of aerodigestive medicine, and I know my limitations. I have almost nothing to do with the liver, colon, heart, teeth, sinuses, etc.
I am an expert in the vagal system, and that includes the whole airway and the whole digestive tract. And yes, all of these parts are connected anatomically and functionally.
As I have become well known as an airway reflux expert, with expertise in non-medical treatment (namely, diet and lifestyle), more and more patients with esophageal reflux (GERD) have come to see me.
A common story is, “I had endoscopy, and I was told that I had Barrett’s esophagus. I was given a pill and told to come back in a year.” Apparently, most GIs think that the only treatment for reflux, no matter how severe, is a purple pill (PPI).
Unlike anatomic (organ-specific) medical specialties, integrated aerodigestive medicine is system-driven and symptom-driven. It combines elements of all of the overlapping aerodigestive tract medical specialties with a special focus on the diagnosis and treatment of airway reflux. Further, as a preventative approach to wellness, integrated aerodigestive medicine emphasizes dietary health, lifestyle education, and behavior modification.
The aerodigestive tract must be treated as a unified system for which physicians are trained. In addition, precision diagnostics (e.g., laryngeal electromyography, airway reflux testing) are the key to accurate diagnosis, and at present, few physicians perform any, let alone all, of them.
So, if integrated aerodigestive medicine is a new “specialty,” who should see such a physician, and for what? Shown below is a list of common integrated aerodigestive medicine symptoms.Here is a list of aerodigestive symptoms: allergies, asthma, burning tongue, chest pain (non-cardiac), choking episodes, chronic cough, chronic throat clearing, COPD (chronic obstructive pulmonary disease); difficulty swallowing, esophageal spasm, excessive throat mucus, food getting stuck, globus (a lump-in-throat sensation), heartburn, hoarseness, indigestion, laryngitis, laryngospasm, nausea, painful speaking (odynophonia), paradoxical vocal fold movement, post-nasal drip, regurgitation, shortness of breath, sinusitis, sleep apnea, throatburn, vocal cord dysfunction, vocal fatigue, vocal nodules and polyps, voice breaks, wheezing
The idea that people with these symptoms need to be seen by a committee of different specialist, one for each problem, makes no sense, particularly since reflux and vagal dysfunction are responsible for most.
For people who don’t have chronic cough but have another reflux-related or neurogenic symptom, you could read this by substituting painful speaking or burning throat for chronic cough and the information and approach will still be relevant.
A doctor practicing integrated aerodigestive medicine, as I do, must have certain skills and diagnostic technology: (1) Ability to obtain and interpret high-definition examination of the nose and throat (transnasal videostroboscopy) with still imaging; (2) Ability to diagnose subtle vocal fold paresis; (3) Ability to calculate an accurate reflux finding score;(4) High-definition esophageal manometry; (5) Ambulatory, double-probe, 24-hour (simultaneous esophageal and pharyngeal) pH monitoring; (6) Laryngeal electromyography; (7) Transnasal esophagoscopy; (8) Pulmonary function testing.
Let’s remember, the vagus nerve is the nerve of the entire aerodigestive tract. I am a doctor of the vagus, and therefore I am a doctor of the aerodigestive tract. I do not, however, practice medicine in a vacuum. I have a team of colleagues to whom I refer when appropriate.
It is a big team because I understand that I have limitations. I am not a sinus surgeon and sometimes one is needed; I am not a pulmonologist and sometimes one is needed, and so forth. No less than 25 stacks of business cards sit on my windowsill for those colleagues to whom I refer patients. They form a network designed to enable me to provide comprehensive care for my patients.
My aerodigestive medicine team: acupuncture, allergy, audiology, cardiology, dentistry, endocrinology, gastroenterology, general surgery (for antireflux surgery), internal medicine, otolaryngology, psychiatry, pulmonology, and speech-language pathology.
I refer to all of those professionals as appropriate, but I remain in charge of the overall health and well-being of my patients. I am the quarterback of the team. I call the plays and I insure that we doctors communicate for the benefit of our patients.
In the future, residency programs in integrated aerodigestive medicine will focus on chronic cough and other aerodigestive symptoms with the understanding that reflux plays a huge role in the severity of disease, and that environmental, dietary, infectious, neurogenic, inflammatory, and emotional factors act together. All must be considered as part of the problem, and the solution should be seen as unique for each individual patient.
In my opinion, a major overhaul of the healthcare system is needed. Health is not a commodity and should never be treated as such. Restructuring the American healthcare system will require a compassionate and un-corporate new paradigm. Integrated aerodigestive medicine provides an excellent model of efficient restructuring.
The whitish lesion is a small vocal cord cancer in a refluxer (life-time non-smoker). The rest of the voice box shows findings of reflux laryngitis.
A recent epidemiologic study reported in the New York Times showed a statistical relationship between heartburn and throat cancer; the authors reported a 78% increase in throat cancer in refluxers with heartburn.
I have spent 35 years studying reflux, particularly the silent type, that is, acid reflux occurring without heartburn. Silent refluxers have symptoms such as hoarseness, chronic throat-clearing and cough, difficulty swallowing, post-nasal drip, and asthma-like symptoms. (See also my Silent Reflux post. Indeed, in 1991, I published data from a serries of 31 patients with throat cancer; 84% had documented reflux, but only 33% had heartburn.
Here below is an excerpt from Dropping Acid: The Reflux Diet Cookbook & Cure on the relationship between reflux and throat cancer.
Reflux and Cancer
One of the most frequent questions patients ask is whether reflux can cause cancer. I believe the answer is an emphatic yes. That is part of the reason this book is so concerned about the acidity of today’s typical diet.
