re·flux n [ L re- back + fluxus flow ] 1: a flowing back 2: a process of refluxing
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 this chapter, I will attempt to describe the whole elephant, drawing in large measure from my almost thirty years of basic scientific and clinical research into reflux disease.1-59
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.
Reflux remains controversial. 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 and LPR are the terms widely used by GIs and ENTs, respectively. See Table 1 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 1
MOST COMMON MEDICAL TERMS FOR REFLUX
Gastroesophageal reflux disease (GERD)
Gastro-oesophageal reflux disease (GORD)
Reflux esophagitis, esophageal erosions
Extraesophageal reflux disease
Supraesophageal reflux disease
Atypical reflux disease
Laryngopharyngeal reflux (LPR)
Silent reflux
In its most elemental form, reflux is the backflow of gastric (stomach) contents into the esophagus (the muscular swallowing tube between the throat and stomach). The term for this is gastroesophageal reflux. Reflux was not actually described until the twentieth century, but severe burning chest pain after eating, known as heartburn, was recognized in antiquity as a predictable outcome of gluttony.1
Reflux as a disease was first reported in 1935 by Winkelstein,60 who described “peptic ulcer of the esophagus.” He postulated that the esophageal injury was due to the backflow of the contents from the stomach. Prior to that, physicians had recognized diseases of the esophagus such as erosions, inflammation, and stricture (narrowing because of scarring), along with the symptom heartburn. However, they believed that those esophageal findings were attributable to diseases such as tuberculosis and gall stones.1
In the 1940s and 1950s, x-ray imaging of the esophagus became popular (using the barium swallow), and the finding of a hiatal hernia became synonymous with a diagnosis of gastroesophageal reflux disease (hiatal hernia is the name for an anatomic finding seen during a barium swallow; it is a kind of deformity of the stomach valve, known as the lower esophageal sphincter, in which the uppermost portion of the stomach slides upward into the chest).
At that time, the only effective anti-reflux medication was Tagamet (an H2-antagonist, similar to today’s Zantac), and for a person with severe heartburn and a hiatal hernia, anti-reflux surgery was often recommended.61,62 We now know that it isn’t that simple; that is, people can have reflux without a hiatal hernia, and people can have a hiatal hernia without having reflux. What is true is that many people with reflux do have such a hernia, which implies a relatively weak lower esophageal valve. However, the presence of a hiatal hernia is not an indication for surgery. Today, laparoscopic anti-reflux surgery (“fundoplication”) is still the treatment of choice for many patients with severe or recalcitrant reflux, especially LPR.41,62,63
In the 1960s and 1970s, clinical (diagnostic) technology matured, including the growing use of esophageal manometry (to assess and measure swallowing and esophageal function),64,65 flexible endoscopes and endoscopy,66 and pH (acid) monitoring systems.67-69 With these diagnostics and some new treatments, a better understanding of managing GERD began to emerge.70-87 LPR, however, was still in the shadows.
Meanwhile, remember those three blind men? It is worthwhile to consider the history of reflux in terms of who discovered what and when. The fragmentation of the understanding of reflux as a disease is in large measure because of turf battles in academic medicine and ignorance of the research from other specialties.
In recent history, otolaryngology (ENT) and gastroenterology (GI) have been sharing the reflux pie, but the father of modern endoscopy was an ENT surgeon named Chevalier Jackson.88 In 1890, Jackson invented the distal-lighted esophagoscope—a hollow, rigid metal instrument for examining the esophagus.1 For most of the twentieth century, Jackson and his disciples in ENT were the ones performing endoscopy of the breathing and digestive passages.
In the late 1960s, with invention of the flexible endoscope,66 many of the specialists in gastroesophageal reflux disease (GERD) became gastroenterologists.
In the early 1980s, there was cooperation and collaboration between GI and ENT,3,5-7 but with the discovery of laryngopharyngeal reflux (LPR), reflux into the larynx (voice box) and pharynx (throat), and with the advent of transnasal esophagoscopy24,33,45,58,89,90 (TNE), cooperation broke down. The problem was one of perception—each group witnessed different reflux manifestations and syndromes in their patients.
