BACK SURGERY

On Wednesday, December 19th 2012, I underwent a four-hour, two-level (L3-L4-L5), lumbar fusion at Lenox Hill Hospital. Prior to my surgery, my surgeon did not explain what I would experience post-operatively or did he tell me how long it would likely take for me to get back on my feet. That is why I wrote this blog, to help others going through what I went through. By the way, I went back to work and I was functional 2½ weeks after the surgery, but it wasn’t easy.

Before telling you about my back surgery experience, let me briefly tell you my medical history. If you would like to skip this part of my story, go straight to the section, “Preparing For Lumbar Fusion Back Surgery” below.

My Medical History

I had compression fractures from an auto accident when I was fifteen years old. I was hospitalized, flat on my back for a week, and then I wore a body cast for three months. (It was made of thick, old-fashioned plaster. This hellish device extended from my under arms to my waist with a grapefruit-sized hole around my belly button to allow easier breathing.) There was no bathing with the cast, just assisted sponge baths … for 3 months.

After six months, I seemingly made a full recovery, and I resumed all my athletic activities. In my twenties, I became a long distance runner. During my five years of surgical training in general surgery and then in otolaryngology (ENT), I ran back and forth to work every day. I had a locker and shower available to me and I left all my work clothes at the hospital. Besides, most days, I just wore greens.

During my residency, I ran a minimum of 16 miles a day. In 1977, I ran my first Boston marathon, and in 1978, I ran my best marathon in Chicago. I finished 77th out of 11,000 runners. Unfortunately, six months later, I ruptured my Achilles tendon playing racket ball, and that was the end of my career as a runner.

In 1978, just before Christmas, I ruptured one of my lumbar disks. About two weeks later, I had a discectomy through a small incision, and the next day, I was back to work. After a period of physical therapy, I went back to running and playing golf and tennis. I ruptured a second lumbar disk that required surgery in 1986. And in 2004, I ruptured the other Achilles tendon, and by then between my bad legs and my bad back, my athletic “career” was over. My athletic activity was restricted to gentle backstroke swimming.

Just after I moved to New York in 2006, I ruptured another disk and could not walk. I had foot drop, which lead to my third back surgery. I viewed an x-ray of my lumbar spine and I was horrified. My L4 vertebrae was very crooked, more so than the leaning Tower of Pizza. As soon as I saw that x-ray, I knew that I probably would have life-long, life-altering back problems.

I had severe degenerative spine disease with chronic back and leg pain. Between hard pavement and uneven sidewalks, jus walking in New York exacerbated my pain. The degenerative process now involved the foramen (openings) for the main nerves to my left leg. After walking a few blocks or sitting for more than an hour, my back and leg pain were severe.

I learned to live with the pain. To get some relief, I sometimes laid down on bathroom floors at restaurant, in the foyer of my box at Carnegie Hall, or wherever I could. Lying down and stretching in certain ways, I could temporarily distract the poor encroached nerves. I had my 4^th back surgery in 2008 to open the neural foramen for my left leg. (It helped for about a year.)

In 2010, I began restorative yoga, weekly acupuncture, swam regularly, lost twenty-five pounds, and stretched twice a day. I also tried other therapies including steroid injections (to no avail). After almost two years of my best efforts to improve my back problems, in late 2012, I decided (after consultation with my doctors) that a two-level lumbar fusion was my best hope for living a normal life with normal activity.

Preparing for Lumbar Fusion Back Surgery … and You Need To!

Remember, I am a surgeon so I have a theoretical advantage in planning my own surgical experience. I don’t know much about orthopedics, so I did some reading and made certain decisions. Mind you, I had received no information about what I might need after surgery or what I might experience from my surgeon. Here are the most important things that I did in preparation for my surgery. Make no mistake about it, these are important!

First. I did not want to have post-operative constipation at any cost, as it would stress my back surgery; and, I knew that I would probably be on narcotic analgesics such as Percocet or Codeine that generally cause constipation. So, a full week before my surgery, I began eating more roughage (organic bran cereal, fruit, and salads) as well as take stool softeners. Specifically, I took three Ducolax before bed with a tablespoon of mineral oil, and three Colase first thing in the morning. I also bought a large bottle of Milk of Magnesia and Senecot to be on hand if I needed even more help.

Second. I knew that I would not be able to bend down to pick things up off the floor, and so I reorganized the locations of my daily-routine items such as toiletries, medications, plastic cups and paper plates, remote controls, etc. Everything was placed at waist-level or higher. (I specifically bought a special caddie for my shower so that shampoo, conditioner, soap, etc. would be easily reachable.) I even moved the toilet paper to a place so that I wouldn’t have to reach for it.

I ordered some helpful devices from Amazon: two graspers, one blunt-ended and one with suction-cup things on the ends, as well as a two-foot-long shoehorn. In addition, I moved a waist-high, four-foot-long table next to my bed (on the opposite side from which I get in and out), and on that table, I placed my bedside lamp, the remote controls for the television, a small laptop computer, a roll of paper towels, a box of Kleenex, hand cream, and some lip gloss. Similarly, I set up the area around the couch in my living room.

I prepared my entire house for a person who was relatively helpless. In the kitchen, the most essential items were left out on a counter. I planned to use one 39 gallon trash container per day (and abandoned recycling during my convalescence), hung at chest level so that the bottom of it just touched the floor. I also instructed my doormen that after my surgery, they would need to come up to my apartment every day to collect the trash.

Third. I knew that I would need help when I can home from surgery, so I worked out a schedule for friends and family to be with me every day. Also, I had one friend who was a cat lover who would come in and play with my cat, feed her, and pooper-scoop the litter box.

All in all, I planned the best that I could. And let me reiterate, none of the above information was provided to me by my surgeon or by any other ancillary staff.

My Surgical Experience

I had a two-level (L3-L4-L5) lumbar fusion performed at the Lennox Hill Hospital on December 19, 2012. After the surgery, my surgeon came to tell me that everything went well. That first day I was on an on-demand morphine pump, and I was pretty much out of it. I think I remember that first evening, I did get out of bed and walked a bit outside the room.

On that first postoperative day, I was already aware that the GI (gastrointestinal) tract had completely shut down. I tried eating some cereal, but I could not swallow, stomach acid came into my mouth, and my abdomen began to swell. The second post-operative day, the pain management team switched me over to Percocet (two every six hours, with morphine shots if needed), and a muscle relaxant (Flexeril). The GI tract problem worsened quickly and I blew up like a frog. Despite that, I continued to get regular meals.

I really couldn’t eat and I had had no bowel movement for two days, but I also had a low-grade fever and symptoms of a urinary tract infection including burning on urination, frequency, and urgency. A medical consultation was put in, and I gave a urine sample for the lab to analyze.

On the evening of day two, I was still having terrible pain but I was afraid to sleep. I was especially concerned about the Flexeril in combination with my other narcotics. Indeed, half a Flexeril put me to sleep immediately.

I was seriously concerned about the possibility of having a respiratory arrest and dying. Consequently, I demanded that I have a pulse oximer (an oxygen monitor), and I hired a private duty nurse form 7p to 7a. Without oxygen, after half a Flexeril, when I started to fall asleep, I noticed that my oxygen saturation would fall into the low 80s, which is not good. So, I used oxygen routinely at night, and I specifically asked my private duty nurse to monitor my respiration. I believe that had I taken all the medication as prescribed without any oxygen, I might have died of a respiratory arrest.

When I was discharged on post-operative day 3, I had not had any kind of consultation with a physical therapist. On day one, a physical therapist saw me walking in the hall and told me “good job,” and the day before I left the hospital, I had an equally brief “visit” … as I was walking in the hall, a young physical therapist decreed from afar, “You’re good to go; I’ll sign you out.”  Wait. What about all my questions?  What about walking? Best to sleep in what position?  I had many questions that were never addressed; I never had a opportunity to ask them. In truth, my total face time with physical therapy during my hospitalization was less than 30 seconds. (I cannot wait to see their bill.)

When I was discharged on post-operative day 3, my GI tract was still completely shut down. I had not had a bowel movement in four days.  The pain management team sent me home on two Percocet every six hours as needed, Flexeril three times a day, and a long-acting morphine twice a day. No one was concerned about my GI tract; no one was concerned about Percocet toxicity; no one was concerned about my follow-up or continuing care. (By the way, retrospectively for two days, I took more medicine, and similar medicines—10 Percocets, 2 Flexerils, and 2 long-acting morphines—than killed Heath Ledger). In truth, my total face time with pain management during my hospitalization was less than 60 seconds. (I cannot wait to see their bill.)

Three hours after my surgical drains were removed, I was discharged on post-operative day 3 with no home healthcare plan whatsoever. I never saw a social worker or home healthcare nurse, and in fact the home-care nursing division informed me that I was ineligible. Who would check to see that I didn’t have an abscess?  What would I do after showering? What about dressing changes?  I didn’t have an appointment to see my doctor until January 3^rd. Would I have no wound or dressing care of any kind for 11 days?

I still had an intermittent low-grade fever and urinary tract infection (UTI) symptoms. After I got home, I started myself on an antibiotic and the UTI cleared within days.

On Sunday, my first full day at home, my GI tract was still completely shut down. I had not had a bowel movement in five days. I stopped all pain medication. I took milk of magnesia, bran cereal, and special fresh yogurt from a health food store. After two days of intense, mind-numbing pain, on my seventh post-operative day, I had a bowel movement.

During my three days of hospitalization, there were other specific horror stories worth recounting. On the second post-operative night while I was still having some fever and concerns about my surgery, I was taken for x-rays of my spine at about 10 p.m. First, they brought a chair that was so uncomfortable that I was unable to sit on it. (Has not anybody asked the question, “What kind of transportation is appropriate for patients who have had spine surgery?”) I refused to be transported in that chair. They eventually found an old fashion wheelchair and I rode down in that. I ended up walking back from x-ray.

I was very concerned about the results of my x-ray. Was something wrong? Why did they get the x-ray then? Do you know that every single day, at least twice a day, I asked, “What were the results of the x-rays of my back?” and the response was, “It’s not in the system yet.”  No one ever told me if my back surgery x-rays were okay … even at the point of my discharge. Talk about accountability!