We have not yet proven that reflux causes laryngeal and vocal cord cancer, but there is strong circumstantial clinical evidence along with bench research to support it.1,7,9,39,114,119-124 We believe that one can get laryngeal cancer without smoking, but not without the presence of reflux.4,39 This section presents six arguments to support this concept
1. Many patients with laryngeal cancer are non-smokers or ex-smokers. We prospectively studied 50 adult patients with early vocal cord cancer.9 Of them, 44 percent (22/50) were active smokers, 42 percent (21/50) were ex-smokers with a median duration of smoking cessation of eight years, and 14 percent (7/50) were lifetime non-smokers. Using pH monitoring, we found that 68 percent of the patients had reflux, almost twice as many as those who were actually smokers. And remember, in the study group, there were seven lifetime non-smokers.9
2. Some people get recurrent, small, reflux-related vocal cord cancers that are periodically removed with a surgical laser. We’ve seen many such cases over the years. Significantly, almost half of those patients stop making cancer when their reflux is controlled. The same is true for patients with pre-cancers called dysplasia and leukoplakia.1,114
3. When different groups of patients are tested for reflux, including those with cough, sore throat, etc., the highest proportion of those demonstrating reflux are the cancer patients. In 1991, we reported abnormal reflux testing in 84 percent of patients with laryngeal cancer, five of whom were lifetime non-smokers.1
4. We compared the reflux (pH) testing results of smokers and non-smokers and found that smokers had twice as much reflux, both in the esophagus and the throat. Cigarette smoking is specifically associated with relaxation of the upper and lower esophageal valves within two minutes, and reflux episodes occur with two-thirds of cigarettes smoked.55,138
5. Our laboratory has examined the impact of reflux on a cellular level in human patients and in animal models and found tremendous similarities in the larynx between patients who have LPR and patients who have cancer. Of those studies, the most important was an analysis of biopsies for the presence of pepsin within the laryngeal tissue. Pepsin was found in 5 percent (1/20) of normal controls without reflux. On the other hand, 95 percent of LPR patients with reflux into the throat had pepsin in their laryngeal biopsy tissue, and 100 percent (5/5) of laryngeal cancer patients tested had pepsin within the cancerous tissue.39,47,55 In addition, extraordinary landmark experiments in cell biology by Nikki Johnston et al. 42,47,48,51.53,54,124 showed that pepsin up-regulates the genes that cause cancer in a way that suggests that pepsin is actually the cause of laryngeal cancer.124
6. There are similarities between laryngeal cancer and esophageal cancer. We have shown the presence of pepsin in reflux laryngitis by a special staining technique. In addition, using biopsies of patients with reflux and laryngeal cancer, we have shown that both have similar protein profiles except for one stress protein, HSP70.4,39,47-49
As previously mentioned, esophageal cancer is the fastest growing cancer in the United States, up 850% since the 1970s. We are also finding Barrett’s Esophagus, a known reflux-related form of pre-cancer, in approximately 7 percent of our LPR reflux patients.33,44,52 It is striking and significant to note that Barrett’s Esophagus is found just as often in ENT patients with silent reflux (symptoms of coughing and hoarseness) as in GI patients with heartburn.134
In summary, there is clinical and scientific evidence that reflux, mainly pepsin, may cause cancer of the larynx and esophagus.
One of our biggest concerns is that a huge population of Americans is potentially at risk to develop cancer, and that we have no methodology for identifying the most susceptible. As clinicians, we can certainly say that we are seeing increasingly more and more reflux in increasingly younger patients; in our opinion, this is an ominous warning sign.
We regret that we cannot prove all of our assertions and beliefs just yet. However, our data and clinical impressions deserve to be in the public domain so that other researchers and clinicians can investigate the relationships we’ve presented. We believe that diet is the missing link and that our diet may be killing us and it is time for us to aggressively explore these variables and fix them.
By the way, people who are rightfully worried about cancer deserve to be checked. The technology has changed. Doctors can now look inside while patients are awake, comfortable, and without pain, using a technique called transnasal esophagoscopy.29,33,58,134 The idea that you can only be checked for cancer in a special facility and under anesthesia is archaic.
(If you are interested in the references, they may be found in Dropping Acid on pages 177-185.)
Excerpted from Dropping Acid: The Reflux Diet Cookbook & Cure (by Jamie Koufman, M.D.)
Standing in front of this corndog and fried food refluxitorium, Larry the Cable Guy tells us to take one Prilosec in the morning and be heartburn free all day long. He implies that if you take AstraZeneca’s purple pill, you can eat anything you want.
Nothing could be further than the truth. In fact, this strategy—cover up the heartburn but don’t control the disease—is probably why acid-reflux-caused esophageal cancer is the fastest growing cancer in the United States, up a whopping 850% since the 1970s.
Purple pills may stop some symptoms but have little or no effect on the progression of the disease. I should know; I am one of the world’s experts on reflux, and virtually every patient who comes to see me with complications of reflux is already on a purple pill, so in truth they don’t work very well.
Purple pills don’t control reflux! They just cover up its more serious manifestations.
The purple pills are a class of drugs called PPIs (proton pump inhibitors). They do not stop reflux, and they never should have been allowed (by the FDA) to be sold over the counter. Here’s why. After people take a PPI, they may feel better. But when they quit taking the PPI, they get rebound hyperacidity. That’s right, when you quit taking purple pills, you make more stomach acid than before. And so sales of purple pills escalate in a vicious cycle: You have heartburn and take purple pills—get some relief—then you stop purple pill—have rebound (worse acidity than before) —then you have to start taking the pills again. Wow! What a great strategy for the greedy drug companies that make the purple pills.
Much safer (and without the rebound hyperacidity) to take on an as-needed basis are the H2A class of drugs, including ranitidine (Zantac) and famotidine (Pepcid). PPIs should be taken under a doctor’s supervision, and when the patient is ready, tapering of the PPI should be done using H2As.
Fact is, the only really effective, long-term treatment of acid reflux is through a healthy diet and lifestyle. Overeating and overdrinking are key factors, and high-fat, high-acid foods are poison. I have written a lot about this topic in this blog and in my New York Times best-selling book, Dropping Acid: The Reflux Diet Cookbook & Cure. Click here for more references on my reflux work
When stupidity and greed collide? Wake up America; what you eat may be eating you!
Reflux is an expensive, high-prevalence disease1-4 and it affects approximately half of patients with laryngeal and voice disorders.5 It remains controversial because there are still no standard diagnostics or treatments.2-4 In addition, divisions between the medical specialties (otolaryngology, pulmonology, gastroenterology) each of which focuses on its own anatomic subdivision, have led to academic turf wars and fragmentation of research and the care of patients with diverse manifestations of reflux, particularly those with laryngopharyngeal reflux (LPR), the often “silent” (no heartburn or indigestion) backflow of gastric (stomach) contents into the laryngopharynx (throat and voice box).
Nevertheless, in addition to causing dysphonia (hoarseness), LPR affects large numbers of otolaryngologic patients with sinusitis, sore throat, globus (a lump-in-the-throat sensation), dysphagia (difficulty swallowing), chronic cough, and other reactive airways diseases such as asthma.2,6,7 Reflux remains a confusing topic even within otolaryngology (ENT), because most otolaryngology residency programs’ curricula often do not include specific training in the diagnosis and management of LPR. Among otolaryngologists, there isn’t even a clear consensus regarding the laryngeal findings.2,8
Having spent thirty-five years studying airway reflux in both laboratory and clinical settings, this chapter presents a paradigm of integrated aerodigestive medicine in which reflux play a unifying role. And therefore the structure of this chapter includes: nosology, epidemiology, etiology, pathophysiology, diagnosis, and treatment.
Nosology (Classification & Nomenclature) of Reflux
The term reflux is derived from two Latin roots, re-. back, and fluere, to flow. Therefore, reflux literally means backflow. The backflow in question here is the backflow of stomach contents into the esophagus and even into the airway, eg, laryngopharynx, trachea, lungs.
Patients and the lay media refer to this problem as “acid reflux,” but medical specialists have many different names and designations for diseases and disorders related to gastric reflux into the esophagus and airway; see Table 1. Specialists have coined different terms to express their different points of view. When describing reflux, gastroenterologists (GIs), for example, generally refer to GERD, gastroesophageal reflux disease, which describes their focus, the esophagus; however, when the airway is involved, GIs use terms like atypical reflux or supraesophageal reflux. Otolaryngologists generally use the term LPR.
