Low-Acid Diet for Recalcitrant Laryngopharyngeal Reflux: Therapeutic Benefits and Their Implications
←
→
Page content transcription
If your browser does not render page correctly, please read the page content below
Annals of Otology. Rhinology & Laryngology 120(5):281-287.
© 20t I Annals Publishing Company. All rights reserved.
Low-Acid Diet for Recalcitrant Laryngopharyngeal Reflux:
Therapeutic Benefits and Their Implications
Jamie A. Koufman, MD
Objectives: Laryngopharyngeal reflux (LPR) is an expensive, high-prevalence disease with a high rate of medical treat-
ment failure. In the past, it was mistakenly believed that pepsin was inactive above pH 4; however, human pepsin has
been reported to be active up to pH 6.5. In addition, it has been shown by Western blot analysis that laryngeal biopsy sam-
ples from patients with symptomatic LPR have tissue-bound pepsin. The clinical impact of a low-acid diet on the thera-
peutic outcome in LPR has not been previously reported. To provide data on the therapeutic benefit of a strict, virtually
acid-free diet on patients with recalcitrant, proton pump inhibitor (PPI)-resistant LPR. I performed a prospective study of
20 patients who had persistent LPR symptoms despite use of twice-daily PPIs and an H2-receptor antagonist at bedtime.
Methods: The reflux symptom index (RSI) score and the reflux finding score (RFS) were determined before and after
implementation of the low-acid diet, in which all foods and beverages at less than pH 5 were eliminated for a minimum
2-week period. The subjects were individually counseled, and a printed list of acceptable foods and beverages was pro-
vided.
Results: There were 12 male and 8 female study subjects with a mean age of 54.3 years (range, 24 to 72 years). The
symptoms in 19 of the 20 subjects (95%) improved, and 3 subjects became completely asymptomatic. The mean pre-diet
RSI score was 14.9, and the mean post-diet RSI score was 8.6 (p = 0.020). The mean pre-diet RFS was 12.0, and the mean
post-diet RFS was 8.3 (p < 0.001).
Conclusions: A strict low-acid diet appears to have beneficial effects on the symptoms and findings of recalcitrant (PPI-
resistant) LPR. Further study is needed to assess the optimal duration of dietary acid restriction and to assess the potential
role of a low-acid diet as a primary treatment for LPR. This study has implications for understanding the pathogenesis,
cell biology, and epidemiology of reflux disease.
Key Words: acid reflux, adenocarcinoma, antireflux, Barrett's esophagus, chronic cough, diet, esophageal cancer, gas-
troesophageal reflux disease, heartburn, hoarseness, laryngopharyngeal reflux, low acid, low fat, pepsin, proton pump
inhibitor.
INTRODUCTION jury — and it is peptic (not acid) injury.'
(Pepsin does, however, require some acid for activa-
Laryngopharyngeal reflux (LPR) is a controver-
tion.) We previously showed that 19 of 20 patients
sial, high-prevalence disease, and it differs from
(95%) with clinical and pH-documented LPR had
classic gastroesophageal reflux disease (GERD) in
tissue-bound pepsin identifiable by Western blot
many ways.'"'" Typically, patients with LPR have
analysis, as opposed to only 1 of 20 control subjects
daytime (upright) reflux without having heartburn
(5%).^ In addition, peptic injury is associated with
or esophagitis.'-^ In addition, one of the most im-
depletion of key protective proteins, including car-
portant differences between LPR and GERD is that
bonic anhydrase, E-cadherin, and most of the stress
the threshold for laryngeal tissue damage is much
lower than that for the esophagus.'-''** As many as
50 reflux episodes (less than pH 4) per day are con- Equally important in understanding the biology
sidered normal for the esophagus, whereas as few of LPR is consideration for the stability and spec-
as 3 reflux episodes per week are too many for the trum of activity of human pepsin.'•* In the past, it
larynx.' was mistakenly believed that pepsin was inactive
above pH 4.' The early experiments on which that
THFRAPEUTIC IMPLICATIONS OF CELL BIOLOGY result was based were performed with porcine pep-
OF LPR
sin, and not human pepsin. Indeed, pig pepsin is in-
The cell biology of LPR holds the key to under- active at greater than pH 4; however, human pepsin
standing the susceptibility of the larynx to peptic in- retains some of its proteolytic activity up to pH 6.5,
From the Voice Institute of New York. New York. NY.