One last story: As I was on my way out the door on that Saturday the 22nd, with a car waiting, engine running, I put on a back-brace that had been supplied, and I thought I had broke one of the strings. Since it was almost the holidays, I wondered if I could get a replacement. Standing at the front desk, the unit secretary offered, “Let me call Sarah, the orthopedic resident; they may have a bunch of those belts in a closet somewhere.”

I waited as long as I could stand and finally went and sat on the only chairs that were by the elevator. Soon thereafter, a young woman got off the elevator. When she was right next to me, I asked, “Hi. Are you Sarah, the orthopedic resident?”

She walked by me without acknowledgement. I waited a couple of minutes, and then I proceeded around the corner. The young woman was talking to a nurse about a patient’s orders. She did not look at me. It was apparent that she was trying hard not to engage me. Her body language said, “I will get to you when I am ready.” Finally, I interrupted, “Excuse me, are you Sarah, the orthopedic resident? Did not you not see me? Did you not hear me? You walked right by me at the elevator?”

She responded, “People do not usually call me that.” I responded, “Well I am Jamie … Jamie Koufman, I am a well-known surgeon, and my surgeon is David. You know David? And you are Sarah, the orthopedic resident, are you not?”

Glaring, she owned up to it. She seemed angry that I was imposing on her. I asked her about my broken belt and she told me that she could do nothing. She then turned back to the nurse in a dismissive manner.

The orthopedic resident, Sarah, was completely without any concern for my welfare. Her treatment of me was highly inappropriate. Her haughtiness and disdain angered me. My parting shot: “Sarah, you are a snotty bitch without one inch of compassion or humility … and you have no right being in medicine.” That experience was/is my last memory of my hospitalization at Lenox Hill.

To put this horrendous experience in perspective, I am a well-known surgeon. Under no circumstances would I ever take care of a patient the way I was treated. Had those people who were involved in my care worked for me, they would all be fired. I underwent major back surgery with no virtually no significant communication from anybody about my status or after care.

Leg Pain and Learning How to Walk Again

From the time I got home, and in spite of pain, I was active. I made sure to change positions every 45 minutes, and I walked several times a day. I was surprised that on the evening of the 9th post-operative day, I began to experience intense new, burning pain in both legs. Both legs?  Before surgery, my pain had been mostly left leg, my right had been fine!  And indeed, this new pain was very intense, more on the right than the left, and I couldn’t sleep. I tried taking a pain pill to no avail. The night pain was terrible and it evolved to be persistently much worse on my “good” right side.

When I went to my doctor to have my staples out on the 11th post-operative day, looking at the x-ray that he obtained that day, he noted that my pelvis was tilted. Had it always been like that he asked.  I didn’t know. He told me that this just was just compensatory for my back pain. He also told me the leg pain was related to the surgery, that the nerves to the legs had been stretched by inserting spacers between the vertebrae. I asked to be started on gabapentin (Neurontin), and I am currently on 300 mg four times a day. It helps, but the right leg is still screaming.

I called a physical therapist on my own, even though no referral was made for physical therapy by my doctor.  The therapist quickly noted that I was tilted to the left when I stood or walked. We began therapy and exercises to correct this problem. But more is now clear to me.

Since my spine surgery, my gait has changed completely. For years I was bent over some and walking as best I could. Now, I was upright enough to carry a book on my head. My gait had changed. Now, I push off my toes differently, and my calves aren’t used to it. I also use my right thigh differently that as I walk, I feel different (but constant) pain in the right leg depending on which leg is bearing weight at the moment.

There is no question that I will have to learn a wholly new gait, and that I will need a good physical therapist to help me accomplish this. Interestingly, this issue of gait change is seldom discussed; see the Hopkins article The Road To Recovery After Lumbar Spine Surgery. In the future, these kinds of issues should be addressed by the surgeon both pre- and post-operatively.

As of this writing, I am three and a half weeks post-surgery.  I assume that my actual surgery went well and that it is just a matter of weeks before I can walk without pain. In truth, I have no idea how long my recovery will take.

The Cost of Spine Surgery

I asked for my medical records and my bill last week. I did get the bill for my surgery; it was $147,378 just for the surgery, that does not include any professional fees. Those will come from surgeon, anesthesia, pain management, physical therapy, etc. I was shocked to see that about $100,000 of the bill was for the plates and screws that now reside in my back. See Bloomberg: Highest-Paid U.S. Doctors Get Rich With Fusion Surgery Debunked by Studies and Newsweek: This Won’t Hurt a Bit

Parting Thoughts

In my opinion, American Healthcare is in a sad state. I suspect that this same surgery would cost about $10,000 in Sweden and that the patient would receive excellent comprehensive post-operative care.

I have undertaken to post this likely-to-be-controversial blog in hopes that it will get peoples’ attention. Change is needed. It appears that the patient has gotten lost in corporate healthcare, which is driven by the profit motive above all else. Personally, I believe that the patient still should come first.

Times have changed. If you are having major surgery at any hospital, you need to have a patient advocate on and at your side. Even though I was heavily medicated, I attempted to be my own advocate (rather unsuccessfully). Your advocate needs to ask and demand answers to important questions and issues. S/he could be a family member, or alternatively, you can actually hire a patient advocate.

Major Conclusion: Today, you need a patient advocate if you are having major surgery if you are to get good care in the hospital. A squeaky wheel still gets oiled first. Without a medically-sophisticated advocate at your side, you are at risk … as I was.

Severe Laryngeal Reflux (LPR)

I have been a laryngologist for almost 40 years, and I was one of the very first to specialize in this field. Laryngology is a medical specialty that focuses on patients with voice disorders and diseases of the larynx (voice box), throat and airway. Quite possibly, I have examined more larynges (plural of larynx) than anyone in the history of civilization, approximately 250,000 of them.

When I look at the larynx, I see things that other doctors don’t see. In particular, I recognize the subtle findings of acid reflux and vocal cord weakness; those being the most common and important underlying causes of hoarseness. The larynx talks to me. It tells the patient’s medical history and it tells me the whole story. I am the larynx whisperer.

How did my story begin? In 1969 I went to medical school with the idea of becoming a general surgeon. I attended Boston University, and during my third-year electives, I had the opportunity to work with three creative visionaries (Drs. Strong, Vaughn and Jako), who were pioneering laser surgery of the larynx.

Imagine my excitement and awe when in 1972 I first saw one-inch-long vocal cords grow to the size of gigantic salamis on a large-screen TV. The images were incredible. The tiny blood vessels looked like a NY subway map. Through the operating microscope, small growths could be removed with precision using laser light. And this was all done through the mouth with no incisions, while the patient slept. It was brilliant. I signed up on the spot.

I finished my residency in 1978, and became the 4th surgeon in the United States to work with the CO2 laser.  My very first business cards declared, “Specializing in Laryngology and the Voice.”  I appealed to my medical colleagues: “Just send me the patients with laryngeal and voice disorders that you don’t want, and the ones that you can’t fix.” I got busy very quickly.

In 1981, I began to notice that some of my patients had unexplained laryngeal inflammation that was severe and causing complications. I removed vocal cord polyps from one patient with precision only to find that she subsequently developed excessive scarring. In another case, I successfully removed a small vocal cord cancer, which healed poorly (unexpectedly) resulting in another bad outcome.

Patients who had surgical complications seemed to show a similar pattern, and some had symptoms of heartburn. Eureka! I figured it out—they had reflux. I began to explore all that was known about reflux in the medical literature, and I found little on how it might affect the larynx and throat. With careful documentation of my observations, I began to be able to describe the reliable findings of reflux laryngitis. Around that same time (1982-83), I got the idea to do reflux testing in the throat using a specially designed pH (acid) monitoring device. For the next 20 years ( as both clinician and scientist), I would spent my career studying reflux as it affected the larynx.

It has taken me all these years to become the larynx whisperer; it has been a personal journey, an evolution of experience and thought. Now it is clear and now I can teach others much of what I know.

For years I had believed that people either had airway or esophageal reflux (not both) with different symptoms, different patterns of reflux and different manifestations; however, that is not the case. Reflux is reflux and why some people develop predominant airway or esophageal symptoms is still unclear, but most people with esophageal reflux also show manifestations of airway reflux even if they deny having airway symptoms. The converse is less true, that is, many people with airway reflux do not have esophageal disease, because much less reflux in the airway can cause trouble

I developed a reflux scoring system for airway (laryngeal) reflux long ago. Unfortunately most physicians are unaware of it; however, I have scored every examination of every patient at every visit for 25 years. Now, I know that most people with reflux, regardless of their symptoms (airway or esophageal reflux) have laryngeal findings of reflux. A look at the larynx tells everything about the status of the entire reflux system; the reflux finding score is a reliable barometer of the whole system.

The Larynx as Barometer of the Reflux System

I used to think that airway reflux (LPR) and esophageal reflux (GERD) were fundamentally dissimilar, that the mechanisms and patterns of reflux were different, which explained why each group of patients had different symptoms.

I thought that the mechanism in LPR was related to a faulty upper esophageal valve (UES, upper esophageal sphincter) and that’s why reflux got into the throat. Similarly, the mechanism in GERD was a leaky the lower valve (LES, lower esophageal sphincter). As it turns out, both valves are dysfunctional in almost all people with reflux regardless of their symptoms. This is a paradigm shift, even for me, and I have been professionally immersed in reflux every day for decades. I thought I understood reflux, but I was wrong.

Here’s why. As a laryngologist, until I wrote Dropping Acid: The Reflux Diet Cookbook and Cure, I was almost exclusively seeing patients with airway reflux. After the book, I began to see just as many patients with primary esophageal reflux who wanted my advice on diet, lifestyle, and treatment in general. As a matter of fact, I began seeing the worst of the worst, people with Barrett’s esophagus, a reflux-caused precancerous condition.