I coined that term LPR in the 1980s specifically to call attention to the fact that the larynx and pharynx were the primary target organs when the refluxate extends above the esophagus. I also coined the term silent reflux because often patients with LPR do not have symptoms of heartburn or indigestion, symptoms that make reflux obvious.
It is worth noting that some people with “silent reflux” have no symptoms. This may occur when a person has nocturnal reflux; and such can be associated with seeming unrelated sinus and lung disease, eg, asthma, recurrent pneumonia, COPD. Indeed, it is possible for LPR to be the underlying cause all of those problems.2-6
Table 1: Most Common Medical Terms for Reflux
Gastroesophageal reflux disease
Extraesophageal reflux disease
Supraesophageal reflux disease
Atypical reflux disease
Why are there so many different terms? Besides otolaryngologists and gastroenterologists, many other specialists, including allergists, pulmonologists, pediatricians, internists, family practitioners, anesthesiologists, and critical care specialists regularly encounter diverse manifestations of reflux disease. Nevertheless, the two most popular terms for reflux across the different groups’ medical literature are GERD and LPR.
Since this reflux post was written for otolaryngologists and reflux patients as well, it makes sense dividing the aerodigestive tract into two basic components, the airway and the esophagus. These overarching anatomic designations are intuitive and appropriately broad. This chapter justifiably might have been termed airway reflux, as the latter term is more encompassing. The terms airway reflux and LPR may be used interchangeably as may the terms esophageal reflux and GERD.
The prevalence of reflux disease—both esophageal reflux (GERD) and airway reflux (LPR)—has increased dramatically in our lifetimes.1-4,9-15 Using a statistical model and an analysis of 17 studies, El-Serag1 showed that the average rate of increase of reflux disease since 1976 was 4% per year (P < .0001).
An even more ominous trend is the skyrocketing increase in the prevalence of esophageal cancer in the U.S.12-14 Based upon National Cancer Institute data, esophageal cancer is the fastest growing cancer in the country having increased 850% since 1975.12 During this same period, its mortality has increased seven-fold despite increased esophageal surveillance.2-4,13,14 In addition, the prevalence of Barrett’s esophagus, the reflux-related precursor to esophageal cancer, is very high.12-14 Furthermore, Reavis, et al. reported that patients with hoarseness and chronic cough (airway symptoms) had Barrett’s esophagus just as frequently (8%) as GERD patients with heartburn.15 Today, routine esophageal screening is recommended for both airway and esophageal reflux patients.2-4,15,16
In the past, reflux was primarily a disease of overweight middle-aged people; however reflux is now common in thin, athletic, young people.3,4,17 This trend toward young patients with severe reflux has been observed by many experienced clinicians.
In 2010, the prevalence of airway and esophageal reflux (GERD and LPR) in the United States was estimated by interviewing a geographically random sample of 656 U.S. citizens.3 The data revealed that an astonishing 40% had reflux disease, 22% having classic esophageal reflux (GERD) and another 18% having airway reflux (LPR).3 There were no statistical differences seen between age, gender, and regions of the country. The most striking and unanticipated finding was that 37% of the 21-30 year-old age group had reflux.3,4
Historically, these trends have been primarily attributed to the obesity epidemic; however, it now appears that food additives (especially acid) in the American diet may be in large measure responsible for the reflux epidemic.3,4
There is considerable overlap between the causes of LPR and GERD, and this makes sense because the initial event for both is a transient LES (lower esophageal sphincter) relaxation that allows a bolus of refluxate to move from the stomach into the esophagus.5 The causes of gastroesophageal reflux (GER) are multifactorial and include many well-described factors2,5,6,8,17-19 (Table 2). Leaving congenital conditions and familial predisposition aside, over-eating, late-night eating, consumption of high-fat foods, fried foods, soft drinks (and other carbonated, caffeinated, and/or acidified beverages), smoking, and ethanol drinking all contribute GER.5
Chemicals like caffeine, ethanol, and theobromine (in chocolate), and medications like theophylline, are all refluxogenic and act by directly relaxing the LES.5 The same is true of fried and fatty foods, which cause the LES to relax, which lead to reflux. Reflux is also caused by anything that increases the intragastric pressure, such as overeating and carbonation, or anything that increases intra-abdominal pressure, such as obesity and exercise. Both increased intragastric and intra-abdominal pressure challenge the resistance of the LES.5
Table 2: Most Common Reported Causes and Risk Factors for Reflux
Tight clothing / belts
Carbonated beverages (all soft drinks actually)
Lying down after eating / Late night eating (within 3 hours of bedtime)
Esophageal dysmotility (lazy esophagus)
High-fat and fried foods (eg, hamburger)
Xerostomia (dry mouth, especially after head & neck irradiation for cancer)
Hypotensive (low) lower esophageal sphincter pressure
One of the least understood, common factors is hiatal hernia (HH). As it turns out, one can have reflux without a HH, and one can have a HH without reflux. Today, we believe that HH decreases the LES pressure by approximately one-third, as the pinchcock effect of the diaphragm on the LES is lost. The size of the HH may, however, have some bearing on reflux, with large hernias being more likely to be associated with reflux.2,5
By comparison with the airway, the esophagus has four robust antireflux defenses.5,20,21 The first line of defense is the LES, and once it opens for any reason, gastric contents enter the esophagus, ie, GER.
The second defense is esophageal acid clearance, which actually is a sequence of events.5 The average person has up to fifty “physiologic” (normal) esophageal acid reflux events each day, occurring mostly after meals. Esophageal acid clearance is how normal pH is established after any reflux event.5
Once a bolus (“ball”) of gastric juice containing acid and pepsin (primary enzyme of stomach) enters the esophagus, a swallow must first clear the volume of the acid bolus, but even after volume clearance by the first swallow, the intraluminal pH remains low. It is only with a subsequent series of swallows, with the delivery of salivary bicarbonate that normal pH is restored. Normal esophageal acid clearance usually takes less than five minutes.5
Esophageal acid clearance requires saliva and salivary bicarbonate. Consequently, it is important for the otolaryngologist to know that xerostomia, particularly iatrogenic (doctor/treatment caused) xerostomia (dry mouth, not enough saliva), following head and neck cancer irradiation, is virtually always associated with reflux. As a logical corollary, esophageal cancer is the most common metachronous (occurring later) cancer following head and neck cancer irradiation, giving further credence to the importance of esophageal acid clearance.