Many reflux patients are frustrated because their doctors only understand classical GERD, so if their symptoms differ, they’re out of luck. While I was writing this book, I gave a preview chapter to a patient who shared it with her local doctor. She then reported to me that her local doctor insisted that her barium swallow showed no signs of reflux, and, that my chapter was “a lot of bunk.” “But he didn’t even read it,” she said. I tell this story here to emphasize that there is still a wide schism between specialties.
Prior to my work on LPR (silent reflux), there were a few brave pioneers who suggested that reflux was not just GERD; 91-100 however, the literature on it was sparse and most of the reports anecdotal. Some of those who deserve credit for seminal thinking on LPR and who most influenced me were Nels Olson,96 Don Cherry,91 Paul Ward,100 Paul Chodosh,94 and Bob Toohill.101 I remember Dr. Olson warning me that LPR was a hot potato subject, and that some of his academic contemporaries had tried to discredit him over his belief that LPR was ubiquitous and caused a myriad of airway diseases. Of course, when Dr. Olson talked about reflux, he referred to it as GERD. In the past two decades, there have been many reports linking reflux to diseases of the ears, nose, throat, and lungs.95-124
In 1991, the year my Triological Society thesis was published,1 I coined the term laryngopharyngeal reflux. I felt we needed a new way to describe the type of “silent” reflux seen in many of our patients. I chose that particular term to call attention to how the symptoms and manifestations were laryngeal and pharyngeal, not esophageal. I also believed that the diagnosis and treatment of LPR were different than for GERD. The idea was to intentionally create a nosological distinction between the specialties so that ENT physicians would consider ideas that did not yet have credibility among GI colleagues.
Incidentally, it was Dr. Walter Bo, chair of the anatomy department at Wake Forest University, who first uttered the term “silent reflux.” In 1988, Walter was my patient. After I explained how one could have reflux without also having heartburn, he rolled his eyes and said, “I get it. I have the silent kind of reflux.” “Yes, Walter,” I said. “That’s it; you have SILENT REFLUX.”
Although I was trained as an ENT (ear, nose, and throat) doctor, I began limiting my practice to laryngology (voice, throat, and swallowing disorders) in 1981, the same year I began noticing patients with laryngeal manifestations of reflux without heartburn. At the time, I was at Wake Forest University, and I went to gastroenterologists there to discuss my patients.
The head of the department was initially skeptical that reflux could actually affect the larynx. So I convinced one of his fellows to help me study my patients with hoarseness using pH devices that were available for monitoring GERD in the GI department.
In 1984, we began to study patients with laryngeal inflammation, whether or not they had GI symptoms; most of them didn’t. The patients actually wore two separate pH monitors—small, soft catheters, one of which went into the esophagus, the other into the throat. Both tubes were connected to minicomputers that continuously measured acidity. The computers recorded any reflux events that occurred and stored the information for subsequent analysis.
Thus was born ambulatory 24-hour double-probe (simultaneous pharyngeal and esophageal) pH monitoring.
We reported our first pH testing results in 1986.5 Yes, the patients with hoarseness had reflux into the throat. By 1987, I had my own reflux-testing laboratory and we were beginning to accumulate data suggesting that LPR patients typically had reflux patterns that were qualitatively and quantitatively different from patients with classic GERD.1,6,7,15,17
Sadly even today, quality reflux testing is only performed in a few places. At the Voice Institute of New York, we routinely employ complete high-definition manometry, ambulatory (simultaneous pharyngeal and esophageal) pH monitoring with ISFET technology and new software that analyzes the data at every pH level,3 and transnasal esophagoscopy. This combination of technologies defines the patterns, mechanisms, and severity of disease so that treatment can be customized for each patient. That is the state of the art.