In other words, patients with severe GERD were consulting me. To my surprise, all of them looked like they had airway reflux (LPR) when I examined their throats. Maybe they looked less inflamed (red), but they all looked swollen (edematous) in a pattern that I recognized to be exclusively related to reflux. That’s right, not allergies, infections, or post-nasal drip causes a larynx to look like reflux. To me, only reflux looks like reflux.

Now, with a lot of experience taking care of patients with “GERD,” I am finding that all refluxers have signs and symptoms of reflux in the larynx. And I now believe that by varying degrees, the entire system is affected by reflux. In other words, almost all patients with reflux, regardless of their symptoms, will have characteristic findings of airway reflux. And when the larynx becomes healthy, the system is healthy … and that is my job, to make that happen.

Reflux Laryngitis (Before Treatment)

Normal (Same Patient After Treatment)

These before- and after-treatment photographs show the larynx of a 40-year-old woman with airway reflux who presented with severe hoarseness, chronic cough, and “asthma”; she was a silent refluxer. [Before (top photo) and after (bottom photo). The V-like structures are the vocal cords; the pre-treatment (upper) is very swollen (blimp-like) by comparison with the photo on the bottom. Also, the back of the larynx (top of the photos) is very much thicker and redder in the before-treatment (upper) photo.]

Specialization: When Being the Best Isn’t Good Enough

Neither gastroenterologists (GIs) nor otolaryngologists recognize and treat airway (laryngeal) reflux; neither have a reliable test for it. And unfortunately, for the most part, ENT doctors do not know what they are looking at when they do examine the larynx. And lung doctors? They still have no idea that reflux accounts for up to 70% of lung disease. Pulmonologists think of reflux last, and when they do, they consult GIs.

When it comes to reflux, the medical establishment has missed the boat by a mile. (You are probably asking yourself how could this happen? Maybe I could be wrong?) Consider this: I recently showed the “reflux laryngitis” photo, the “before treatment” one (above), at a national convention of ENT doctors where I lectured on reflux. I asked for a show of hands to the question, “Is this larynx abnormal?” No hands went up. Then, I asked, “Okay, is this larynx normal?” Again, no hands went up. Hundreds of otolaryngologists in the audience looking at a photo that unequivocally showed reflux, and all I could hear was crickets. Not one of the doctors even dared to venture a guess.

Dear reader — and silent reflux sufferer — that is the sad state of the art!

This is about reflux friendly eating

The world is changing and the most significant trends in the contemporary management of reflux-related disease are: (1) The prevalence of reflux and esophageal cancer is increasing;^1-9 (2) The medical treatment failure rate with PPIs (proton pump inhibitors) is increasing;^1-3,10 and (3) Effective reflux management depends mainly on dietary and lifestyle variables.^1,2,11

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 than a generation ago. As the world’s diet has become Americanized, reflux has followed.  See and purchase my best-selling book, Dropping Acid: The Reflux Diet Cookbook & Cure … yes, it’s a cure for many people.

Increasing Prevalence of Reflux Disease and Reflux-Related Esophageal Cancer

The prevalence of acid reflux disease—both esophageal reflux (i.e., GERD, gastroesophageal reflux disease) and airway reflux (i.e. LPR, laryngopharyngeal reflux)—has increased dramatically in our lifetimes.^1-5 Using a Poisson model and an analysis of 17 prevalence studies published from 1976-2005, El-Serag⁴ 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.^6-8 Based upon National Cancer Institute data, esophageal cancer is the fastest growing cancer in the country having increased 850% since 1975.⁶ During this same period, its mortality has increased seven-fold  despite increased esophageal surveillance.^1,6-8 In addition, the prevalence of Barrett’s esophagus, the reflux-related precursor to esophageal cancer, is very high.^8,9 Furthermore, Reavis, et al. reported that patients with hoarseness and chronic cough (airway symptoms) had Barrett’s esophagus just as frequently (8%) as reflux patients with heartburn.⁹ Today, routine esophageal screening is recommended for both symptomatic airway reflux and esophageal reflux patients.^1,2,12,13

Reflux Disease Is Now Common in Young People

In the past reflux was primarily a disease of overweight middle-aged people. But now we are finding that many reflux patients are neither obese nor older.^1,2,14 This trend toward younger and younger, not-overweight, patients with more and more severe reflux has been observed by other experienced clinicians.¹⁵

In 2010, we estimated the prevalence of airway and esophageal reflux (LPR and GERD) in the United States by interviewing a geographically random sample of 656 U.S. citizens.^1,2 (The interviews carefully elicited all reflux symptoms and medications.) The data revealed that an astonishing 40% had reflux disease, 22% having classic esophageal reflux (GERD) and another 18% having airway reflux (LPR).^1,2 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.^1,2

Cell Biology of Reflux: Clinical Implications

The popular term acid reflux is a misnomer. It is pepsin (not acid) that does most of the airway and esophageal tissue damage from reflux; however, pepsin requires acid for its activation.^{1,2,11,13,16-21} Therein lies the cause of some of the confusion regarding the pathophysiology of reflux disease. Pepsin causes inflammation and damages airway mucosa, especially the surface epithelium, in a variety of ways.

First, pepsin destroys the protective mucus barrier.^16,22 Second, it damages the mortar between squamous epithelial cells (E-cadherin), allowing pepsin to penetrate deeply to the active basal layers of the epithelium.^1,20 Third, once pepsin binds to cell membranes, it is endocytosed; and once inside the cell depletes vital protective proteins, including carbonic anhydrase and stress proteins.^{1,2,19-21,23-27} Interestingly, using laryngeal cell lines, Johnston et al.²⁸ has reported that pepsin upregulated genetic markers for squamous cell carcinoma.

In patients with LPR, post-cricoid biopsies show pepsin in the tissue demonstrated by Western blot analysis and immunohistochemistry (IHC). We have previously reported that 95% of patients with clinical and pH-documented LPR had tissue-bound pepsin (5% of controls).²³ In addition, pepsin requires very little acid to become active, i.e., proteolytic (digests protein).^13,16,20,21

Figure 1 shows the pepsin IHC of a biopsy from the posterior glottis of a patient with airway reflux. Once pepsin is tissue bound, acid from any source can activate it; that’s why acidic foods and beverages cause inflammation.^1,2,11,16

Figure 1: Reflux Laryngitis: IHC for Human Pepsin 3b

Pepsin is the brown material and it is found both intracellular and extracellular. It is important to recognize that human pepsin is remarkably stable, and it retains proteolytic activity up to pH 6.5 depending on the substrate.²¹ At pH 6.5, for example human pepsin 3b (by far the most abundant type) is able to digest collagen.²¹ Peak peptic activity (100%) occurs at pH 2, but there is still some (~10%) activity at pH 6²¹; see Figure 2. In other words, clinical reflux disease (LPR) is associated with tissue-bound pepsin,^19-21,23-28 and we have previously shown that laryngeal damage occurs at pH 5.0 or less.²⁰

Figure 2: Human Pepsin 3b Activity Curve²¹

The clinical significance of finding 50-90% of peptic activity in the pH 4.6-2.5 range is that almost all bottled and canned foods and beverages (all soft drinks) today are manufactured in that pH range to kill bacteria and prolong shelf life.^1,2

How the World’s Diet Has Changed Since WWII

The dramatic increases in reflux over the past forty years cannot be explained by the obesity epidemic alone. Coincident with the reflux epidemic, the world’s diet has changed.^1,2 In our lifetimes, there have been four unhealthy dietary trends²:

(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)

The last of these trends—increased dietary acid—may hold the key to understanding the contemporary reflux epidemic and the dramatic increases in esophageal cancer.^1-10

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.”^1,2,29-31 How was this accomplished? Through acidification of bottled and canned foods, which was intended to prevent bacterial growth and prolong shelf life.^1,2,29 From the 1979 Title 21 Act:

“Acidified foods should be so manufactured, processed, and packaged that a finished equilibrium pH value of pH <4.6 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.”^1,2,31

Today, two generations later, the FDA has never wavered from this path and has apparently 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 reflux and esophageal cancer epidemics appears to closely follow soft drink consumption.^2,32,33

Fig. 3: These Beverages (many deemed "Healthy") Are Very Acidic (pH 2.4-2.9). Click on photo to enlarge???

At the end of World War II, the average American consumed four (4) eight-ounce soft drinks per week. In 2010, the average 12-29-year-old young American drank forty-nine (49) eight-ounce soft drinks per week, an average of seven per day.^2,33 The number provided by the America Beverage Association for this group is 606 liters per year, or almost two liters a day.³³

In addition to acid as a major food additive, the FDA allows over 300 other chemicals be added to food that are “generally regarded as safe” (GRAS).^1,2,30,31 Many of these GRAS food additives were “grandfathered in” in the 1970s without the benefit of contemporary state-of-the-art scientific scrutiny.^2,31 Thirteen percent of these additives are acids, and there is no evidence that the FDA (or anyone else) has ever studied the long-term effects of these GRAS.

Excessive Dietary Acid Is the Missing Link

Why are reflux disease and esophageal cancer epidemic? Many years ago, when esophageal cancer was relatively uncommon, reflux patients usually presented in middle age. Today, we are seeing comparable disease in patients in their 20s.¹ Over-acidity in the diet is the missing link, which explains the reflux epidemic and the increasing rates of Barrett’s and esophageal cancer.²

Today, even “organic” baby food is acidified. We measured the pH of an “organic” banana baby food and found the pH to be 4.3. Normally, the pH of banana is about 5.7. But this so-called “organic” banana had had acid added. Indeed, most bottled and canned foods and beverages are pH <4,^1,2 because phosphoric, acetic, ascorbic, and/or citric acids are added. Sometimes the food label may just read “vitamin C enriched” or “vitamin C enhanced.”

Dietary and Lifestyle Modification

In the twenty years since publication of my Triological thesis,¹⁶ the number of Americans with reflux disease has doubled.^1,4 In addition, it is clear that when it comes to reflux diseases, particularly airway reflux, the medical establishment has missed the boat by a mile. Furthermore, it is now clear that for airway reflux, the PPI-treatment failure rates (regardless of dose) are very high. Medication does not control reflux for most people, especially those with silent airway reflux. And, if the medication does help, should such patients have to stay on medication for life?