Presented at the meeting of the American Broncho-Esophagological Association. Las Vegas, Nevada. April 28-29.2010.
Correspondence: Jamie A. Koufman. MD. Voice Institute of New York. 200 W 57th St. Suite 1203, New York, NY 10019.
281
282 Koufman, Low-Acid Diet for Laryngopharyngeal Reflux
TABLE 1. TRADITIONAL ANTIREFLUX DIET AND
LIFESTYLE MODIFICATION PROGRAM
If you use tobacco, quit, because smoking causes reflux.
Do not wear clothing that is too tight, especially trousers,
corsets, and belts.
Avoid exercising, especially weight-lifting, swimming,
jogging, and yoga, after eating.
Do not lie down after eating; do not eat within 3 hours of
bedtime.
Elevate the head of your bed if you have nighttime reflux
(hoarseness, sore throat, and/or cough 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,
Human pepsin activity curve. (Data from Johnston et citrus fruit or juice, carbonated beverages (soda), beer, hard
al.'") liquor, wine, mints, and chocolate.
depending on the substrate.•'' The pepsin activity this induction refiux diet to exclude all recognized
curve is shown in the Figure.'"* Peak peptic activity reflux trigger foods, as well as anything that we iden-
(100%) occurs at pH 2, but there is still some (10%) tified to be acidic (below pH 5). Eggs and red apples,
activity at pH 6.'"* In other words, clinical disease for example, used to be on the induction diet, but
(LPR) is associated with tissue-bound pepsin,^ and we found that those foods caused problems for some
laryngeal damage occurs at pH 5.0 or less.* of our patients, so they were removed. Thus, the ap-
CLINICAL CONSIDERATIONS proved foods and beverages list for the induction re-
flux diet evolved to its present form (Table 2),
For more than 25 years, LPR was diagnosed in
my practice by the symptoms and findings of LPR
MATERIALS AND METHODS
and by ambulatory 24-hour (simultaneous pharyn-
geal and esophageal) pH monitoring,'"^•'' Treatment All of my adult patients with pH-documented
for moderate to severe LPR was typically twice-dai- LPR on "maximum" antirefiux therapy (twice-daily
ly proton pump inhibitors (PPIs) with an H2-recep- PPIs with an H2-receptor antagonist at night) were
tor antagonist at bedtime and an antireflux dietary eligible for the study if they were failing to improve
and lifestyle modification program (Table 1). on medical treatment and did not have potentially
life-threatening manifestations of LPR. Specifically
There was some customization of the eonvention- excluded were patients with airway stenosis, laryn-
al antireflux protocol, eg, one cup of coffee a day, geal neoplasia, and/or pulmonary disease. Medical
no citrus, no carbonated beverages. We have long treatment failure was defined as no improvement
recognized that some patients who drank excessive in symptoms — according to a validated outcomes
amounts of carbonated beverages might gain control measure, the reflux symptom index (RSI)'*'^ —
of their LPR simply by eliminating those beverag- on office visits at least 2 months apart. Incidental-
es. Indeed, carbonated beverage consumption is one ly, it has been my routine practice for the past 25
of the most common identifiable causes of medical years to have all patients complete the RSI at every
treatment failure in LPR. visit.
With our 2007 study'"* showing peptic activity Before inclusion in the low-acid diet study, pa-
up to pH 6,5, and having previously found (by im- tients were offered other alternatives such as chang-
munohistochemical analysis) pepsin within the tis- ing their antireflux medications or evaluation for
sue biopsy specimens of patients with LPR,^ we antireflux surgery. If the low-acid reflux diet was
recognized that tissue-bound pepsin in these pa- elected (Table 2), patients had to agree to be compli-
tients might be activated by exogenous hydrogen ant with the conditions of the diet, which was very
ions from any source, including dietary ones. Con- restrictive (nothing below pH 5). For example, the
sequently, in 2008 we began measuring the pH of diet allows no fruit except bananas and melons. Pa-
common foods and beverages and restricting pa- tients were counseled about what they could and
tients with LPR from consuming anything below could not eat and were provided with a handout that
pH 5 for a trial period of 2 weeks. To our surprise, explained the purpose of the diet and its scientific
this appeared to have outstanding therapeutic bene- basis, as well as a list of foods and beverages that
fits for many patients. were allowed. Study subjects were instructed to eat
In the ensuing few years, we continued to refine only from the list of the items in Table 2 for 2 weeks
Koufman, Low-Acid Diet for Laryngopharyngeal Reflux 283
TABLE 2. INDUCTION REFLUX DIET because 1) the strict, low-acid, induction reflux diet
Agave carried no risk of harm; 2) the diet was a logical ex-
Aloe vera tension of the traditional antireflux diet; 3) alterna-
Artificial sweetener (maximum 2 teaspoons per day) tive therapeutic alternatives were neither denied nor
Bagels and (non-fruit) low-fat muffins precluded; and 4) there was no risk of violation of
Banana (great snack food) patient confidentiality, as no one but the author had
Beans (black, red, lima, lentils, etc) access to the study data.