By 1989, we already understood that the mechanisms and patterns of reflux in LPR were different than those of GERD.1,3-7,23,27,33 Most GERD patients had heartburn, esophagitis, dysmotility, and a supine (nocturnal) reflux pattern with prolonged periods of acid/pepsin exposure.1-3,5-7,10,17,27,32,33 Conversely, LPR patients usually did not have heartburn or esophagitis, and an upright (daytime) reflux pattern predominated.1-3,5-7,32,33 A summary of the typical differences between LPR and GERD is shown below.
Table 2
SUMMARY OF THE TYPICAL DIFFERENCES BETWEEN GERD & LPR
PPIs = Proton pump inhibitors (such as Nexium, Protonix, Prilosec, Prevacid, and Zegerid)
One of the key differences between LPR and GERD is that the thresholds for laryngeal and esophageal damage are quite different.1,39,42,49 Based on normative pH monitoring data, one can have up to 50 esophageal reflux (pH <4) events, occurring mostly after meals, and that is considered normal. In the larynx, as few as three episodes a week may be too many.1 In addition, pepsin, and not acid, is the primary injurious component of the refluxate.1,28,39,125-128 From animal experiments, we know that acid and pepsin in combination (i.e., activated pepsin) produces more tissue damage than any other combination of enzymes. Adding bile salts to the mix, for example, reduces the potency of the refluxate.1,127,128
The GI and ENT literature both agree that it is pepsin and not acid that produces tissue damage.1,127,128 Unfortunately, some of the GI literature suggests that pepsin is inactive above pH 4; however, those experiments were done using pig pepsin.126 Our laboratory has unequivocally demonstrated that human pepsin is active up to pH 6.54 See the pepsin activity curve in “What You Eat Could Be Eating You,” page 24.
Most of the important bench research including reflux-related cell biology was performed in my laboratory at Wake Forest University and with collaborators in the United Kingdom.28,39,42,47-49,51,53-57 The papers were reported in prestigious, peer-reviewed medical journals, yet it would seem that this robust scientific literature has gone largely unnoticed outside the specialty of ENT.
Here is a summation of the most important findings and their implications for understanding reflux disease:
• Pepsin, the main digestive enzyme of the stomach, can attach (bind) to tissue and destroy protein, gain access to the cell, and disrupt normal cellular function.39,42,48,49,53-55,124,129
• Pepsin requires some acid for its activation, and human pepsin is active across the pH range from 1–6, with 100 percent activity at pH 2 and 10 percent activity at pH 6.54
• Patients with reflux laryngitis (LPR) have pepsin on and within their laryngeal tissue, and that pepsin can remain attached for a long time, which may be reactivated by acid from any source, including acidic foods and beverages.42
• In studies to date, the tissue-damage protein profiles for reflux laryngitis and for laryngeal cancer are similar;3,39 see Table 4.
• Reflux is associated with the development of Barrett’s Esophagus, a precursor of esophageal cancer; it occurs as frequently in patients with LPR symptoms as it does in patients with classical GERD.131-135
• Clinically, patients with reflux symptoms improve when the amount of acid in the diet is limited.136 Dr. Koufman reported results of a clinical trial of a series of patients with recalcitrant LPR. (Recalcitrant was defined as failed treatment on high-dose anti-reflux medicines.) These patients were treated with the Induction Reflux Diet (nothing below pH 5) for a minimum of two weeks; and 95 percent improved significantly, and notably some became completely symptom free.136
• Finally, the prevalence of all forms of reflux is increasing, especially among the younger population in the United States.137
In attempting to describe the whole elephant, I must reiterate that the three blind men exemplify the fragmentation of the medical community. In 2009, I spoke on “Specialization: When Being the Best Isn’t Good Enough,” in a presidential address to the American Broncho-Esophagological Association. In that speech, I urged that the specialties of otolaryngology, gastroenterology, and pulmonology might be merged to form a new “specialty,” Integrated Aerodigestive Medicine. The problem with specialists, I argued, is that they only know about a defined anatomic zone; however, reflux is a disease of the entire aerodigestive tract, the components of which are shown in the Table 3.
These anatomic zones are all connected to each other and it is preposterous to presume that reflux disease respects the boundaries of our medical specialties. It is puzzling, for example, why pulmonary doctors have been slow to embrace reflux as an important cause of pulmonary disease.8,15,106,107 In my opinion, LPR is responsible for up to 70 percent of lung disease.