For most patients with reflux, “cleaning up” their diet and their lifestyle is the essential therapeutic action for getting well.^1,2 When a patient’s reflux is bad, there is a (downward) vicious cycle going on. The more one refluxes; the more one refluxes. This is because reflux causes inflammation of the esophagus and its valves, and that inflammation further compromises the esophageal and valve function. Thus, more reflux begets worsening esophageal function, which in turn, begets more reflux. This is a downward spiral.

Thankfully, the opposite is true, that is, as inflammation and reflux improves, esophageal and valvular function improves as well so that there is less subsequent reflux. The point is that healthy function can be restored and that diet and lifestyle are far more important than medication; however, for many patients with severe reflux dietary and lifestyle changes are needed as well as medication at the beginning. That is why the Induction (“Detox”) Reflux Diet helps so much: Reduce acid and pepsin coming from below (from the stomach) for two weeks using medication, and at the same time, reduce damaging acid (that activates pepsin) coming from above during that same two week period. (Today, many of our patients are being treated by diet alone, i.e., without medication.)

Evolution of the Induction (“Detox”) Reflux Diet

For more than 25 years, LPR patients in the author’s practice were prescribed PPIs with or without a nighttime H2-antagonist, as well as limited nutritional and lifestyle counseling. The latter consisted of a list of do’s and don’ts (Table 1).

Table 1: Traditional Antireflux Diet and Lifestyle Modification Program
If you use tobacco, you must quit, because smoking causes reflux
Don’t wear clothing that is too tight, especially trousers, corsets, and belts
Avoid exercising, esp. weight-lifting, swimming, jogging, and yoga after eating
Do not lie down just after eating; do not eat within 2-3 hours of bedtime
Elevate the head of your bed if you are a nighttime refluxer (hoarse in the morning)
Limit your intake of red meat, butter, cheese, eggs, and anything with caffeine
Completely avoid fried food, high-fat meats, onions, tomatoes, citrus fruit (and fruit juice),
carbonated beverages (soda), beer, hard liquor, wine, mints, and chocolate

For many years we recognized that carbonated beverages, particularly caffeinated cola drinks, were a major risk factor for the development of airway reflux. Indeed, excessive consumption of carbonated beverages continues to be the single most common identified cause of medical treatment failure among our patients.^1,2 Based upon clinical experience, we also began to limit our patients’ intake of citrus and hot (pepper) sauces. Other than those few specifics, the antireflux diet did not change much over the years; that is, until recently.^1,2,11

With publication of the 2007 paper, Activity/stability of human pepsin: Implications for reflux attributed laryngeal disease,²¹ showing peptic activity up to pH 6.5; and having previously reported finding pepsin in the laryngeal biopsies of most patients with LPR^20,23; we recognized that tissue-bound pepsin in LPR might be activated by exogenous hydrogen ions from any, including a dietary source.^1,2 Consequently, we began measuring the pH of common foods and beverages and restricting airway reflux patients from consuming anything pH <5 for a trial period of two weeks. This appeared to be beneficial for patients.

In 2008, we began to systematically measure the pH of common foods and beverages, and as a consequence of finding acid in almost everything we tested, we began to strictly limit the acid intakes of our LPR patients, with outstanding results. As we measured the pH of more and more foods, the Induction Reflux (“Detox”) Diet evolved. Soon we had lists of good and bad foods and beverages. In the ensuing years, we refined the Induction Reflux Diet to exclude recognized reflux “trigger” foods as well as anything pH <5.^1,2 The basic elements of the Induction Reflux Diet in its present form are shown in Table 2, and Table 3 provides the complete list for the Induction Reflux Diet.

Table 2: Basics of the Two-Week Induction Reflux Diet
Grilled/baked/broiled/boiled fish, shellfish, and poultry
All vegetables (except onions, tomatoes, garlic, and peppers)
Breads, rice, grains, low-sugar cereals, oatmeal, and tofu
Melons, bananas, ginger, agave, Manuka honey, chamomile tea
Low-fat soy, almond, coconut or cow milk, alkaline water pH >8
Finally, one cup of coffee or caffeinated tea per day allowed

Table 3: Induction Reflux Diet: What You Can Eat
Agave
Aloe vera (read label: make sure no acid added)
Artificial sweetener (max. 2 teaspoons per day)
Bagels and (non-fruit) low-fat muffins
Banana (great snack food)
Beans (black, red, lima, lentils, etc.)
Bread (especially whole grain and rye)
Caramel (max. 4 tablespoons per week)
Celery (great snack food)
Chamomile tea (most other herbal teas are not acceptable)
Chicken (grilled/broiled/baked/steamed; no skin)
Chicken stock or bouillon
Coffee (max. one cup per day; best with milk)
Egg whites
Fennel
Fish (including shellfish, grilled/broiled/baked/steamed)
Ginger (ginger root, powdered or preserved)
Graham crackers
Herbs (excluding all peppers, citrus, garlic, and mustard)
Honey (Manuka honey is preferred honey)
Melon (honeydew, cantaloupe, watermelon)
Mushrooms (raw or cooked)
Oatmeal (all whole-grain cereals)
Olive oil (max. 2 tablespoons per day)
Parsley
Popcorn (plain or salted, no butter)
Potatoes (all of the root vegetables except onions)
Rice (healthy, especially brown rice, is a staple during induction)
Skim milk (alternatively, soy or Lactaid skim milk)
Soups (homemade with noodles and low acid veggies)
Tofu
Turkey breast (organic, no skin)
Vegetables (raw or cooked, but no onions, tomatoes, garlic, or peppers)
Vinaigrette (max. 1 tablespoon per day; you must toss salads)
Whole-grain breads, crackers, and breakfast cereals

We have previously reported successful results of the Induction Reflux Diet in twenty patients with recalcitrant (PPI-resistant) airway reflux.¹ All twenty of the study subjects claimed excellent compliance with the prescribed diet, and 95% improved on the low acid diet. Three subjects became completely asymptomatic, and another went from an initial RSI (reflux symptom index) of 28 to a post-diet RSI of 4. The mean pre-diet RSI³⁴ (an index based on patient reported symptoms taken at each visit) was 14.8 and the mean post-diet RSI was 8.6 (P= 0.023); the mean RSI improvement was Δ-6.3. The mean pre-diet RFS³⁵ (reflux finding score based on laryngoscopy) was 12.0, and the mean post-diet RFS was 8.3 (P< 0.001).¹

Four Phases of Dr. Koufman’s the Reflux Diet

There are four phases of my reflux diet: (1) Induction, (2) Transition, (3) Maintenance, and (4) Longevity. To reiterate, the purpose of the two-week Induction Reflux Diet is to wash out pepsin and restore more normal functioning of antireflux defenses.

The Induction Reflux Diet has been the cornerstone of the author’s dietary and lifestyle program for patients with both airway and esophageal reflux. An additional adjunctive therapy that has been added within the last year is alkaline water. We evaluated a natural artesian alkaline (pH 8.8) water (Evamor™) in the laboratory and found that it instantaneously and permanently denatured pepsin; it also had good buffering capacity.¹¹

The Induction Reflux Diet is still recommended for just the first two weeks with a gradual reintroduction of some additional fatty foods and other “historically refluxogenic” foods. Cheese, eggs, meats, sauces, and condiments are allowed in moderation as flavorings, but the key elements of the other phases of the reflux diet are that it remains relatively low-acid (not no-acid) and low-fat (not no-fat).

With fatty foods in particular, we teach patients moderation, using tasty fats as flavorings rather than as main ingredients. We also introduce the concept of pH balancing. The idea is that favored acidic foods may be combined with non-acidic foods. Acidic fruits, for example, that are not allowed to be eaten by themselves may be fine if added to breakfast cereal with milk (preferably low-fat milk) that has a high pH. Many of my patients report that alkaline water is a key variable to their recovery.

Finally, during the reflux diet, particularly during induction, there is no eating allowed within four hours of bed. Even if a person eats healthy food, eating too late can be a problem. It actually takes 4 hours for the stomach to empty completely. After the induction, the time between eating and recumbency can be 2-4 hours.

Here’s an example. I had a patient who was a restaurant manager. He would get off work at 11 p.m., and by midnight, he’d have eaten dinner and already gone to bed. He was frustrated that his reflux medication wasn’t helping as he awoke every morning with terrible heartburn and sometimes in the middle of the night, too. To make matters worse, he also told me that dinner was usually his biggest meal of the day. When he told me his story, I explained that he didn’t have a chance of beating his reflux as long as he was eating dinner before bed, he replied,” I pretty much knew that you were going to say that; I guess that I am going to have to make some big changes, huh?”  “Not really,” I told him, just take a break to eat your dinner before 8 p.m.”

Night eating is a major cause of reflux, obesity, diabetes, hypertension, snoring, and sleep apnea. Reflux patients who go to bed with a full stomach are going to reflux. Just as bad, by the way, is lying on the sofa after dinner. Actually, the best thing a person can do after dinner is take a walk. Even after induction, night eating is one of the biggest risk factors for both airway and esophageal reflux.

Based upon many years of examining pH-monitoring data, we know that most patients with airway reflux (LPR) are upright (daytime) refluxers, often with many (relatively short) periods of laryngopharyngeal acid/pepsin exposure. On the other hand, for airway reflux patients with supine (nocturnal) reflux, acid/pepsin contact times are often hours long. Such prolonged reflux episodes result in far more severe laryngopharyngeal inflammation and damage. Indeed, a single 2-6 hour supine nocturnal reflux event can produce hoarseness, sore throat, and cough symptoms that can last several weeks.

After induction, comes Phase II, Transition. This phase requires trial and error on the part of the patient as foods and beverages are added back. I usually start by adding back egg yolks, condiments, and some additional fruits (those that are relatively low-acid, such as pears and red apples) and some meats (those that are relatively low-fat, such as white pork and lean beef).