The third esophageal antireflux defense is esophageal epithelial resistance.2,5,20-24
The esophageal mucosa (lining) is more resistant to damage from acid and pepsin than any other aerodigestive structure, except the stomach. Remarkably, when inflamed, the esophageal mucosa secretes bicarbonate.5,20-22 All mammalian cells contain an important enzyme, carbonic anhydrase, which helps maintain intercellular acid-base balance by hydrolyzing CO2 to form bicarbonate. Carbonic anhydrase is usually found in the basal layer of the epithelium. That is the case in the normal esophagus; however, with esophagitis, the carbonic anhydrase diffuses through the superficial layers so that the esophagus actually secretes bicarbonate. This is an amazing defense, which is not shared by the laryngeal epithelium.5
The fourth defense is the UES (upper esophageal sphincter, also called the cricopharyngeus), is actually not an esophageal antireflux defense, because it is the primary barrier to airway reflux (LPR).5
Pathophysiology of LPR
From both theoretical and practical perspectives, while LES failure is at fault in GERD; in LPR, the UES is faulty. Under normal circumstances, UES pressure increases in response to esophageal acid exposure; but in patients with LPR, this protective reflexive function fails.5 Why the upper valve fails in LPR is uncertain; however, it is also clear that UES failure is reversible with effective antireflux treatment.2
Cell Biology of Airway Reflux
The biggest difference between the airway and the esophagus is simply that the airway epithelium (outer liming membrane) is profoundly fragile and easily damaged by gastric reflux compared to the esophageal epithelium (that is relatively robust). To understand these differences, the cell biology of LPR holds the key.2,20-27
First, it is important to recognize that the tissue damage is due to pepsin; it is peptic (not acid) injury.2-5,20-27 Second, it is tissue-bound pepsin that causes tissue injury. Johnston et al. reported that pepsin was found by Western blot determination in 95% of laryngeal biopsies in patients with documented LPR.27 Third, peptic injury is associated with depletion of key protective proteins including carbonic anhydrase, E-cadherin, and the stress proteins.20-24
Equally important in understanding the biology of LPR is consideration for the stability and spectrum of activity of human pepsin.24 Human pepsin retains some of its proteolytic activity well above pH 4.0 depending on the substrate. For example, pepsin can destroy collagen up to pH 6.5.24 Clinical LPR is associated with tissue-bound pepsin,27 and based upon both experimental and pH-monitoring data, it is that clear laryngeal epithelial damage occurs at pH 5; whereas, the threshold for esophageal epithelial damage is pH 4.21 Figure 1 shows the relationship between pH and the proteolytic activity of pepsin. Note that 40% of peptic activity remains at pH 5.
Figure 1: The Human Pepsin 3b Activity Curve24
Initiation and Promotion of Reflux
From a clinical perspective, there is another way of looking at the pathophysiology of reflux. For most reflux patients, airway reflux has an “initiation phase” (actual reflux of acid and pepsin into the laryngopharynx with binding of pepsin to the epithelium) and a “promotion phase,” which is dependent on additional LPR and/or a source of dietary (HCl) acid. (The terms “initiation” and “promotion” are borrowed from the carcinogenesis literature and in this model pepsin is the initiator and “subsequent” dietary acid is the promoter.) In other words, pepsin is only found (and manufactured) in the stomach; initiation requires a true gastro-esophageal-pharyngeal reflux event or events. Once pepsin is tissue-bound, proteolytic activation is promoted by acid, usually from acidic foods and beverages.3,4 In other words, once pepsin is tissue-bound to laryngopharyngeal structures, hydrogen ions from any source can be the promoters.
The initiation-by-pepsin and promotion-by-dietary-acid model helps explain why for so many LPR patients pharmacologic acid-suppression is ineffective, that is, without dietary intervention medical treatment usually fails. At best, acid suppression from below is only half of the peptic-injury equation.3,4
It also explains why dietary bingers do poorly. Imagine a college student who is well-behaved most of the time, but on Saturday nights he goes out drinking, and on his way home stops for cheeseburgers, fries, and a soda. Tipsy and with a stomach full of acidic high-fat food, he falls asleep and refluxes all night. He awakes in the morning dysphonic with a sore throat and cough.
He has tissue-bound pepsin all over his laryngopharynx, and that is his initiation. First thing in the morning, he drinks orange juice pH<4, then during the day he drinks almost a half gallon of soft drinks (pH<3). Amazingly, in 2010, the average 12-29-year-old American drank 160 gallons of soft drinks; that’s almost a half-gallon per day.3 And that is acid promotion! Even if the student does not have another actual reflux event for a week, his airway reflux peptic damage is active, and tissue inflammation and injury can escalate over time dietary acid alone. The more acid he consumes, the more the tissues are affected including the UES and LES. In other words, after initiation has occurred, promotion can progress (or even escalate) inflammation and tissue damage leading to further impairment of anti-reflux defenses.
Based upon pH-monitoring data, most patients with airway reflux (LPR) are upright (daytime) refluxers; however when an LPR patient has supine (nocturnal) reflux, tissue damage tends to be more severe. When it comes to initiation, nighttime reflux is far more injurious than daytime reflux. For many LPR patients, regardless of dose of acid-suppressive medications, late-night eating must be curtailed before effective treatment can begin.
Reflux has the characteristics of a vicious cycle, a downward spiral. The more a person refluxes, the worse esophageal function is affected, which in turn leads to worsening reflux. This downward spiral may continue until symptomatic decompensation causes the patient to seek medical attention. Fortunately, it is also true that recovery is an upward spiral. The less a patient has acid and pepsin in the airway (or esophagus), the more likely recovery of the body’s natural antireflux defenses.
Diet: Where Epidemiology & Pathophysiology Meet
The dramatic increases in reflux over the past forty years cannot be explained by the obesity epidemic alone. The increases appear to be mostly related to other dietary and lifestyle-related factors. Coincident with the reflux epidemic, America’s diet has changed.In our lifetimes, there have been four unhealthy dietary trends:
(1) Increased saturated fat
(2) Increased high-fructose corn syrup
(3) Increased exposure to organic pollutants (e.g., DDT, PCBs, dioxins)
(4) Increased dietary acidity (and other food additives as well)
The last of these trends—increased dietary acid—may hold the key to understanding the growing reflux epidemic with its associated and dramatic increases in esophageal cancer.2-4 Dietary aid appears to be the missing link: In 1973, following an outbreak of food poisoning, the U.S. Congress mandated that the Food and Drug Administration (FDA) take responsibility for assuring the safety of processed food by establishing “Good Manufacturing Practices.”3,4 How was this accomplished? Through acidification of bottled and canned foods, which was intended to prevent bacterial growth and prolong shelf life.3,4 From the 1979 Title 21 Act:
“Foods should be so manufactured, processed, and packaged that a finished equilibrium pH value is achieved. If the finished equilibrium pH is 4.0 or below, then the measurement of acidity of the final product may be made by any suitable method.”3,4
Today, two generations later, the FDA has never wavered from this path and has never questioned the possibility that acidification of the food supply might have potential adverse health consequences. In other words, the FDA encourages food manufacturers to reduce the pH of their products to less than 4.0, the same pH level as stomach acid (Figure 3). In the U.S., the arc of the reflux and the esophageal cancer epidemics closely follows soft drink consumption.2,32,33
At present, almost everything in a bottle or can is acidified to discourage bacterial growth and prolong shelf life. Bottled and canned foods and beverages are almost always pH <4,2-4,31-34 because ascorbic and/or citric acids are added. Sometimes the food label can be vaguer; it may just read “vitamin C enriched” or “vitamin C enhanced.”3,4 That is not really added to give you vitamins; it is done for purposes of acidification alone.