I am an expert on LPR and silent reflux. I actually coined both terms. I recognize, however, that I am still one of the blind men in spite of my desire to take care of whole patients. This work points to the urgent need for collaborative research, particularly in translational cell biology that crosses specialty lines.
In a later section of this chapter, “The Missing Link,” you will see that there is another gaping hole in our knowledge: We know almost nothing about environmental medicine and about the health risks of what we eat. I fear that within our lifetimes we have all been part of an appalling scientific experiment in which unintended and unforeseen consequences of well-intentioned scientists—whose focus was to make food safe from bacterial contamination—might have led us to a national public health crisis. Reflux is ubiquitous and its consequences are serious, even deadly.
Table 3
COMPONENTS OF THE AERODIGESTIVE TRACT
Nose and sinuses
Mouth (oral cavity)
Throat (pharynx)
Voice box (larynx)
Swallowing tube (esophagus)
Stomach and upper intestines
Breathing tube (trachea) and lungs
One of the most frequent questions patients ask is whether reflux can cause cancer. I believe the answer is an emphatic yes. That is part of the reason this book is so concerned about the acidity of today’s typical diet.
We have not yet proven that reflux causes laryngeal and vocal cord cancer, but there is strong circumstantial clinical evidence along with bench research to support it.1,7,9,39,114,119-124 We believe that one can get laryngeal cancer without smoking, but not without the presence of reflux.4,39 This section presents six arguments to support this concept.
1. Many patients with laryngeal cancer are non-smokers or ex-smokers. We prospectively studied 50 adult patients with early vocal cord cancer.9 Of them, 44 percent (22/50) were active smokers, 42 percent (21/50) were ex-smokers with a median duration of smoking cessation of eight years, and 14 percent (7/50) were lifetime non-smokers. Using pH monitoring, we found that 68 percent of the patients had reflux, almost twice as many as those who were actually smokers. And remember, in the study group, there were seven lifetime non-smokers.9
2. Some people get recurrent, small, reflux-related vocal cord cancers that are periodically removed with a surgical laser. We’ve seen many such cases over the years. Significantly, almost half of those patients stop making cancer when their reflux is controlled. The same is true for patients with pre-cancers called dysplasia and leukoplakia.1,114
3. When different groups of patients are tested for reflux, including those with cough, sore throat, etc., the highest proportion of those demonstrating reflux are the cancer patients. In 1991, we reported abnormal reflux testing in 84 percent (21/25) of patients with laryngeal cancer, five of whom were lifetime non-smokers.1
4. We compared the reflux (pH) testing results of smokers and non-smokers and found that smokers had twice as much reflux, both in the esophagus and the throat. Cigarette smoking is specifically associated with relaxation of the upper and lower esophageal valves within two minutes, and reflux episodes occur with two-thirds of cigarettes smoked.55,138
5. Our laboratory has examined the impact of reflux on a cellular level in human patients and in animal models and found tremendous similarities in the larynx between patients who have LPR and patients who have cancer. Of those studies, the most important was an analysis of biopsies for the presence of pepsin within the laryngeal tissue. Pepsin was found in 5 percent (1/20) of normal controls without reflux. On the other hand, 95 percent of LPR patients with reflux into the throat had pepsin in their laryngeal biopsy tissue, and 100 percent (5/5) of laryngeal cancer patients tested had pepsin within the cancerous tissue.39,47,55 In addition, extraordinary landmark experiments in cell biology by Nikki Johnston et al. 42,47,48,51.53,54,124 showed that pepsin up-regulates the genes that cause cancer in a way that suggests that pepsin is actually the cause of laryngeal cancer.124
6. There are similarities between laryngeal cancer and esophageal cancer. Figure 1 below shows the presence of pepsin in reflux laryngitis by a special staining technique (Figure 1A), and within a Barrett’s Esophagus biopsy specimen (Figure 1B). Dropping Acid 168
Figure 1: PEPSIN IMMUNOCHEMISTRY (IHC)
A. Reflux laryngitis showing pepsin by IHC
B. Pepsin in Barrett’s Esophagus by IHC
The table below summarizes the cell biology findings. As you can see, reflux and laryngeal cancer have the same protein profiles except for one stress protein, HSP70.4,39,47-49
Table 4
TISSUE PROFILE OF LPR, CARCINOMA, AND CONTROLS
As previously mentioned, esophageal cancer is one of the fastest growing cancers in the United States, and we are finding Barrett’s Esophagus, a known reflux-related form of pre-cancer, in approximately 7 percent of our LPR reflux patients.33,44,52 It is striking and significant to note that Barrett’s Esophagus is found just as often in ENT patients with silent reflux (symptoms of coughing and hoarseness) as in GI patients with heartburn.134
In summary, there is clinical and scientific evidence that reflux, mainly pepsin, may cause cancer of the larynx and esophagus.