Three-egg omelets are made with just one yolk as an example of low-fat (not no-fat) eating, and when it comes to meats, portion control is as important. Patients are instructed to use/order all dressings, condiments, cheeses, and sauces on the side so that they can use relatively small amounts. Wine and cocktails may be added back with the admonition that these must be limited to one per day, and not too late in the evening.

During the Transition Phase, which can last months, there must be a lot of trial and error with foods. The truth is that everyone with reflux is different, and even foods that are forbidden during the induction phase may be well-tolerated, including onions, tomatoes, garlic, and peppers.  These are all idiosyncratic foods, that is some patients can tolerate some but not others, and some are better cooked than raw, e.g., tomatoes and onions. Some people can tolerate garlic flavorings but not garlic itself … and so on.

It is also important to point out that different patients have different trigger foods, which are foods that cause symptoms, sometimes immediate symptoms like throatburn.  Even items on the best-for-reflux food list are trigger foods for some patients.

During the transition phase, the key endpoints are the patient’s symptoms and the laryngeal examination. The author employs the Reflux Finding Score (RFS) for every reflux patient at every visit and the RFS should be lower (more normal) as time passes. In addition, during Transition, I attempt to get patient off antireflux medications, at least off PPIs.  H2-antagonists, such as ranitidine, can be used up to 150 mg q.i.d. without problems, even during pregnancy. Furthermore, H2-antagonists are perfectly acceptable as ad hoc medications, taken as needed.  Ranitidine may be preemptively taken before dinner and before bed by patients if they know they are going to be eating later than usual or eating foods that may be problematic. The same is not true of PPIs that often are associated with hyperacidity “rebound” after they are discontinued.

During the Third Phase, Maintenance, the patient can sustain a “healthy lifestyle” such that her/his reflux is under control for a prolonged period. In addition, during this phase, the patient will easily manage eating in restaurants, and he/she will feel that healthy eating is easy.

We call the final, Fourth Phase, Longevity, the patient has no reflux, is close to her/his ideal body weight, and effortlessly eats at home or dines out without fear of having reflux. In this phase, patients are not on reflux medication. Sound too good to be true? Longevity takes work and persistence, and sometimes the help of a nutritionist. But it is true that normal physiology can be established in many reflux patients with incredibly outstanding long-term outcomes. This is, after all, proof that reflux is primarily a disease of what we eat and when we eat it.

In summary, excessive acid and fat in the diet, as well as late night eating and alcohol in excess, are the most important reversible lifestyle-related factors contributing to the development of chronic airway (and esophageal) reflux. For the reflux sufferer, tobacco and highly-acidic beverages, such as soft drinks, should be totally and permanently avoided.

With customized dietary and lifestyle modifications, about two-thirds of reflux patients can be managed successfully. Without such, all other treatments are usually doomed to failure.  One final note: From a public health point of view, it would probably be very beneficial to have the pH of all bottled and canned foods and beverages printed (by law) on nutritional labels. Please help any way you can with this effort!

References

1. Koufman JA. Low-Acid Diet for Recalcitrant Laryngopharyngeal Reflux: Therapeutic Benefits and Their Implications. Ann Otol Rhinol Laryngol 120:281-87, 2011.
2. Koufman JA, Stern JC, Bauer MM. Dropping Acid: The Reflux Diet Cookbook & Cure. Reflux Cookbooks LLC (The Reflux Cookbooks LLC), Midpoint Trade Books (Distributor), New York, 2010.
3. 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.
4. El-Serag HB. Time trends of gastroesophageal reflux disease: A systematic review. Clin Gastroenterol Hepatol 2007;5:17-26.
5. Altman KW, Stephens RM, Lyttle CS, et al. Changing impact of gastroesophageal reflux in medical and otolaryngology practice. Laryngoscope 2005;115:1145-53.
6. 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.
7. 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.
8. 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.
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.

10.  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.
11.  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.
12.  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.
13.  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.
14.  Halum SL, Postma GN, Johnston C, Belafsky PC, Koufman JA. Patients with isolated laryngopharyngeal reflux are not obese. Laryngoscope 2005;115:1042-5.
15.  Koufman JA. Personal communications with Dr. Robert Sataloff (Philadelphia, PA) and Dr. John Hunter (Portland, OR)
16.  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.
17.  Lillemoe KD, Johnson LF, Harmon JW. Role of the components of the gastroduodenal contents in experimental acid esophagitis. Surgery 1982;92:276-84.
18.  Johnson LF, Harmon JW. Experimental esophagitis in a rabbit model. Clinical relevance. J Clin Gastroenterol 1986;8 (Suppl 1):26-44.
19.  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.
20.  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.
21.  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.
22.  Orlando RC, Powell DW, Carney CN. Pathophysiology of Acute Injury in Rabbit esophageal Epithelium. J Clin Invest 1981;68:286-93.
23.  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.
24.  Knight J, Lively MO, Johnston N, Dettmar PW, Koufman JA. Sensitive pepsin immunoassay for detection of laryngopharyngeal reflux. Laryngoscope 2005;115:1473-8.
25.  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.
26.  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.
27.  Samuels TL, Johnston N. Pepsin as a marker of extraesophageal reflux. Ann Otol Rhinol Laryngol 2010;119:203-8.
28.  Johnston N, Yan JC, Hoekzema CR, et al. pepsin promotes Proliferation of Laryngeal and Pharyngeal Epithelial Cells. Laryngoscope 2012;122:1317-25.
29.   “Acidified Foods.” Code of Federal Regulations—Title 21—Food and Drugs Chapter I, Department Of Health And Human Services Subchapter B—Food for Human Consumption Part 114. United States Food and Drug Administration. Arlington, VA, Washington Business Information, 2010.
30.  “Generally Recognized as Safe Food Additives: FDA Database of Selected GRAS Substances.”  United States Food and Drug Administration. National Technical Information Service, Springfield, VA, 2009.
31.  “Food Safety: FDA Should Strengthen Its Oversight of Food Ingredients Determined to Be Generally Recognized as Safe (GRAS).”  GAO-10-246: United States Government Accountability Office, February 3, 2010.
32.  Bellis M. Introduction to Pop: The History of Soft Drinks Timeline. About.com (http://inventors.about.com/od/sstartinventions/a/soft_drink.htm)
33.  Lobbying 2009: American Beverage Association. Center for Responsive Politics. (http://www.opensecrets.org/lobby/clientlbs.php?year=2009&lname=American+Beverage+Assn&id) March, 2010.
34.  Belafsky PC, Postma GN, Koufman JA.  Validity and reliability of the reflux symptom index (RSI). J Voice 2002;16:274-7.
35.  Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS).  Laryngoscope 2001;111:1313-17.

The White House

Office of the Press Secretary
______________________________________________________________________________________________________
For Immediate Release

President Barack Obama: Presidential Proclamation — Monday, July 30, 2012

Close the Kitchen by 8p Day

Whenever possible, I have an early family dinner with Michelle, Sasha, and Malia at about 6:30 p.m.  Unfortunately, most of the evening meals at official White House functions, especially State Dinners, are much later than that. This trend towards late night eating is unhealthy.

Today, one-in-twelve Americans have asthma, and it is much higher for poor, non-white children. It is likely that unhealthy bedtime snacks play a role in this “asthma” epidemic, as eating soon before bed is associated with acid reflux disease. Besides acid reflux, late-night eating is associated with the development of many other expensive, high-prevalence diseases such as obesity, diabetes, hypertension (high blood pressure), snoring, sleep apnea, and esophageal disease, including cancer.

NOW, THEREFORE, I, BARAK OBAMA, President of the United States of America, in accordance with a joint resolution of the Congress approved July 24, 2012 as amended (38 U.S.C. 309), do hereby proclaim July 30, 2012 as Close the Kitchen by 8 pm Day. I direct the appropriate officials of the Government to display the flag of the United States on all Government buildings on this day, and I call upon all citizens to observe this day by not eating after 8:00 p.m., and if you have school-age children, not after 6:30 p.m.; and no bedtime snacks. Further to the intent of this Proclamation, which is to raise public awareness about the health risks of late-night eating, I, BARAK OBAMA, do encourage all Americans with possible acid reflux disease to make dinner time early as possible so that the kitchen can routinely close by 8.

IN WITNESS WHEREOF, I have hereunto set my hand this thirtieth day of July, in the year of our Lord two thousand twelve, and of the Independence of the United States of America the two hundred and thirty-sixth.

BARACK OBAMA

There is pepsin in Barrett's (IHC shown)

Identify – Treat – Drop the Acid

Acid reflux is epidemic today, and it is the cause of esophageal cancer, which has become the fastest growing cancer in the United States. It has increased 850% since the 1970s!

Reflux affects 125 million Americans 22% with typical esophageal reflux, the symptoms of which are heartburn and indigestion, and another 18% with airway reflux, the symptoms of which are hoarseness, post-nasal drip, chronic cough, asthma, sinusitis, lump-in-the-throat sensation, and difficulty swallowing. Sometimes airway reflux is called “silent reflux” or “LPR” (laryngopharyngeal reflux).

Remember, our goal here is not just early detection of cancer, but rather cancer prevention. For this, there are three key steps for people with reflux symptoms: (1) esophageal screening to indentify those at risk for developing esophageal cancer (EC); (2) effective medical treatment; and (3) long-term, antireflux dietary (and lifestyle) modification, which means truly healthy eating—with the addition of a couple of supplementary esophageal superfoods. And yes, healthy eating appears to be the single most important factor in EC prevention.

STEP I: Esophageal Screening for People with Any/All Reflux Symptoms

It is important to note that people with airway reflux, even without any heartburn, are at equal risk to develop esophageal cancer and its precursor, Barrett’s esophagus. Indeed, today about 8% of people with reflux have Barrett’s. That converts to over ten (10) million people. All of these people need early screening examinations of the esophagus by transnasal esophagoscopy (TNE). TNE is quick, well-tolerated by people, and requires no sedation. It is done in the doctor’s office, and right after this kind of endoscopy, people can return to normal activity. And yes, it is as effective as sedated endoscopy (EGD) to diagnose trouble in the esophagus (www.TransnasalEsophagoscopy.com).