Knowing what we now know about the cell biology of reflux, the stability and activity of pepsin, and the contemporary American diet, it may be reasonable to postulate that acidification of America’s food supply is in large measure responsible for the reflux epidemic. Dietary acidity appears to be fundamental to the pathophysiology of airway reflux; and dietary acid appears to be the crucial factor in the prevalence (including neoplasia) and outcomes of reflux disease as it affects the laryngopharynx.3,4 See also the section on “Treatment.”
The symptoms and manifestations of airway reflux go beyond those typically associated with esophageal reflux (Table 3), and there are red flags that make airway reflux highly likely. Waking in the middle of the night from a sound sleep coughing (and even gasping for air like a fish out of water, i.e., laryngospasm), chronic cough for more than two months (with a normal pulmonary evaluation), a sensation of a lump in the throat (globus) that is there all the time, except when the patient is actually eating, morning hoarseness, chronic-intermittent hoarseness and difficulty swallowing (dysphagia) all can be symptoms of LPR.
Table 3: Symptoms and Conditions Reportedly Related to Airway Reflux
Regurgitation Dental caries and erosions
Chest pain Esophageal spasm
Shortness of breath Esophageal stricture
Choking episodes Esophageal cancer
Hoarseness Reflux laryngitis
Vocal fatigue Larynx (laryngeal) cancer
Voice breaks Endotracheal intubation injury
Chronic throat clearing Contact ulcers and granulomas
Excessive throat mucus Posterior glottis stenosis
Post-nasal drip Arytenoid fixation
Chronic cough Paroxysmal laryngospasm
Dysphagia Globus pharyngeus
Difficulty swallowing Laryngeal cancer
Difficulty breathing Vocal cord dysfunction
Choking episodes Paradoxical vocal fold movement
Lump-in-throat sensation Vocal nodules and polyps
Food getting stuck Pachydermia laryngitis
Airway obstruction Recurrent leukoplakia
Wheezing Polypoid degeneration
Vocal cord dysfunction
Sudden Infant Death Syndrome
Sinusitis and allergic symptoms
What about asthma? Is it a symptom of reflux? There is one question that every clinician should ask when a patient says they have asthma, particularly adult-onset asthma, “When you have breathing difficulties, do you have more trouble getting air in or out?” If the patient says, “IN,” they do not have asthma. Their symptoms are due to reactive airway disease secondary to airway reflux.
At present, there is no one diagnostic reflux test for LPR that provides more accurate information than pharyngeal/UES/esophageal manometry combined with ambulatory 24-hour dual-probe (simultaneous pharyngeal and esophageal) pH monitoring.2 Impedance monitoring is, in the author’s experience, a second choice for diagnosing airway reflux though it is a good supplement to pH testing as it may identify injurious non-acid reflux. Under development are new diagnostic tests that are specific for airway reflux and utilize pepsin as a marker. The author currently uses a combination of diagnostics.
1. Clinical Parameters: The Reflux Symptom index28 (RSI) and The Reflux Finding Score29 (RFS)
When taken together the RSI and the RFS are the most reliable clinical diagnostics, and they are recommended for routine use by the otolaryngologist. The RSI (a nine-item, symptom severity scale) is completed by the patient, and it is a validated reflux outcomes instrument29 (Table 4). when a patient has a RSI of >15, s/he has a 90% chance of having pH-documented LPR.2
Table 4: The Reflux Symptom Index (RSI)
The RSI should be completed by every patient prior to being seen by the clinician, and the clinician should complete the RFS after each laryngoscopy, even if it is to note that the RFS was nil. The RFS is a system for grading the laryngeal findings of LPR (Table 5).
Theoretically, the RFS can be calculated on the fly during a visual laryngoscopy; however, grading the RFS after the examination is completed from an archived laryngeal image is preferred, and that image should show the larynx in abduction, not adduction. This grading system was developed using images obtained by transnasal flexible laryngoscopy (TFL), and TFL is the preferred examination. The RFS is a weighted nine-item scoring system devised by the author in 1986 and subsequently reported.8,29 The RFS is particularly useful in diagnosing LPR. In addition, when calculated at each visit, it is an excellent parameter to evaluate the effectiveness of therapy. Patients who are successfully treated will have a normal (less that 4) RFS. Below are descriptive parameters for each of the nine items:
Pseudosulcus vocalis refers to subglottic edema that gives the vocal fold the appearance of being three-dimensional, almost having the appearance of an open hotdog bun. The normal non-swollen, non-inflamed vocal fold appears to be a two-dimensional structure. Pseudosulcus is a finding usually associated with reflux and diffuse laryngeal edema. (Pseudosulcus can also sometimes be a “normal” finding when the vocal folds are atrophic, eg, presbylaryngis.) A finding of pseudosulcus gets two points in the RFS system.
Figure 2: LPR Findings (A. Before and B. After Treatment)
Ventricular obliteration. The ventricle is a grove-like structure or recess between the true and false vocal folds. When it is normal and open, the ventricular band is sharp and the depth of the ventricle glistens. If, however, both the true and false folds are swollen, the ventricle can be partly or completely obliterated. Partial ventricular obliteration scores two points, and complete ventricular obliteration scores four points in the RFS. The case, Figure 2-A, shows partial ventricular obliteration that resolves after treatment (Figure 2-B).
Erythema, the third item, is graded two points for red arytenoids and four points for diffuse laryngeal erythema. In reality, erythema is grossly overcalled. The main finding of LPR is edema not erythema. The normal vascularity of the posterior larynx will vary a lot depending upon the brightness of the light source.
Vocal fold edema is graded as follows: “1 Mild” for slightly swollen vocal folds; “2 Moderate” if pseudosulcus is present; “3 Severe” if there is sessile or polypoid swelling that is occupying some of the intra-fold space; and “4 Polypoid” for Reinke’s edema.
Diffuse laryngeal edema is the most subjective finding of the RFS. It relates to the size of the glottal opening (chink) relative to the size of the entire larynx. Normally, the area of the glottal chink at near-full abduction occupies 50% of the total area. (Diffuse laryngeal edema is rarely graded more than one or two points.)
Posterior commissure hypertrophy is graded as follows: “1 Mild” when the moustache of the posterior commissure is still upwardly concave; “2 Moderate” when edge of the posterior commissure is straight; “3 Severe” when it is convex into the endolaryngeal lumen; and “4 Obstructing” when it is obstructing the airway.
Figure 3: Example of Tiger-Stripe Post-Cricoid Edema (Arrow)
A. (left): Before treatment for LPR; the reflux finding score is 11 (partial ventricular obliteration 2, vocal fold edema 2, diffuse laryngeal edema 1, posterior commissure hypertrophy 2, post-cricoid edema 2, endolaryngeal mucus 2). B. (right): After treatment; normal, the RFS is 0.
Tiger-stripe post-cricoid edema. Tiger-stripe post-cricoid edema is a highly reliable reflux finding (Figure 3). Under normal circumstances, the post-cricoid region is smooth. When swollen, it may give the appearance of having wet, edematous stripes. (Tiger-striping was not originally reported8,29 but added later.) Tiger-stripe edema is usually seen in patients who are supine (nocturnal) refluxers.