Bread (especially whole grain and rye)
RESULTS
Caramel (maximum 4 tablespoons per week)
Celery (great snack food) There were 12 male and 8 female subjects with a
Chamomile tea (most other herbal teas are not acceptable) mean age of 54.3 years (range, 24 to 72 years). All
Chicken (grilled, broiled, baked, or steamed; no skin) of the study subjects claimed complete compliance
Chicken stock or bouillon
with the prescribed diet. Nineteen of the 20 subjects
Coffee (maximum 1 cup per day; best with milk)
(95%) improved on the low-acid diet, and 1 got
worse. Three subjects became completely asymp-
Egg whites
tomatic, and another went from an initial RSI score
Fennel
of 28 to a post-diet RSI score of 4. The mean pre-
Fish (grilled, broiled, baked, or steamed)
diet RSI score was 14.9, and the mean post-diet RSI
Ginger (ginger root, powdered, or preserved)
score was 8.6 (p = 0.020); the mean RSI improve-
Graham crackers
ment was 6.3. The mean pre-diet RFS was 12.0, and
Herbs (excluding all peppers, citrus, garlic, and mustard)
the mean post-diet RFS was 8.3 (p < 0.001). The
Honey data are shown in Table 3.
Melon (honeydew. cantaloupe, watermelon)
Mushrooms (raw or cooked) DISCUSSION
Oatmeal (all whole-grain cereals)
In 1981,1 was emergently consulted to see a pa-
Olive oil (maximum 2 tablespoons per day)
tient with airway obstruction. Portable endoscope in
Parsley hand, I rushed to the hospital to see a stridulous pa-
Pasta (with nonacidic sauce) tient. She calmly pointed to her throat and gasped,
Popcorn (plain or salted, no butter) "Can't breathe...acid reflux." After a quick bedside
Potatoes (all of the root vegetables except onions) endoscopy, I took her to the operating room and re-
Rice (healthy, especially brown rice, a staple during induction) moved the two largest obstructing vocal process
Skim milk (alternatively, soy or Lactaid skim milk) granulomas that I have ever seen before or since.
Soups (great homemade with noodles and vegetables) The patient was placed on a postoperative regimen
Tofu of high-dose cimetidine, head-of-bed elevation, and
Turkey breast (organic, no skin) a restricted diet: no fried food, no coffee, no toma-
Turnip toes, onions, garlic, cheese, chocolate, or mints, as
Vegetables (raw or cooked, but no onion, tomato, or peppers) well as no late eating. Under that treatment, the pa-
Vinaigrette (maximum 1 tablespoon per day; toss salads) tient got well. She was my introduction to LPR.
Whole-grain breads, crackers, and breakfast cereals
In the 30 years since, reflux medications have
evolved, and now many patients with LPR are start-
or until the first follow-up visit thereafter. ed on "maximal antireflux treatment" consisting of
I performed a laryngeal examination with each of- twice-daily PPIs (before breakfast and before the
fice visit, as is the routine for management of LPR. evening meal) and an H2-receptor antagonist at bed-
The reflux finding score (RFS)20 was calculated for time.2' Although this regimen results in better acid
each patient for each visit; however, for this study, suppression than did previous medical therapy, there
it was not blinded, as it was anticipated that there is still a significant rate of medical treatment failure
would be no significant change in the RFS. We have (10% to 17%).22-23 It is presumed that PPI failure is
previously reported that the laryngeal findings of due to a "bioavailability" problem (ie, poor drug ab-
LPR do not usually change as quickly as the symp- sorption).22
toms.'*^ (I never expected the degree of improvement More than a decade ago, we recognized that car-
in the RFS that was found.) For statistical analysis bonated beverages, particularly caffeinated cola
I used Students' /-test for the pre-diet and post-diet drinks, were a major risk factor for LPR. Indeed, ex-
RSI and RFS data. cessive consumption of carbonated beverages was
Institutional Review Board approval was not the single most commonly identified cause of medi-
sought for this study, as it was deemed unnecessary cal treatment failure among our patients with LPR.