There may come a time when all adults should have routine TNE esophageal screening, but in the meanwhile, at present we recommend that all people with esophageal and airway reflux symptoms undergo TNE examinations. Then, people who are found to have Barrett’s esophagus (EC pre-cancer), pre-Barrett’s (an irregular Z-line), and esophagitis are all at risk for the development of EC; and therefore need to be on antireflux medication and learn about esophageal health. What does esophageal health mean? It’s a low-acid, low-fat, pH-balanced diet.

When we do a TNE, we may or may not perform a brush biopsy to get preliminary histologic information. If there is any question about the findings, the diagnosis, or the biopsy on TNE, we send the patient to a gastroenterologist for EGD with Seattle Protocol biopsy and potential ablation if in fact there is dysplasia, especially high-grade dysplasia.  (See also, Save Money: Throw Out the Baby.)

STEP II: Effective Medical Treatment

For people who have airway reflux, we almost always recommend twice-daily (before breakfast and before the evening meal) PPIs (proton pump inhibitors), such as Prilosec, Protonix, and Nexium, as well as an H2-antaonist, such as Zantac, before bedtime. Sometimes this regimen is called “maximum” medical treatment. Meanwhile, we recommend this dosing for any patient with Barrett’s esophagus or an irregular Z-line (pre-Barrett’s).

The visual in the ads on television that show little acid pumps (in the stomach) giving up at the sight of a purple pill simply isn’t so. None of the acid-suppressive medications, regardless of dose, actually turns the acid off. At best, it cuts the acid in half. That is why we recommend the higher dose for really “at risk” people, at least at the beginning of the treatment program. The idea is to try and produce around the clock acid suppression. Most of the drugs that claim that once-daily is enough actually work well for about sixteen hours. What about the other eight?  By the way, “beginning of the treatment program” usually means 6-12 months or until the tissue heals.

STEP III: Healthy Low-Acid Low-Fat Eating

It may come as a surprise to you, but what you eat may be eating you. Here’s the scoop. When you reflux, acid and pepsin (the powerful digestive enzyme of the stomach) comes up. When the pepsin attaches itself to your tissues (in your throat, esophagus, lung, etc.), then it’s off to the races. Pepsin is the cause of tissue damage. The clincher is that pepsin requires acid to activate it. In other words, without acid, pepsin can’t wreak its havoc.

In the last few years, we have discovered that acid in the foods and beverages that we consume causes most of the trouble. The single greatest risk factor for the development of reflux disease is the consumption of soft drinks. According to the American Beverage Association, in 2010 the average 12-29-year-old consumed 160 gallons of soft drinks; that is almost one-half gallon per day; and all are very acidic. BTW, I recently diagnosed Barrett’s in two 28-year-old heavy soda-drinkers. Barrett’s used to be a problem only seen in middle-aged people.

Does diet make a real difference? We are now seeing reversal (cure) of biopsy-proven Barrett’s esophagus in some of our patients. What does it take? (1) maximum antireflux treatment (all the meds); (2) a strict low-acid, low-fat, pH-balanced diet; (3) alkaline water (Evamor is the very best and is recommended); and (4) Manuka honey twice a day (after breakfast and before bed).

Our book is Dropping Acid: The Reflux Diet Cookbook & Cure. Our reflux diet is the healthiest, most sustainable diet in the world. It is like an extension of the healthy-heart diet that emphasizes the additional element of low-acid. This, we believe, is the key to esophageal health.

Next: The Four Phases of Dr. Koufman’s Low-Acid Barrett’s Diet

This is the voice box of a patient with severe airways reflux. Indeed, it is so swollen that the airway (breathing passages) are narrowed.

This may come as a surprise, but reflux is more complicated and controversial than almost any other common disease.^1-3 Reflux is like the elephant in the famous tale 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 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. “Aha, you are both wrong,” he says. “The elephant is rather like a giant leaf.” Each of the blind men embraces a part of the truth, but none understands its entirety.

In the case of reflux, the three blind men might be represented by three medical specialties, each one focusing on a different part of the aerodigestive tract: (1) The otolaryngologist (ENT physician) specializes in the ears, nose, and throat; (2) the gastroenterologist (GI physician) specializes in the esophagus (the swallowing tube that connects the throat with the stomach); and (3) the pulmonologist (PUL physician) specializes in the lungs. Many other medical specialties encounter patients with reflux as well, including internists, family practitioners, pediatricians, and critical care specialists.

Part of the problem is that each medical specialty has its own language and set of diseases related to reflux. While “acid reflux” is the most common lay term for the disease, GERD, gastroesophageal reflux disease, and LPR, laryngopharyngeal reflux, are the terms widely used by GIs and ENTs, respectively. See the table below for a list of common terms for reflux.

That there are so many different terms for reflux suggests fragmentation within the medical community with regard to the mechanisms and manifestations of disease. To make matters worse, most medical specialists remain unaware of the literature and research from other specialties. At least the three blind men in the fable shared their findings with each other—because medical specialists don’t.

Table: Most Common Medical Terms for Reflux
Gastroesophageal reflux disease (GERD)
Gastro-oesophageal reflux disease (GORD) [U.K.]
Reflux esophagitis, esophageal erosions
Extraesophageal reflux disease
Supraesophageal reflux disease
Gastropharyngeal reflux
Atypical reflux disease
Heartburn / Erosive esophagitis
Barrett’s esophagus
Esophagopharyngeal reflux
Laryngopharyngeal reflux (LPR)
Silent reflux
Esophageal reflux
Airways reflux
Throat reflux

In 1987, I coined the term LPR, specifically to differentiate my patients with throat reflux from those with esophageal reflux, that is, GERD. A year or so later, Dr. Walter Bo and I came up with the term “silent reflux,” is a very useful and descriptive term. Dr. Bo was the chair of the anatomy department at Wake Forest University. In 1988, Walter was my patient and he had LPR. After I explained how one could have reflux without also having heartburn, Walter rolled his eyes and said, “I see … I have the silent kind of reflux.” “Yes, Walter,” I said. “That’s it; you have SILENT REFLUX.”

Meanwhile, since writing Dropping Acid: The Reflux Diet Cookbook & Cure—the sales of which have been trending upwards ever since its publication—it has become clear that people (i.e., non-physicians) find the terms laryngopharyngeal reflux and gastroesophageal reflux disease (even just LPR and GERD) cumbersome and overly medical. The terms have obvious meaning to doctors: LPR means the backflow of gastric contents into the laryngopharynx (the throat and the voice box), and GERD means the backflow of gastric contents into the esophagus (the swallowing tube that connects the throat and stomach).

I propose to change the terminology forever.  The most encompassing and descriptive terms are AIRWAYS REFLUX and ESOPHAGEAL REFLUX.

I am an airway reflux expert. I recently estimated that in my medical practice I have seen, and cared for, over 100,000 patients with airway reflux. These include thousands of patients misdiagnosed as having asthma, sinusitis, allergy, and laryngitis.

Common Symptoms of Airways Reflux
Nasal congestion, sneezing, and/or runny nose
Ear fullness, popping, or intermittent echoing
Unexplained progressive dental and gum disease
Difficulty swallowing or painful swallowing
Chronic throat clearing and post-nasal drip
Awaking from sleep coughing or wheezing
A lump-in-the-throat sensation
Hoarseness or voice breaks
Shortness of breath
Trouble sleeping
Chronic cough
Sinusitis
Asthma

One parting thought: In my practice, of 100 patients who present with a diagnosis of “asthma,” only 15% actually have it. If you want to know the difference between real asthma and reactive airways disease secondary to reflux, here’s the pearl: If you have more trouble getting air “in” rather than “out” during an “asthma attack,” it’s not asthma! (By the way, the word NOSOLOGY refers to the classification or nomenclature of diseases.)

Next post: THE TRUTH ABOUT ASTHMA VS. PSEUDO-ASTHMA

1st Corollary – Conflicting elements are held together by function & purpose

•   •   •

2nd Axiom – Decompensation is preceded by often ignored warning signs

2nd Corollary – During early destabilization, imbalance is assessable

•   •   •

3rd Axiom – Last straw principle: When threshold is exceeded, collapse occurs

3rd Corollary – Recovery requires stabilization and repair of all essential elements

Barrett's esophagus as seen by transnasal esophagoscopy (TNE)

Esophageal screening by Transnasal Esophagoscopy (TNE) will provide better healthcare for Americans at a much lower cost.

The Reuter’s article, Special Report: Cancer screening feeds overdiagnosis debate, by Frederik Joelving (April 20, 2012) contains erroneous premises and incorrect information so that its conclusions are all wrong. It appears that Joelving would like to throw the baby out with the bath water! Here are the facts:

• Acid reflux is epidemic, and reflux-caused esophageal cancer—having increased 850% since the 1970s—is now the fastest growing cancer in America … by far.
• Acidity in the American diet is the cause of the reflux epidemic, and proper dietary treatment for reflux is highly effective. Reflux disease can be reversed!
• People with airway (“silent”) reflux—with hoarseness, chronic cough, and breathing difficulties (including asthma)—are more likely to have esophageal cancer and precancer (Barrett’s esophagus) than people with typical acid reflux with heartburn and indigestion.
• People with both esophageal and airway reflux should have esophageal screening examinations by TNE.