The brown material in biopsy specimens shown in Figure 1A & 1B is pepsin stained by a special technique. It’s easy to see how dietary acid from above could stimulate that pepsin the same way as could acid from below.
One of our biggest concerns is that a huge population of Americans is potentially at risk to develop cancer, and that we have no methodology for identifying the most susceptible. As clinicians, we can certainly say that we are seeing increasingly more and more reflux in increasingly younger patients; and this in our opinion, is an ominous warning sign.
We recognize that we may be criticized as alarmists, and we regret that we cannot prove all of our assertions and beliefs just yet. However, our data and clinical impressions deserve to be in the public domain so that other researchers and clinicians can investigate the relationships we’ve presented. We believe that diet is the missing link and that our diet may be killing us, and it is time for us to aggressively explore these variables and fix them.
By the way, people who are rightfully worried about cancer deserve to be checked. The technology has changed. Doctors can now look inside while patients are awake, comfortable, and without pain, using a technique called transnasal esophagoscopy.29,33,58,134 The idea that you can only be checked for cancer in a special facility and under anesthesia is archaic.
Why is reflux epidemic? Why is esophageal cancer one of the fastest growing cancers in America? Why are so many people with reflux failing medical treatment? We believe that the answer is related to high levels of dietary acid. How and when did this happen?
While this story of the reflux epidemic focuses on acid, we should point out that since WWII there have been four significant dietary trends, counting the increased acidification of prepared foods and beverages, there are: Increased saturated fat; increased sugar (low-glycemic index carbs); and increased use of preservatives, stabilizers, thickeners, and artificial sweeteners. Here’s the story.
Table 5
LANDMARKS AND MILESTONES IN THE AMERICAN DIET
Coca-Cola was invented in 1886 by a pharmacist in Atlanta, and Pepsi Cola came along a few years later.140 These were fountain drinks and weren’t actually bottled until the twentieth century. Coca-Cola rose to prominence as America’s drink during and after WWII. While the recipe and ingredients have changed over the years, this drink and others like it have always been very acidic. The current pH (acidity) of Coca-Cola is 2.8, as acidic as stomach acid itself.
The American Bottlers of Carbonated Beverages was formed in 1919. After many years and a few name changes, they became a national lobby.
The first diet soda pop made its debut in 1952. This represented a new potential market for the soda industry, but it also introduced a host of additives and chemicals. Today, some diet drinks are more acidic than their non-diet counterparts.
In 1955, Roy Kroc started the McDonald’s Corporation. Most baby boomers can remember when they first encountered McDonald’s. (Personally, I recall buying a hamburger in Dedham, Massachusetts, in the early 1960s for 19 cents.)
By 1962, instant foods, such as instant milk and instant pudding, were common in almost every American household. These products were essentially carryovers from WWII rations made palatable for the consumer. Incidentally, it was also around then that I believe the term “mystery meat” was first invented.
In 1963, McDonald’s began advertising meals for families. It was a milestone for marketing and public relations, as well as a paradigm shift—the idea that this type of fast food was appropriate for family dining, that you could get an inexpensive meal outside the home in a fast-food restaurant. Until then, people looked on fast food as inferior, but through this marketing coup, fast food became integral to the American diet. This meant more soda pop, more beef, more fries, and more saturated fat for the nation’s consumers.