284 Koufman, Low-Acid Diet for Laryngopharyngeal Reflux
TABLE 3. RESULTS
Reflux Symptom Index Score Reflux Finding Score
Age Before After Before Afler
Subject (y) Sex Diet Diet Change Diet Diet
1 29 F 28 4 24 13 8
2 70 F 4 3 1 12 5
3 72 F 10 0 10 10 0
4 53 M 10 8 2 10 9
5 61 M 29 35 -6 12 12
6 41 M 18 15 3 13 10
7 62 M 20 8 12 11 9
8 57 M 1 0 1 10 4
9 82 F 2 0 2 14 9
10 33 M 12 10 2 14 11
11 65 M 27 16 11 16 II
12 52 F 21 12 9 14 9
13 63 M 13 7 6 9 5
14 60 M 7 4 3 9 9
15 60 F 7 3 4 12 11
16 59 M 19 7 12 11 10
17 52 F 21 16 5 14 11
18 24 M 22 9 13 12 11
19 39 M 15 8 7 12 8
20 52 F 12 7 5 12 4
Mean 54.3 14.9 8.6 6.3 12.0 8.3
On the basis of clinical experience, we also limited themselves on the reflux diet, are permitted when
our patients' intake of citrus fruits and hot (pepper) added to breakfast cereal with milk, preferably low-
sauces. Other than these few specifics, the antireflux fat milk, which has a high pH. In other words, the
diet has not changed much over the years — that is, cereal and milk buffer the acidic fruit; ie, they pH-
until recently. In 2008, we began measuring the pH balance the dish.
of common foods and beverages, and as a conse-
quence of finding acid in almost everything we test- It is important to recognize that these ideas and
ed, we began to limit the acid intakes of our patients their practical applications in clinical practice have
with LPR, with surprisingly good results. evolved over a period of many years. By reporting a
series of worst-case, PPI-resistant patients who had
The clinical results reported herein are particular- successful outcomes with a strict low-acid diet, it is
ly striking and significant because "maximum anti- my hope to stimulate interdisciplinary research in
reflux therapy" was failing in the study patients. In the areas of reflux, nutrition, and the American diet.
the months since this paper was presented, many ad- Indeed, the contemporary American diet appears to
ditional patients with LPR have been treated with a be making Americans sick.
low-fat, low-acid diet as the cornerstone of therapy,
SCIENTIFIC BASIS FOR DIETARY ACID RESTRICTION
with or without adjunctive antireflux medications. IN REFLUX MANAGEMENT
The induction reflux diet is still recommended for Despite the popular use of the term "acid reflux"
the first 2 to 4 weeks with a gradual reintroduction among the lay public, most of the clinical manifesta-
of some fatty foods and other historically "refluxo- tions of LPR and GERD are due to pepsin.'--''•5''-9.ii-i7
genic" foods. Cheese, eggs, meats, sauces, and con- Pepsin is responsible for tissue injury and inflam-
diments are allowed in moderation, but the key ele- mation, and the confusion stems from the fact that
ments of the maintenance reflux diet are that it re- pepsin requires acid activation.''**The pepsin activ-
mains relatively low in acids and low in fat. ity profile (see Figure), the cell biology of LPR, and
With fatty foods in particular, we teach patients clinical experience with pharyngeal pH monitoring
moderation, and to use tasty fats as flavorings, not all suggest that the threshold of the larynx for peptic
as main ingredients. We also introduce the concept injury is far less than that of the esophagus.'-**" '"^
of pH balancing. The idea is that acidic foods may Surprisingly little acid is needed for peptic activa-
be combined with nonacidic foods. Strawberries, tion, and pepsin remains mildly proteolytic up to pH
for example, which are not allowed to be eaten by 6.5.'"* In addition, tissue-bound pepsin can be acti-
Koußnan, Low-Acid Diet for Laryngopharyngeal Reflux 285
vated by hydrogen ions from any (including a die- appeared to provide us with a reasonable approxi-
tary) source,'"* mation of a national sample.) The interviews were
It appears that the key to the development of clini-
carefully conducted to elicit all reflux symptoms
cal laryngeal disease is the presence of tissue-bound
and medications, both over-the-counter and physi-
pepsin,^-^ which causes depletion of protective cell
cian-prescribed. Respondents were considered to
proteins such as earbonie anhydrase, E-eadherin,
have a tendency to reflux if they had multiple re-
and the stress ("heat-shock") proteins,^-^'^'•'' John-
flux symptoms and/or took reflux medications. For
ston et al* demonstrated (in vitro and in vivo) that
the purposes of this survey, respondents with only
peptic laryngeal damage occurs at pH 5. It was ba-
one symptom, such as hoarseness or cough, were
sic science that led us to consider the possibility that
not considered to have reflux, as one symptom may
the contemporary reflux epidemic might be related
have many different causes.