  Reflux and Reflux-Related Esophageal Cancer is Epidemic

  The prevalence of acid reflux disease has increased dramatically in our lifetimes.^1-6 Analysis of 17 prevalence studies showed that the rate of growth of reflux disease has been 4% per year since 1976.² In the last decade alone in ENT (ear, nose and throat) practice, office visits for reflux increased 500%.³

  In 2010, we estimated the prevalence of reflux (GERD and LPR) in America by interviewing 656 people waiting to purchase discount theater tickets (at TKTS) in Times Square in New York City.^1,5 The data revealed that an astonishing 40% (262/656) of the study group had reflux disease with 22% (144/656) classic esophageal reflux (aka GERD, gastroesophageal reflux disease) and another 18% (118/656) with silent (airway) reflux (aka LPR, laryngopharyngeal reflux).⁶ The most striking and unanticipated result was that 37% of the 21-30 year-old age group had reflux.⁵ In the past, reflux was primarily a disease of overweight, middle-aged people. But now we are finding that many of our reflux patients are neither old nor obese.⁷

  An even more ominous trend is that the prevalence of esophageal cancer in the United States has increased 850% since 1975.^1,4 During this same time period its mortality (deadliness) has increased seven-fold.⁵ In addition, the prevalence of esophageal precancer (Barrett’s esophagus) is also increasing, and it is just as high in people with hoarseness, sore throat, and chronic cough as it is in people with heartburn and indigestion.⁸

  In addition, today, asthma is very often overdiagnosed and misdiagnosed. The author (JK) recently reported a series of patients with a chief complaint of chronic cough for 10 years and found that reflux was mistaken for asthma by physicians 80% of the time.⁹ (If you have “asthma,” and if during breathing attacks you have more trouble getting air “in” rather than “out” (wheezing), you don’t have asthma; you have reactive airways disease because of reflux.)

  Dietary Acid May Be the Missing Link

  Coincident with the reflux epidemic, the American diet has changed dramatically.^1,10 Since the 1960s, there have been four parallel unhealthy dietary trends: (1) increased saturated fat, (2) increased high-fructose corn syrup, (3) increased exposure to organic pollutants (e.g., DDT, PCBs, dioxins), and (4) increased acidity.¹⁰ The last of these trends—increased dietary acid—may hold the key to understanding the contemporary reflux epidemic and the dramatic increases in Barrett’s esophagus and esophageal cancer.

  In 1973, following an outbreak of food poisoning (botulism), Congress enacted Title 21, mandating that the Food and Drug Administration (FDA) assure the safety of processed food crossing state lines by establishing “Good Manufacturing Practices.”^1,10-12 How was this accomplished? Through acidification of bottled and canned foods, intended to prevent bacterial growth and prolong shelf life. Today, almost all food that is bottled or canned is pH <4.^11-13

  Today, in the office, I saw a woman from Seattle whom I had first seen a year ago. She had originally come to see me because she knew that I would help her find the best diet for her Barrett’s esophagus with the idea that it might be reversed. (She had been previously diagnosed, biopsy-proven Barrett’s, by a gastroenterologist shortly before coming to see me.)  I knew that pepsin was produced in Barrett’s, and I knew that a low-acid diet was likely to be beneficial. So today, my patient showed me a recent endoscopy/biopsy report from her gastroenterologist: Now a year later, her Barrett’s was gone. How? Low-acid, low-fat, pH-balanced eating with Manuka honey (t.i.d.) and alkaline water. FLASH: Barrett’s esophagus reversed by healthy diet!  In other words, this patient chose lifestyle and dietary modifications over ablation — she had no procedures for her Barrett’s — with the best possible result.

  Connect the dots. While it may sound like a conspiracy theory; it is true. Dietary acid appears to be the primary factor in the prevalence, mechanisms, manifestations (including cancer), and outcomes of reflux disease. Until now, it appears that fundamental nutritional questions related to how food has been preserved for the last two generations may have been overlooked.^1,10,13 In the meanwhile, the proof of the pudding is that people with reflux disease, including some with Barrett’s esophagus, significantly benefit from a low-acid diet. Contrary to popular belief, reflux disease is reversible.^1,10

  Who Should Be Screened for Esophageal Cancer?
  

  Last month alone, I found Barrett’s esophagus in two refluxers in their 20s. Reflux used to be a disease of people in middle age. Not any more. Now, we are seeing advanced disease in young people, and in thin people, too. It’s no longer a disease of just the obese. In fact people with airway reflux tend not to be overweight. But here is a statistic for you: In 2010, the average 12-29-year-old American consumed 160 gallons of acidified soft drinks, almost a half-gallon per person per day (American Beverage Association data).

  I recently reported that a staggering 63% of patients with chronic cough had significant esophageal pathology, including 47% with esophagitis and 8% with Barrett’s.⁹ The problem with reversible-by-healthy-diet reflux disease is that it needs to be properly diagnosed to be properly treated.^1,9,10

  Today, 40% of Americans have reflux (22% with esophageal reflux another 18% with airway reflux). If any disease needs screening it is reflux. The introduction of transnasal esophagoscopy (TNE) a decade ago provided an important advance in the care of patients with reflux, dysphagia (swallowing problems), and esophageal pathology.¹⁴ The TNE endoscope offers brilliant illumination, excellent image quality, and the capability to obtain biopsies. TNE is inexpensive, well-tolerated by the vast majority of patients, though it is performed in a comfortable, seated, awake patient who can walk out the door as soon as the procedure is complete.

  The esophageal examination test that is expensive and wasteful is EGD (esophagogastroduodenoscopy) under aesthesia, and not TNE, but some medical specialists have a huge financial stake in maintaining the status quo of EGD. Last year in the U.S., 10 million sedated EGDs were performed at a “facility fees” cost of $10 billion (and that doesn’t include physician fees or biopsies).

  TNE is one of the most important and cost-effective advances in the diagnosis and prevention of serious disease in the past decade. Who should have it? The 100 million Americans with reflux. It is foolish to lump TNE with any other screening tests that have low yield and high cost. Save the baby!

  References

  1. Koufman JA. Low-Acid Diet for Recalcitrant Laryngopharyngeal Reflux: Therapeutic Benefits and Their Implications. Ann Otol Rhinol Laryngol 120:281-87, 2011.

  2. El-Serag HB. Time trends of gastroesophageal reflux disease: A systematic review. Clin Gastroenterol Hepatol 2007;5:17-26.

  3. Altman KW, Stephens RM, Lyttle CS, et al. Changing impact of gastroesophageal reflux in medical and otolaryngology practice. Laryngoscope 2005;115:1145-53.

  4. 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.

  5. 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.

  6. Koufman JA, VanHorn G. The Prevalence of Reflux in America—The Times Square Study. (Unreported data), 2010 (manuscript in prepartion).

  7. Halum SL, Postma GN, Johnston C, Belafsky PC, Koufman JA. Patients with isolated laryngopharyngeal reflux are not obese. Laryngoscope 2005;115:1042-5.

  8. 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.

  9. Koufman J. Diagnosis and management of non-pulmonary chronic cough. Presented at the annual meeting of the American Broncho-Esophagological Association, April 19, 2012, San Diego, CA (submitted to the Annals of Otology, Rhinology & Laryngology).

  10. Koufman JA, Stern JC, Bauer MM. Dropping Acid: The Reflux Diet Cookbook & Cure. Reflux Cookbooks LLC (Brio Books), Minneapolis MN, 2010.

  11. “Acidified Foods.” Code of Federal Regulations—Title 21—Food and Drugs Chapter I, Department of Health and Human Services Subchapter B—Food for Human Consumption Part 114. United States Food and Drug Administration. Arlington, VA, Washington Business Information, 2010.

  12. “Generally Recognized as Safe Food Additives: FDA Database of Selected GRAS Substances.”  United States Food and Drug Administration. National Technical Information Service, Springfield, VA, 2009.

  13. “Food Safety: FDA Should Strengthen Its Oversight of Food Ingredients Determined to Be Generally Recognized as Safe (GRAS).”  GAO-10-246: United States Government Accountability Office, February 3, 2010.

  14. 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.

Thursday, March 7, 2012. I’ve experienced something unique this year, both my personal experience and in my medical practice, in my patients. I’ve been calling it the “never ending virus” for two month already. Here is my personal case history:

In mid-December I felt that I was coming down with an upper respiratory infection (URI), with excessive sneezing, a runny nose, and fatigue. Just before Christmas, about a week after the onset of the first symptoms, I developed a terrible dry cough. Five days after that when I arrived in Florida for a golf holiday, I found myself sick in bed with what seemed like the flu, but without fever, and a terrible cough. The malaise was so severe I got out of bed only to go to the bathroom, drink water, eat cereal, or soup. On the third day in bed, I developed right maxillary sinusitis (with fullness and pain in my face and teeth). With effort I made it to the drug store to pick up an antibiotic, and thankfully, the sinusitis resolved within a few days. After four days in bed, and oh yes, drinking Nyquil like it was water, on the last day of my holiday vacation, I got up feeling weak and dizzy, and looking the mirror it looked like I’d lost a significant amount of muscle mass.

The next week (back at work), I was exhausted. The following week the cough got worse again, and it was keeping me from sleeping. The fatigue was difficult and I saw my doctor, who on chest auscultation (examination) thought that I might have pneumonia. So, he put me on Levaquin, a strong antibiotic. My lungs cleared quickly, but I went straight downhill having had a serious side-effect of the Levaquin, one that involved all my muscles and joints. I even got fluid in my knee. Moving and walking was difficult, but I continued to work. I was concerned about the Levaquin complication because I did not know how long it would take for my joints to get better. (Now six weeks later, my joints are fine except for my left knee that remains rather stiff.)

At the end of January I was feeling pretty good except for my joints, when all of a sudden, it began all over again. I developed the same URI with sneezing, copious rhinorrhea (runny nose), and cough.  I thought that one developed immunity from a virus after a URI; nevertheless, I felt that I was starting my fourth recrudescence. It took about ten days for it to subside, and this time no complications. By mid-February I was back to my normal self with good energy. But again one day, I again began coughing with sneezing and runny nose all over again. This came and went in two days. Meanwhile, through the month of February I was using an allergy nasal spray thinking it might be allergies, but it is not allergy, this strange affliction.

To set my illness in perspective: M 29-year-old daughter had this URI with severe cough for six weeks, not unusual for a viral URI. My sister has had a similar on and off again respiratory infection for a three months now; and recently, David Letterman (with apparent nasal congestion) announced, “I’ve had a cold for five months now.”

Now come my patients. Today, I saw a 25-year-old man with symptoms of an on-again-off-again URI for a month. On examination, his entire nose and throat looked like a severe respiratory URI with mucus of varying viscosity everywhere. The watery stuff was dripping down from above, like a waterfall, and there was thick, white, almost Elmer’s-glue-like mucus on the pharynx, and the entire larynx (voice box) was swollen with watery edema. And there was  and mucus everywhere. That is the pattern of an acute upper respiratory infection, but young people don’t get sick for 4-6 weeks. Another strange thing, I have some singers coming in with no real symptoms except for mild hoarseness who appear to have findings of a rip-roaring URI; see below.