Figure 3: Severe LPR with Tiger-Stripe Post-Cricoid Edema (arrow)
The RFS is 17 (complete ventricular obliteration 4, vocal fold edema 4, diffuse laryngeal edema 3, posterior commissure hypertrophy 2, post-cricoid edema 2, endolaryngeal mucus 2). Endolaryngeal mucus. Thick, white, tenacious mucus on the vocal folds counts as two points in the RFS. Finally, arytenoid granuloma, granulation, and/or (contact) ulceration counts as two points as well.
2. Pepsin Immunoassay30: Spit Test Screening for Airway Reflux
The author has developed and is now using a “spit-in-a-cup test” that detects pepsin in airway secretions or saliva. The test is performed by putting a small sample of the patient’s saliva in buffer and then in a lateral flow device (similar to a pregnancy test). As a screening test for LPR, the sensitivity of the assay is 82% and its specificity is 100%. This useful screening test will become commercially available as soon as it receives FDA approval.
3. Ambulatory 24-hour pH-Monitoring with or without Impedance Testing
For the author, ambulatory, 24-hour, double-probe (simultaneous pharyngeal and esophageal) pH monitoring has been her gold-standard LPR diagnostic for twenty-five years. Impedance testing provides less information as there are no reliable pharyngeal data. Due to poor manufacturing quality control, in the author’s reflux-testing laboratory, antimony sensors have been replaced with more accurate ISFET technology. Finally, pharyngeal pH monitoring using an “aerosolized” sensor in the pharynx has proven to be highly inaccurate and not worthwhile as a clinical test.
Pharyngeal pH-Monitoring is especially useful if the data are examined in a number of ways: (1) Using pH >4.0 as a threshold, (2) using pH >5.0 as a threshold, (3) calculating mean pharyngeal pH, and (4) calculating the pharyngeal reflux injury score2 (RIS), which is a summation of the time at each pH level multiplied by the peptic activity coefficient; the RIS is comparable to the DeMeester score for overall pharyngeal reflux severity.2
pH-Monitoring following high-definition pharyngeal/UES/esophageal manometry will t only insure accurate pH-probe placement, but the data may also alter therapy, eg, a prokinetic medication may be added to the treatment regimen for patients with esophageal dysmotility.
5. Transnasal Esophagoscopy (TNE) with or without Biopsy9,16
Patients with both airway and esophageal reflux should be screened for esophageal disease as 8-10% will be found to have Barrett’s esophagus, a precursor to esophageal cancer.15 In addition, other pathology (eg, Candida esophagitis, erosive esophagitis, varices) is found in another 25% of LPR patients.9 The highest percentage of esophageal pathology (63%) is seen in LPR patients with a chief complaint of chronic cough [Koufman JA, unpublished data, 2013].
It is important to note that although esophageal endoscopy is necessary to rule out esophageal pathology, esophagoscopy is NOT the diagnostic test of choice for LPR. Indeed, it has been reported that up to 80% of LPR patients have normal esophagoscopy.9
6. Barium Swallow Esophagography
A generation ago, the barium swallow/esophagogram was routinely used to evaluate reflux. Unfortunately, this technology is relatively insensitive and non-specific, and the finding of a hiatal hernia alone has little clinical significance. Barium studies should be reserved for patients in whom structural esophageal abnormalities are suspected.5
7. Therapeutic Trial with Antireflux Medication
The world is changing and two of the most significant trends in the contemporary management of reflux-related disease are (1) that the medical treatment failure rates with PPIs (proton pump inhibitors) are increasing,3,4,19 and (2) that effective reflux management depends on dietary and lifestyle variables.2-4 Presumably this is because globalization and urbanization have brought about dramatic changes in where, when, and what people eat.
Fifty years ago, most people ate at home, and prepackaged foods and beverages were uncommon. Today, most big soft drink and fast-food companies are global brands, and by comparison people everywhere are being exposed to much higher levels of food additives (especially acids) than a generation ago. As the world’s diet has become Americanized, reflux has followed.
For many years, a therapeutic trial with PPIs (proton pump inhibitors) was considered a useful diagnostic test for LPR. Clearly, acid-suppressive medications alone no longer constitute an appropriate therapeutic trial and such is no longer considered to be reliable or cost-effective. It now appears that dietary and lifestyle issues are even more important than medication for the effective treatment of airway reflux.
Before leaving this section on the diagnosis of LPR, it is important to reemphasize the value of the laryngeal examination with determination of the RFS. In the author’s opinion, examination of the larynx, regardless of the severity of airway reflux symptoms, holds the key to understanding reflux within the entire aerodigestive system. This point cannot be overemphasized: sequential laryngeal examinations, using the RFS are the best way to evaluate the progress of treatment. The larynx is a window through which the clinician can view and assess the condition of the upper aerodigestive tract. It is the crossroads and it is responsive enough to accurately reflect the status of the entire system.
Airway reflux (LPR) can be associated with minor symptoms (e.g., throat clearing) or with life-threatening disease (e.g. laryngeal stenosis, airway obstruction, and cancer). So it stands to reason that there cannot be any one-size-fits-all therapeutic regimen. Meanwhile, there are medical, lifestyle, dietary, and surgical treatment options.
There are several different approaches to medical treatment: antacids, acid suppressants, mucosal protection, and promotility agents. These may be used alone or in combination depending on the patients reflux pattern and disease severity.
Antacids, once the cornerstone of antireflux treatment, are now just reserved for patients with mild and intermittent symptoms, or as adjunctive therapy to alleviate primarily heartburn in patients with recalcitrant disease. Today, proton pump inhibitors (PPIs) are the most commonly used antireflux drugs, followed by H2-antagonists. There are many different PPIs on the market today and they account for $15 billion in annual sales in the U.S. alone.
PPIs give the best acid suppression of any antireflux medication. However, their use has become more controversial in recent years due to concerns about rebound hyperacidity following drug cessation, side effects, as well as short- and long-term complications. When they are used for airway reflux, they should be given in a twice-daily dose (before breakfast and before the evening meal). Patients with nocturnal reflux are also usually given an H2-antagonist at bedtime as the latter work better during sleep than PPIs.
In the past, clinicians recommended twice-daily PPIs (before breakfast and before the evening meal) with an H2-antagonist at bedtime for LPR patients. Today, there are concerned about the long-term safety and efficacy of PPIs, particularly the double-dose regimen.
Prokinetic agents (including reglan, erythomycin, and domperidone) can help improve esophageal function (peristalsis) and sphincter function. Their use should be reserved for patients who demonstrate poor esophageal motility and/or sphincter function. Reglan and domperidone should be used with caution as they can cause significant and permanent side effects. Reglan has numerous side effects including irreversible tardive dyskinesia and Domperidone is not FDA approved in the United States.
Many patients with airway reflux need long-term medical treatment, but many also can get off medications after the acute phase improves as long as they remain compliant with a reasonable maintenance antireflux diet.