to the eontemporary Ameriean diet. The data revealed that an astonishing 40% (262
of 656) of the study group had reflux disease, with
INCREASING PREVALENCE OF REFLUX DISEASE AND
REFLUX-RELATED ESOPHAGEAL CANCER
22% (144 of 656) having classic GERD and another
18% (118 of 656) having LPR. There were no statis-
The prevalence of acid reflux disease (GERD tical differences between age groups, genders, and
and LPR) has inereased dramatieally in our life- regions of the country. The most striking and unan-
times.2'* •-•'' Using a Poisson model and an analysis of ticipated result was that 37% of the 21- to 30-year-
17 prevalence studies, El-Serag^** showed that since old age group had reflux.
1976, the mean rate of increase of GERD has been a
staggering 4% per year (p < 0,0001 ), In the past, reflux was primarily a disease of over-
weight, middle-aged people. Now, we are finding
Altman et aP^ reported that office visits to otolar- that many of our reflux patients are neither old nor
yngologists for LPR increased almost 500% from obese.'" This trend toward younger and younger pa-
1990 to 2001, Those authors hypothesized that the tients with more and more severe reflux has been
increase was due to obesity and a greater awareness noted by other experienced clinicians (J, Hunter and
of LPR by otolaryngologists^S; however, reportedly, R, Sataloff, personal communications, 2011),
only 27% of the study patients were counseled about
CHANGES IN AMERICAN DIET IN PAST FIFTY YEARS
an antireflux di
Coincident with the reflux epidemic, the Amer-
An even more ominous trend is the skyrocketing
ican diet has changed dramatically,-""^'' Since the
increase in the prevalence of esophageal cancer in
1960s, there have been four parallel unhealthy die-
the United States.^^-^o The US National Cancer In-
tary trends: 1) increased saturated fat; 2) increased
stitute data from 2005 reveal that esophageal cancer
high-fructose corn syrup; 3) increased exposure to
had increased 600% since 1975 (from 4 to 23 cases
organic pollutants (eg, DDT, PCBs, dioxins); and
per million).2'' During this same period, its mortality
4) increased acidity.^^"^^ The last of these trends —
rate inereased sevenfold, despite increased esopha-
increased dietary acid — may hold the key to un-
geal surveillance^^-^''; the histopathology has been
derstanding the contemporary reflux epidemic and
trending toward more deadly, poorly differentiated
the dramatic increases in Barrett's esophagus and
esophageal cancer^^'^^-^"*
In addition, the prevalence of Barrett's esopha-
In 1973, after an outbreak of food poisoning
gus (a reflux-related precursor to esophageal can-
cer) is also very high,2''-^o Reavis et aP^ reported
(botulism), the US Congress enacted Title 21, man-
that patients with hoarseness, sore throat, and chron-
dating that the US Food and Drug Administration
ic cough (LPR symptoms) had Barrett's esophagus (FDA) ensure the safety of processed food cross-
just as frequently (7% to 10%) as did patients with ing state lines by establishing "Good Manufactur-
GERD and heartburn. Thus, routine esophageal ing Practices,"-'^'^'* How was this accomplished?