Findings: thick and thin mucus, diffuse inflammation (redness and granularity of all the nose/throat tissue)

Furthermore, many of my patients shared my experience of getting well, only to have full blown recrudescences (this terrific word means “breaking out anew”). Different people’s manifestations of this NEVER-ENDING VIRUS tend to remain constant for each individual, meaning that the on-again-off-again-on-again pattern is usually with the same symptom complex in each person. (I was the only person I know who developed typical URI symptoms, then sinusitis, then pneumonia.) Most people with this URI either do or don’t develop cough.

I’ve spoken to colleagues in internal medicine and expressed concern about “the never-ending virus,” but I have not gotten any answers. Here is why I am concerned. Usually after a URI one has immunity; you don’t get the same virus back again just after it’s over. That just doesn’t happen in my experience, but that is what is happening this year. It’s almost as though the virus in our community this year does not confer immunity against itself. Of  concern is the question of why?  Why doesn’t the immune system banish this virus by producing antibodies after the infection? Instead, it comes back again and again like a bad penny. I am posting this because I am interested in other people’s experience, particularly people who work in the fields of infectious disease and immunology.

In conclusion, the URI virus in our community this year does not follow a recognized pattern; the usual post-URI immunity seems to be lacking. Of course the big question is might this NEVER-ENDING VIRUS be different? Could it possibly be altering the immune system in some pernicious way? Would that not explain its bizarre recurring pattern?

Final note: Yesterday I was sneezing and coughing again, and now I must say I’ve had this NEVER-ENDING VIRUS for a full two months. HELP!

The Never-Ending Virus is “SILENT” in Some Patients

Today, a patient with laryngopharyngeal (airway) reflux came in saying that her reflux symptoms (chronic throat clearing, a sensation of a lump in the throat, sore throat and hoarseness) were much worse. When I examined her I found the same evidence of an acute URI that I described above; however, she didn’t think that she was sick. (The photos from her exam are shown below.) This is a “silent: URI? The whole thing here is very odd!

Click on the picture to see it in greater detail: the mucus is like glue!

Have you ever wondered why there are so many different (medical) terms for acid reflux?  There are so many terms because different  medical specialist groups use different terms that they invented to describe their viewpoints.  The table below shows the most common ones.

Most Common Medical Terms for Acid Reflux
Gastroesophageal reflux disease (GERD)
Laryngopharyngeal reflux (LPR)
Gastro-oesophageal reflux disease
Extraesophageal reflux disease
Supraesophageal reflux disease
Esophago-pharyngeal reflux
Gastropharyngeal reflux
Atypical reflux disease
Esophageal erosions
Barrett’s esophagus
Reflux esophagitis
Reflux laryngitis
Silent reflux
Esophageal reflux
Airway reflux

Reflux is like the elephant in the famous tale 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 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. “Aha, you are both wrong,” he says. “The elephant is rather like a giant leaf.” Each of the blind men embraces a part of the truth, but none understands its entirety.

In the case of reflux, the three blind men are represented by three medical specialties, each one focusing on a different part of the aerodigestive tract: (1) The otolaryngologist (ENT physician) specializes in the ears, nose, and throat; (2) the gastroenterologist (GI physician) specializes in the esophagus (the swallowing tube that connects the throat with the stomach); and (3) the pulmonologist (PUL physician) specializes in the lungs. Many other medical specialties encounter patients with reflux as well, including internists, family practitioners, pediatricians, and critical care specialists.

GIs are unfamiliar with the signs and symptoms of airway reflux, but they insist on using diagnostic tests designed for esophageal reflux to evaluate airway reflux, because that’s what they know and understand.

Many gastroenterologists make their livings performing sedated endoscopies, mainly  esophagoscopy (aka EGD, esophagogastroduodenoscopy) and colonoscopy. This involves intravenous sedation, recovery, and it is sometimes associated with serious (even life-threatening) complications.

Sedated EGD is overkill for screening the esophagus for pathology such as Barrett’s in patients with acid reflux. We recommend transnasal esophagoscopy instead. Transnasal esophagoscopy (TNE) can be done in the doctor’s office without sedation, with comfort, and without complications.  Is TNE new? Not really. At the Voice Institute of New York, we have been performing TNE routinely for more than a decade. Gastroenterologists, however, have been reluctant, or at least slow, to embrace this technology. Why?

Last year, there were 10,000,000 sedated endoscopies done in the United States by approximately 10,000 gastroenterologists (GIs). If every GI did endoscopy (which they don’t), then each would have performed 1,000 last year,  that is, 20 per week or 4 per day.

The “facility fees” alone for sedated endoscopy were $10,000,000,000, that’s right, $10 billion!  The average facility fee for endoscopy last year was $1,000. And that’s just the fee that the endoscopy facility received; this does not include the doctors’ professional fees. Do the math; if the GI doctor owned her/his endoscopy facility, and many are owned by groups of GIs, the take “facility fee” take-home would be $1,000,000, that is $1,000 per X 1,000 procedures). GI doctors appear to have a significant conflict of interest in favor of sedated EGD procedures.

When GIs perform sedated EGDs, usually they do not examine the throat. Indeed, the endoscope is usually passed blindly, that is, without viewing the path into the esophagus. This is one of the reasons that GIs do not recognize airway reflux. By the way, it is time to stop using all those different terms for acid reflux. It now makes sense just to use two: ESOPHAGEAL REFLUX and AIRWAY REFLUX.

Patients with Airway Reflux DO NOT Usually Have Esophageal Reflux

We have published articles examining how ineffective GI diagnostics were in patients with airway reflux. We found that 80% of patients with airway reflux did not have esophageal findings of reflux. This is because the airway is 500 times more susceptible to damage from reflux than the esophagus. The latter organ is robust by comparison so that the acid/etc. can pass through the esophagus quickly and then do damage to structures in the airway. In addition, we found that the positive predictive value of esophageal (only) reflux (pH) monitoring in patients with airway reflux was 49%.  Would you get a test that got it right less than half of the time?  And impedance testing isn’t much better.

GIs also do not understand the importance and impact of diet in people with airway reflux. A month ago, I had a patient come see me from Oregon. She had airway reflux, and I started her on the Reflux Induction Diet and antireflux medication. A few days ago she returned dramatically improved. “Your reflux diet makes all the difference in the world,” she reported; then she added, “I went back to my GI and told him what happened, and you know what he said?  ‘I have reflux too, but I don’t want to change my diet; I love burgers and fries and all … so I take pills and they help’.”  After that interaction the patient confided that she wouldn’t be seeing that GI doctor ever again.

Almost One in Five Americans Have Airway Reflux

In the Time Square Study, we found that 22% of Americans had esophageal reflux and 18% had airway reflux. Not surprisingly, many of the people with airway reflux had “silent reflux,” meaning that they suffered acid reflux without heartburn or indigestion. These numbers are a wake-up call. It is time to recognize that airway reflux is common, important, and still under-diagnosed and under-treated. What are the symptoms?

Symptoms of Airway Reflux
Hoarseness
Chronic cough
Choking episodes
Difficulty swallowing
Lump-in-the-throat sensation
Food and/or pills getting stuck
Too much throat mucus
Chronic throat clearing
Shortness of breath
Post-nasal drip
Sore throat
Sinusitis
Asthma

“Asthma” is a very interesting presenting symptom in my clinic. True asthma is characterized by wheezing, trouble getting air out. About 8% of people with airway reflux have reactive airway disease, including laryngospasm, paradoxical vocal fold movement, and pseudo-asthma. With reflux, patients have difficulty getting air in (not out), and they almost always know the difference.

“When you have an ‘asthma’ attack, do you have more trouble getting the air in or out,” I ask, and 90% my patients respond “IN” without hesitation. Most people with adult-onset asthma actually have reflux-related reactive airways disease, and  when the reflux is effectively treated, the “asthma” usually disappears. The same is true of chronic cough symptoms; most are due to reflux.

At present, ENT (ear, nose, and throat) doctors are the ones to see for people with airway reflux, not gastroenterologists. Here is a slight but important paradox: Endoscopy (esophagoscopy, TNE) is not how you diagnose airway reflux. That takes a throat examinations and sometimes special (pH) testing. If one has reflux, however, a screening endoscopy should be performed to rule-out significant esophageal disease. We now know that people with airway and esophageal reflux have a similar incidence of esophageal cancer and pre-cancer. Silent reflux causes just as much cancer and the non-silent type.

Meanwhile, what is missing? What is needed?  In a way, the biggest problem with airway reflux is that most physicians, even those who recognize its symptoms, don’t have a way to confirm the diagnosis. At the Voice Institute of New York, we do special airway reflux testing, and we are now working on two new diagnostics for airway reflux; see www.KoufmanReflux.com. The first is a spit-in-a-cup screening test (similar to a pregnancy test) that detects pepsin, the principle enzyme of the stomach. Pepsin is only made in the stomach so that if a person has detectable pepsin in their spit, they have acid reflux (either airway or esophageal reflux). In preliminary testing, the spit test for pepsin is approximately 90% accurate.  This is terrific for a screening test. We hope that we can have the test, known as Koufman Reflux Test Strips (YouTube video) on the market by the summer of 2012. It will help physicians and their patients by making the right diagnosis.

Also under development by Koufman Diagnostics, is a definitive,  turn-key, airway reflux pH testing system that may be employed by any physician regardless of medical specialty (e.g., pulmonology, gastroenterology, otolaryngology, family practice) to make a definitive diagnosis of airway (and/or esophageal) reflux. The system uses ambulatory pH-monitoring technology with foolproof probe-placement and a software that makes interpretation foolproof.  This test is also coming this year.

If you think you have airway reflux, see an ENT doctor, or come see me here at The Voice Institute of New York.  Also, the book,  Dropping Acid: The Reflux Diet Cookbook & Cure, may help.

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