Lifestyle and Dietary Treatment
Control of dietary and lifestyle factors are probably more important that antireflux medication; although, when patients present with severe reflux, particular those with reactive airways diseases such as chronic cough, laryngospasm, and asthma, the clinician must use acid-suppressive medications as well as diet/lifestyle modifications in combination.
Obesity and reflux go together especially when the patient overeats, consumes a lot of fried and fatty foods, chocolate, carbonated beverages, and eats late at night. Those are among the high-risk behaviors for reflux disease. Interestingly, smoking also causes reflux. However, it is important to recognize that many patients with LPR are thin, athletic, and generally eat healthy food. For that group, an overly acidic diet and lifestyle issues such as late night eating are commonest reflux risk factors.
One of the most difficult problems in treating reflux patients is how much variation there is from patient to patient. While fried food, ethanol, and soft drinks in excess are almost universally associated with reflux, many other marginal (eg, acidic fruits like papaya and strawberries) or idiosyncratic foods (eg, nuts, tomatoes, onions, garlic, peppers) or even “healthy” foods (eg, banana, pears, oatmeal) can trigger reflux in some people.
When a patient has severe LPR, it is well worth prescribing a two-week induction (“detox”) reflux diet in which nothing consumed that is pH <5; no eating within four hours of bed, and consumption of alkaline (pH >8) water.3,4, 31 While this seems severe, it really works to get patients better fast.3 Recommendations for dietary and lifestyle modifications are summarized in Table 6.
Table 6: Recommended Lifestyle and Dietary Modifications for Reflux
General Lifestyle Recommendations
If you use tobacco, quit. Smoking causes reflux
Don’t wear clothing that is too tight, especially trousers, corsets, bras, and belts
Avoid exercising right after eating (especially weightlifting, jogging, and yoga)
Do not lie down right after eating, and do not eat anything within three hours of bedtime
Elevate the head of your bed if you’re a nighttime refluxer; that is, if you have symptoms
of hoarseness, sore throat, and/or cough in the morning
An overweight patient should start a low-acid, pH-balanced diet
Worst For Reflux Foods and Beverages to Avoid
Onions (This is an “idiosyncratic” food that affects some people, not others)
Peppers / Hot Sauce (All peppers including bell and black pepper)
Citrus fruit/juice (These are naturally too acidic and more is added)
Fried Food (This is restaurant food and different from sautéed)
Fatty Meats (bacon, pork, lamb, some fatty steak cuts like rib eye)
Alcoholic beverages (More than one drink and you’ll probably reflux)
Chocolate (Sorry, this is one of the most common reflux trigger foods)
Almost all bottled/canned beverages (except water), all soft drinks are acidified
Really avoid all carbonated beverages (Coke, Pepsi, and all sodas including seltzer)
Anything that you eat before bed is a “worst for reflux” food
The Best-For-Reflux Food and Beverage List
Bananas (A rich, low-acid fruit, strangely a trigger food for 5% of people)
Melons (Best fruits for most refluxers: watermelon, cantaloupe, honeydew, etc.)
Aloe Vera (Great thickener and good for digestion, make sure no acid added)
Salads and Vegetables (A staple, excluding onions, tomatoes, garlic and peppers)
Rice and Whole Grains (Best is brown rice, Bulgur wheat, and healthy bread)
Oatmeal (One of the best breakfast foods that there is and great with banana)
Ginger (Spicy, zesty flavor but good for reflux–try ginger tea, candy, jam, etc.)
Poultry (Baked, grilled, but never fried; sorry, skinless preferred; high protein)
Tofu (Tofu, coagulated soy milk in many forms is a vegetarian staple protein)
Fish (All seafood— raw, grilled, baked, boiled, or boiled—is good for reflux)
The primary effective surgical option for the treatment of reflux is a laparoscopic Nissen laparoscopic fundoplication. The term “fundoplication” refers to wrapping fundus (the dome of the stomach) around the esophagus and then plicating (sewing it) there to produce a tight angle where the esophagus enters the stomach. This surgical procedure is by far the single most effective treatment for both esophageal and airway reflux. There is controversy surrounding which LPR patients are the best candidates for a fundoplication. When chosen correctly it is an extremely effective procedure. Indeed, surgical treatment is often recommended for patients with lung disease related to reflux and for patients who cannot tolerate or fail medical treatment.
The diagnosis of LPR is difficult because there is no gold-standard diagnostic test; nevertheless, the reflux symptom index and the reflux finding score are invaluable and reliable clinical measures.
Airway reflux (LPR) has different pathophysiology than esophageal reflux (GERD) based upon the relative sensitivity of airway (compared to esophageal) epithelium to peptic injury. In addition, the sine qua non for laryngeal tissue injury is the presence of tissue-bound pepsin, because once pepsin is attached to epithelium, any source of hydrogen ions, including dietary acid, will maintain extended periods (days or weeks) of proteolytic activity.
Because of this distinctive mechanism, dietary and lifestyle modifications, particularly low-acid diet, is essential for treatment to be effective.
- El-Serag HB. Time trends of gastroesophageal reflux disease: A systematic review. Clin Gastroenterol Hepatol 2007;5:17-26.
- Koufman JA. Perspective on Laryngopharyngeal Reflux: From Silence to Omnipresence. Classics in Voice and Laryngology. Branski R, Sulica L, Eds. Pages 179-266, Plural Publishing, San Diego, 2009.
- Koufman JA. Low-Acid Diet for Recalcitrant Laryngopharyngeal Reflux: Therapeutic Benefits and Their Implications. Ann Otol Rhinol Laryngol 120:281-87, 2011.
- Koufman JA, Stern JC, Bauer MM. Dropping Acid: The Reflux Diet Cookbook & Cure. Reflux Cookbooks LLC (Midpoint Distributors), New York, NY, 2010.
- Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): A clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope 1991;101 (Suppl. 53):1-78.
- Koufman JA, Amin M, Panetti M. Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders. Otolaryngol Head Neck Surg 123:385-388, 2000.
- Koufman JA, Block C. Differential diagnosis of paradoxical vocal fold movement. Amer J Speech and Hearing. 2008;17:327-34.
- Belafsky PC, Postma GN, Koufman KA. Laryngopharyngeal reflux symptoms improve before changes in physical findings. Laryngoscope 111: 979-981, 2001.
- Koufman JA, Belafsky PC, Daniel E, et al. Prevalence of esophagitis in patients with pH-documented laryngopharyngeal reflux. Laryngoscope 2002;112:1606-9.
- El-Serag H, Becher A, Jones R. Systematic Review: Persistent Reflux Symptoms on Proton Pump Inhibitor Therapy in Primary Care and Community Studies. Alimentary Pharmacology and Therapeutics. Blackwell Publishing, Ltd., Pages 1-18, 2010.
- Altman KW, Stephens RM, Lyttle CS, et al. Changing impact of gastroesophageal reflux in medical and otolaryngology practice. Laryngoscope 2005;115:1145-53.
- Pohl H, Welch HG. The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence. J Natl Cancer Inst 2005;97:142-6.