screening for both LPR and GERD was (and still is) Through acidification of bottled and canned foods,
recommended.29 .-''0 which was intended to prevent bacterial growth and
prolong shelf life. For two generations, the FDA has
INCREASED PREVALENCE OF REFLUX IN YOUNG never wavered from this path, apparently without
PATIENTS ever considering the possibility that the acidifica-
In 2010, we estimated the prevalence of reflux tion of America's food supply might have potential
(GERD and LPR) in the United States by interview- adverse health consequences. From the 1979 Title
ing 656 adult US citizens while they were waiting 21
in line to purchase discount theater tickets in Times Acidified foods should be so mantifactured, processed,
Square in New York City, (This specific location and packaged that a finished equilibrium pH value of 4,6
286 Koufman, Low-Acid Diet for Laryngopharyngeal Reflux
or lower is achieved. If the fini.shed equilibrium pH is cer was relatively uncommon, reflux patients usu-
4.0 or below, then the meastirement of acidity of the final ally presented in middle age. Today, we are seeing
product may be made by any suitable method. lApril 1,
2002; US Government Printing Office. 21CFR114.80]
comparable disease in patients in their twenties (J.
Hunter and R. Sataloff, personal communications,
In other words, the FDA actually encourages food 2011). Overacidity in the diet may be the missing
manufacturers to reduce the pH of their products to link that explains the reflux epidemic, as well as in-
less than 4.0, the same pH levej as stornach acid.' In creasing rates of Barrett's esophagus and esopha-
addition to acetic, ascorbic, citric, and hydrochloric geal cancer.
acids as food additives, the FDA allows more than
300 other chemicals that are "generally regarded as At present, even baby food is acidified. We tested
safe" (GRAS)."--''^ Many of these GRAS food addi- the acidity of an "organic" banana baby food and
tives were approved in the 1970s without the benefit found it to be pH 4.3; normally, banana is pH 5.7.
of contemporary methods of scientific testing and The label of the so-called "organic" banana prod-
''*''^ uct revealed that it had had both ascorbic and citric
acids added. Indeed, almost all bottled and canned
Furthermore, in 1997, the FDA was directed to foods and beverages contain ascorbic acid and/or
provide specific criteria for food manufacturers to citric acid; sometimes the packaging is less obvious
report their use of GRAS additives in their prod- and may just read "vitamin C-enriched" or "vitamin
ucts; inexplicably, as of this writing, those criteria C-enhanced."-''3
have still not been established.-^^ Thus, with regard
to food additives, the food industry remains com- Knowing what we now know about the cell biol-
pletely self-regulated.-''-^-'^ ogy of reflux, the stability and activity of pepsin,
and the contemporary American diet, it is reason-
In 2010, the US Government Accountability Of- able to postulate that the acidification of America's
fice, a bipartisan group of scientists, published a food supply may be responsible for the reflux epi-
scathing report on the FDA's lack of oversight of demic. Diet may be the primary factor in the preva-
food manufacturing.-^.^ In particular, they were crit- lence, mechanisms, manifestations (including neo-
ical of the FDA's negligence in failitig to monitor plasia), and outcomes of reflux disease, particular-
GRAS food additives, as referenced above.•''^-^-'' In ly as it affects the laryngopharynx and esophagus.
searching the literature, it appears that neither the Further research is needed to investigate this ques-
FDA nor the scientific community have examined tion. Until now, it appears that fundamental nutri-
the acidity question. No one, it appears, has con- tional issues related to how food has been preserved
sidered the possibility that the acidification of the for the past two generations may have been over-
nation's food might have potentially adverse health looked. Dietary acid may turn out to have serious
consequences; today, almost all food that is bottled adverse health effects on the general population,
or canned is below pH 4.^-^ and how food is preserved may soon become a per-
It is interesting to note that the Amish, who grow plexing public health conundrum. In the meanwhile,
and consume their own organic food, have aerodi- it seems likely that patients with LPR will benefit
gestive tract cancer rates (eg, larynx, pharynx, from a low-acid diet. ' -•
esophagus) that are only 37% the rates of controls.^'
In attempting to explain those findings, the authors CONCLUSIONS
emphasized that the Amish do not drink alcohol or
smoke tobacco, but they did not discuss or consider A strict low-acid ("acid-free") diet appears to be
the possible health benefits of a diet devoid of acids beneficial for patients with pH-documented LPR.
and other food additives.^'' ' ' In this study, the diet was shown to improve both
the symptoms and the laryngeal findings of patients
DIETARY ACID AS POSSIBLE MISSING LINK IN with recalcitrant (PPI-resistant) LPR. Also raised by
REFLUX EPIDEMIC this study are broader public health policy issues re-
Why are reflux disease and esophageal cancer lated to FDA-mandated acidification of manufac-
epidemic? Many years ago, when esophageal can- tured foods and beverages.