By 1965, canned soda pop was available in vending machines, and diet and regular soda came in many flavors. No longer just soda-fountain drinks, these beverages were available 24 hours a day, 7 days a week, for anybody who had a dime and a nickel.
In 1966, the American Bottlers of Carbonated Beverages changed its name to the National Soft Drink Association and went on to become a powerful lobby, successfully fighting consumer groups that attempted to limit access to soda pop in venues such as public schools. In 2004, it changed its name again, this time to the American Beverage Association. In 2009, the ABA spent over $19 million on marketing, promotion, and lobbying, with 25 lobbyists at seven different firms on its payroll—an increase in spending of 1000 percent over the previous election cycle.141 Recently, they have helped defeat laws to raise taxes on high-sugar drinks. You can read more about this online at the Center for Responsive Politics—“Lobbying 2009: American Beverage Association.”141
When high-fructose corn syrup (HFCS) was introduced in the late 1960s, our food supply really changed. Within two decades, it found its way into use in American soda products and other sweetened beverages, as well as other food products. HFCS is more fattening (more calories, ounce per ounce, than sugar) and less expensive than sugar. Since the introduction of HFCS, the public’s consumption of it has grown to equal that of cane and beet sugar. It has recently become a target in America’s battle against the obesity epidemic. Once HFCS became an ingredient in soda, soda became more fattening and higher in lowglycemic sugar.
In response to an outbreak of botulism in 1973, Congress passed Title 21, a law giving the Food and Drug Administration the power to regulate canned and bottled goods that crossed state lines.
The introduction of “New Coke” in 1985 was met with loud boos and great disdain by angry “Coke-aholics,” who complained that it was a syrupy drink without any kick. Coke lovers called it “worse than Pepsi.” At the time, I knew that the “new” Coke was simply a ruse to substitute high-fructose syrup for sugar. Indeed, when “Coke Classic” returned to the market and “New Coke” disappeared, corn syrup had been successfully substituted for real sugar, completing one of the most brilliant cost-savings ploys in manufacturing and marketing history.
In 1990, Congress passed the Nutrition Labeling and Information Act to help guide consumers in making healthy choices about the food they purchase, and to encourage manufacturers to produce healthier products. It suggests a dawning realization that consumers have a right to know what, exactly, they are eating.
By 2003, the obesity epidemic was national news, with a focus on saturated fat and low-glycemic sugar. Meanwhile, despite all the labeling efforts, Americans continued to consume a large portion of their calories from “junk food.”
In 2009, the average annual sugar intake per person was a staggering 142 pounds, the average sodium intake per day was 4500 mg, and the average daily saturated fat intake was approximately 20 grams.142
Title 21 underwent major revisions and was expanded in 1979 with the creation of “Good Manufacturing Practices.” These practices set higher levels of certain food additives and acidity levels in pre-packaged food to discourage bacterial growth and reduce the likelihood of bacterial contamination. The idea that acidification of the food supply might have adverse consequences was not considered in any of the documented discussions about food safety.143
The acidification of food has long been used as a means to preserve it, but it wasn’t until the modern era that the process evolved to prevent and regulate bacterial growth in food traveling long distances to sit on a store shelf. The FDA’s system of “Good Manufacturing Practices” through Title 21 regulations does not regulate what acids and preservatives within a broad group are used; it only requires the pH to be below 4.6, a level low enough to discourage most bacteria. In fact, Title 21 encourages acidification of foods and beverages to pH 4.0 and below:
“Acidified foods shall be so manufactured, processed, and packaged that a finished equilibrium pH value of 4.6 or lower 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.”[April 1, 2002; U.S. Government Printing Office, 21CFR114.80]
That sentence implies that the FDA is incentivizing manufacturers to acidify their product to pH <4.0. “Any suitable method” would presumably allow testing with just a pH meter to show that the pH was less than 4.0.