- Lund O, Hasenkam JM, Aagaard MT, Kimose HH. Time-related changes in characteristics of prognostic significance in carcinomas of the oesophagus and cardia. Br J Surg 1989;76:1301.
- Conio M, Blanchi S, Lapertosa G, et al. Long-term endoscopic surveillance of patients with Barrett’s esophagus. Incidence of dysplasia and adenocarcinoma: A prospective study. Am J Gastroenterol 2003;98:1931-9.
- Reavis KM, Morris CD, Gopal DV, Hunter JG, Jobe BA. Laryngopharyngeal reflux symptoms better predict the presence of esophageal adenocarcinoma than typical gastroesophageal reflux symptoms. Ann Surg 2004;239:849-56.
- Amin MR, Postma GN, Setzen M, Koufman JA. Transnasal esophagoscopy: A position statement from the American Broncho-Esophagological Association. Otolaryngol Head Neck Surg 2008;138:411-3.
- Halum SL, Postma GN, Johnston C, Belafsky PC, Koufman JA. Patients with isolated laryngopharyngeal reflux are not obese. Laryngoscope 2005;115:1042-5.
- Postma GN, Tomek MS, Belafsky PC, Koufman JA. Esophageal motor function in laryngopharyngeal reflux is superior to that of classic gastroesophageal reflux disease. Ann Otol Rhinol Laryngol 2001;110:1114-6.
- Amin MR, Postma GN, Johnson P, Digges N, Koufman JA. Proton pump inhibitor resistance in the treatment of laryngopharyngeal reflux. Otolaryngol Head Neck Surg 2001;125:374-8.
- Axford SE, Sharp S, Ross PE, Pearson JP, Dettmar PW, Panetti M, Koufman JA. Cell biology of laryngeal epithelial defenses in health and disease: Preliminary studies. Ann Otol Rhinol Laryngol 2001;110:1099-1108.
- Johnston N, Bulmer D, Gill GA, Panetti M, Ross PE, Pearson JP, Pignatelli M, Axford A, Dettmar PW, Koufman JA. Cell biology of laryngeal epithelial defenses in health and disease: Further studies. Ann Otol Rhinol Laryngol 2003;112:481-91.
- Gill GA, Johnston N, Buda A, Pignatelli M, Pearson J, Dettmar PW, Koufman J. Laryngeal epithelial defenses against laryngopharyngeal reflux (LPR): Investigations of pepsin, carbonic anhydrase III, pepsin, and the inflammatory response. Ann Otol Rhinol Laryngol 2005;114:913-21.
- Johnston N, Dettmar PW, Lively MO, Koufman JA. Effect of pepsin on laryngeal stress protein (Sep70, Sep53, and Hsp70) response: Role in laryngopharyngeal reflux disease. Ann Otol Rhinol Laryngol 2006;115:47-58.
- Johnston N, Dettmar PW, Bishwokarma B, Lively MO, Koufman JA. Activity/stability of human pepsin: Implications for reflux attributed laryngeal disease. Laryngoscope 2007;117:1036-9.
- Lillemoe KD, Johnson LF, Harmon JW. Role of the components of the gastroduodenal contents in experimental acid esophagitis. Surgery 1982;92:276-84.
- Samuels TL, Johnston N. Pepsin as a marker of extraesophageal reflux. Ann Otol Rhinol Laryngol 2010;119:203-8.
- Johnston N, Knight J, Dettmar PW, Lively MO, Koufman J. Pepsin and carbonic anhydrase isoenzyme III as diagnostic markers for laryngopharyngeal reflux disease. Laryngoscope 2004;114:2129-34.
- Belafsky PC, Postma GN, Koufman JA. Validity and reliability of the reflux symptom index (RSI). J Voice 2002;16:274-7.
- Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope 2001;111:1313-17.
- Knight J, Lively MO, Johnston N, Dettmar PW, Koufman JA. Sensitive pepsin immunoassay for detection of laryngopharyngeal reflux. Laryngoscope 2005;115:1473-8.
- Koufman JA, Johnston N. Potential Benefits of pH 8.8 Alkaline Drinking Water as an Adjunct in the Treatment of Reflux Disease. Ann Otol Rhinol Laryngol 121:431-34, 2012.
THE PREVALENCE OF ACID REFLUX IN AMERICA: THE TIMES SQUARE STUDY
Until now, the prevalence of acid reflux was unknown. In addition, it is clear that not all refluxers have classic gastroesophageal reflux disease (GERD). Many people have symptoms and manifestations of reflux without having heartburn or indigestion, including hoarseness, post-nasal drip, sinus, chronic cough, difficulty swallowing, a sensation of a lump in the throat, and sore throat. This latter group has laryngopharyngeal reflux (LPR), sometimes called silent reflux.
We interviewed 1,010 people (U.S. citizens) in Times Square in New York City, who were in line waiting to buy discount theater tickets (at TKTS). Thus, we obtained a random sample of respondents from all over the nation. The data showed that 40% of the American population had reflux. Twenty-two percent (22%) had known (diagnosed by a doctor) GERD; another 18% had reflux symptoms (including LPR and GERD) but weren’t under a doctors care. One of the biggest surprises in this study was that young people in the 20-30 year-old age group had almost as much reflux (37%) as older people.
Since the days of Chevalier Jackson, esophagoscopy has undergone numerous changes. Recently, with the introduction of the thin, high-resolution distal chip camera esophagoscope (VE-1530, Pentax Precision Instrument Corporation, Orangeburg, New York), the esophagoscope can be inserted through the nose in the upright position with topical anesthesia alone without the use of intravenous or per oral medications. This allows the otolaryngologist to perform esophagoscopy as an in-office procedure. In addition, air insufflation, irrigation, and biopsies can be performed. The entire upper aerodigestive tract from the nasal vestibule to the gastroesophageal junction (GEJ) is easily and safely visualized.
Continue reading Transnasal Esophagoscopy: Revisited (over 700 Consecutive Cases)
The distal-lighted, rigid esophagoscope was invented by Chevalier Jackson more than a century ago, and until the 1960s, with the introduction and popularization of flexible fiberoptic endoscopy, esophagology was the domain of the otolaryngologist. In the last 50 years, other medical specialties (eg, pulmonology, pediatric surgery, gastroenterology) have joined in the evolution of aerodigestive tract endoscopy. (See also www.transnasalesophagosocpy.com).
Continue reading Transnasal esophagoscopy
In otolaryngologic practice, recognition of many of the clinical manifestations of laryngopharyngeal reflux (LPR) have gained acceptance; however, the prevalence of otolaryngologic and respiratory disorders caused by LPR remains unknown. In part, this appears to be because currently used diagnostics for LPR often rely on testing methods and normative standards that were established for the diagnosis of classic gastroesophageal reflux disease (GERD), which may not be appropriate for use in diagnosing LPR.
Continue reading Sensitive Pepsin Immunoassay for Detection of Laryngopharyngeal Reflux compared with 24-hour double-probe (esophageal and pharyngeal) pH monitoring