REFERENCES
1. Koufman JA. The otolaryngologic manifestations of gas- 2. Koufman JA. Perspective on laryngopharyngeal reflux:
troesophageal reflux disease (GERD): a clinical investigation from silence to omnipresence. In: Branski R. Sulica L. eds.
of 225 patients using ambulatory 24-hour pH monitoring and Classics in voice and laryngology. San Diego. Calif: Plural Pub-
an experimental investigation of the role of acid and pepsin in lishing. 2009:179-266.
the development of laryngeal injury. Laryngoscope 1991; 101
(suppl53):l-78. >- .. . ••. i ,- • 3. Koufman JA. Wiener GJ. Wu WC. Castell DO. RefluxKoußnan, Low-Acid Diet for Laryngopharyngeal Reflux 287
laryngitis and its sequelae; the diagnostic role of 24-hour pH Academy of Otolaryngology-Head and Neck Surgery. Otolar-
monitoring. J Voice I988;2;78-9. yngol Head Neck Surg 2002;127;32-5.
4. Postma GN, Tomek MS, Belafsky PC, Koufman JA. 22. Amin MR, Postma GN, Johnson P, Digges N, Koufman
Esophageal motor function in laryngopharyngeal reflux is supe- JA. Proton pump inhibitor resistance in the treatment of laryngo-
rior to that of classic gastroesophageal reflux disease. Ann Otol pharyngeal reflux. Otolaryngol Head Neck Surg 2001;125;374-
Rhinol Laryngol 2001 ;110; 1114-6. 8.
23. El-Serag H, Becher A, Jones R. Systematic review: per-
5. Axford SE, Sharp S, Ross PE, et al. Cell biology of laryn-
geal epithelial defenses in health and disease; preliminary stud- sistent reflux symptoms on proton pump inhibitor therapy in
ies. Ann Otol Rhinol Laryngol 2001 ;110; 1099-108. primary care and community studies. Aliment Pharmacol Ther
2010;32;720-37.
6. Amin MR, Postma GN, Johnson P, Digges N, Koufman 24. El-Serag HB. Time trends of gastroesophageal reflux dis-
JA. Proton pump inhibitor resistance in the treatment of laryngo-
ease; a systematic review. Clin Gastroenterol Hepatol 2007;5;
pharyngeal reflux. Otolaryngol Head Neck Surg 2001 ; 125;374-
17-26.
8.
25. Altman KW, Stephens RM, Lyttle CS, Weiss KB. Chang-
7. Koufman JA, Belafsky PC, Bach KK, Daniel E, Postma ing impact of gastroesophageal reflux in medical and otolaryn-
GN. Prevalence of esophagitis in patients with pH-documented
gology practice. Laryngoscope 2005;I15;1145-53.
laryngopharyngeal reflux. Laryngoscope 2002; 112:1606-9.
26. Pohl H, Welch HG. The role of overdiagnosis and reclas-
8. Johnston N, Bulmer D, Gill GA, et al. Cell biology of sification in the marked increase of esophageal adenocarcinoma
laryngeal epithelial defenses in health and disease: further stud-
incidence. J Nati Cancer Inst 2005 ;97 ; 142-6.
ies. Ann Otol Rhinol Laryngol 2003;! 12:481-91.
27. Lund O, Hasenkam JM, Aagaard MT, Kimose HH. Time-
9. Johnston N, Knight J, Dettmar PW, Lively MO, Kouf-
related changes in characteristics of prognostic significance in
man J. Pepsin and carbonic anhydrase isoenzyme III as diagnos-
carcinomas of the oesophagus and cardia. Br J Surg I989;76;
tic markers for laryngopharyngeal reflux disease. Laryngoscope
1301-7.
2004; 114;2129-34.
28. Conio M, Blanchi S, Lapertosa G, et al. Long-term en-
10. Halum SL, Postma GN, Johnston C, Belafsky PC, Kouf-
doscopie surveillance of patients with Barrett's esophagus. In-
man JA. Patients with isolated laryngopharyngeal reflux are not
cidence of dysplasia and adenocarcinoma; a prospective study.
obese. Laryngoscope 2005; 115:1042-5.