A corollary question to consider is what kind of food additives are being used to achieve these FDA-regulated acidity levels. It turns out there are 333 substances that are FDA approved—they are affectionately referred to as GRAS, for “Generally Recognized as Safe.”144, 145
In February 2010, the Government Accountability Office146 (GAO), a non-partisan group appointed by Congress to investigate federal agencies, published a scathing report to Congress.
Here is the first paragraph of “Food Safety: FDA Should Strengthen Its Oversight of Food Ingredients Determined to Be Generally Recognized as Safe (GRAS).”147
“FDA’s oversight process does not help ensure the safety of all new GRAS (“Generally Recognized as Safe”) determinations. FDA only reviews those GRAS determinations that companies submit to the agency’s voluntary notification program—the agency generally does not have information about other GRAS determinations companies have made because companies are not required to inform FDA of them. Furthermore, FDA has not taken certain steps that could help ensure the safety of GRAS determinations, particularly those about which the agency has not been notified. FDA has not issued guidance to companies on how to document their GRAS determinations or monitored companies to ensure that they have conducted GRAS determinations appropriately. Lastly, FDA has yet to issue a final regulation for its 1997 proposed rule that sets forth the framework and criteria for the voluntary notification program, potentially detracting from the program’s credibility.”
This states that not only was there inadequate oversight of the approval process, but that food manufacturers themselves and not the FDA were left to determine the “safety” of the additives they chose to employ in their products. For all intents and purposes, this process is industry self-regulated, providing the food additives comply with the list of approved GRAS substances. This is like asking tobacco manufacturers to tell us whether cigarette smoke is harmful or not.
Throughout the scientific community and in the literature and published reports dealing with food safety and food additives, we have not seen concerns raised about the possible adverse health consequences of food acidification. By the way, 13 percent of the GRAS substances are acids, including hydrochloric acid, which is considered a safe food additive.
An interesting report in September 2009 from the Ohio State Medical Center found that the age-adjusted incidence of all cancers among Amish adults in Ohio was 60 percent that of other adults, and only 37 percent of the control group for “tobacco-related” cancers139—including of the pharynx, larynx, and esophagus. In addition to the fact that the Amish drink and smoke less, the authors never specifically discussed the role of diet. We suggest that one possible explanation for the favorable cancer rates among the Amish is that they don’t eat highly acidified and preservative-laden food.139
It is important to remember that reflux causes many different symptoms other than heatburn and indigestion. Silent reflux affects the voice box, throat, and lungs, and causes symptoms of cough, sore throat, hoarseness, and asthma, among others. Those are the most common symptoms for which people see doctors in America. Therefore, it is important for both doctors and patients to recognize that reflux is not always classic reflux (gastroesophageal disease, GERD). Based upon the author’s experience, it is likely that reflux is grossly under-diagnosed and under-treated. For a review of the symptoms, see “How Do I Know if I Have Reflux?” on page 31.
Why is reflux epidemic and why are esophageal cancer rates soaring? The cell biology (basic science) of reflux in conjunction with clinical experience has shown that a highly acidic diet is harmful for people with reflux. Amazing as it may seem, until now no one has investigated this problem, but even more amazingly no one has ever considered the possibility that there might be adverse health consequences of systemic acidification of America’s food.
We believe that acidic food is indeed the reason reflux is epidemic and the reason that esophageal cancer (and pre-cancer, i.e., Barrett’s esophagus) is increasing in prevalence so dramatically. From our point of view, we try to eat fresh, organic, non-processed foods and generally avoid acids. For most people, there is probably a middle road—having a glass of orange juice or soda pop once in a while doesn’t cause reflux disease—but if that’s all you drink day in and day out, it’s likely to be a problem. For people with known reflux disease, a period of “acid/pepsin detox” makes good sense.
People will ask if we have proven these claims beyond a reasonable doubt—that dietary acid causes disease. We respond that we have cited here sound scientific evidence and the state of the art of clinical medicine. We believe that our data are compelling and speak for themselves. It is likely that we are dealing with an important public health issue. Yes, we are worried about the implications of all this, aren’t you?