Am J Gastroenterol 2003;98;193l-9.
11. Knight J, Lively MO, Johnston N, Dettmar PW, Kouf- 29. Reavis KM, Morris CD, Gopal DV, Hunter JG, Jobe BA.
man JA. Sensitive pepsin immunoassay for detection of laryn- Laryngopharyngeal reflux symptoms better predict the presence
gopharyngeal reflux. Laryngoscope 2005;l 15;1473-8.
of esophageal adenocarcinoma than typical gastroesophageal
12. Gill GA, Johnston N, Buda A, et al. Laryngeal epithelial reflux symptoms. Ann Surg 2004;239:849-58.
defenses against laryngopharyngeal reflux; investigations of E- 30. Amin MR, Postma GN, Setzen M, Koufman JA. Trans-
cadhcrin, carbonic anhydrase isoenzyme III, and pepsin. Ann nasal esophagoscopy; a position statement from the American
Otol Rhinol Laryngol 2OO5;114:913-21. Broncho-Esophagological Association. Otolaryngol Head Neck
13. Johnston N, Dettmar PW, Lively MO,etal. Effect of pep- Surg 2OO8;I38;411-4. [Erratum in Otolaryngol Head Neck Surg
sin on laryngeal stress protein (Sep70, Sep53, and Hsp70) re- 2009;140;280.]
sponse: role in laryngopharyngeal reflux disease. Ann Otol Rhi-
31. Bellis M. Introduction to pop: the history of soft drinks
nol Laryngol 2006;l 15;47-58.
timeline. About.com (http;//inventors .about.com/od/sstartinven-
14. Johnston N, Dettmar PW, Bishwokarma B, Lively MO, tions/a/soft_drink.htm). Accessed March 2010.
Koufman JA. Activity/stability of human pepsin; implications
32. Lobbying 2009: American Beverage Association. Cen-
for reflux attributed laryngeal disease. Laryngoscope 2007; 117; ter for Responsive Politics, (http://wvvw.opensecrets.org/lobby/
1036-9. clientlbs.php?year=2009&lname=American+Beverage+Assn
15. Samuels TL, Johnston N. Pepsin as a marker of extra- &id). Accessed March 2010.
esophageal reflux. Ann Otol Rhinol Laryngol 2OIO;119:203-8,
33. Koufman JA, Stem JC, Bauer MM. Dropping acid: the
16. Lillemoe KD, Johnson LF, Harmon JW. Role of the com- reflux diet cookbook and cure. Minneapolis, Minn: Reflux
ponents of the gastroduodenal contents in experimental acid Cookbooks. 2010.
esophagitis. Surgery 1982;92;276-84.
34. Acidified foods. Code of Federal Regulations — Title 21
17. Johnson LF, Harmon JW. Experimental esophagitis in a — Food and Drugs Chapter 1, Department of Health and Human
rabbit model. Clinical relevance. J Clin Gastroenterol 1986;8 Services Subchapter B — Food for Human Consumption Part
(suppi l):26-44. 114. United States Food and Drug Administration. Arlington,
18. Belafsky PC, Postma GN, Koufman JA. Validity and reli- Va: Washington Business Information, 2010.
ability of the reflux symptom index (RSI). J Voice 2002; 16:274- 35. Generally recognized as safe food additives: FDA da-
7. tabase of selected GRAS substances. United States Food and
19. Belafsky PC, Postma GN, Koufman JA. Laryngopharyn- Drug Administration. Springfield, Va: National Technical Infor-
geal reflux symptoms improve before changes in physical find- mation Service, 2009.
ings. Laryngoscope 2001 ; 111 ;979-81. 36. Food safety: FDA should strengthen its oversight of
20. Belafsky PC, Postma GN, Koufman JA. The validity food ingredients determined to be generally recognized as safe
and reliability of the reflux finding score (RFS). Laryngoscope (GRAS). GAO-10-246, United States Government Account-
2001;! 11:1313-7. ability Office, February 3, 2010.
21. Koufman JA, Aviv JE, Casiano RR, Shaw GY. Laryn- 37. Westman JA, Ferketich AK, Kauffman RM, et al. Low
gopharyngeal reflux: position statement of the Committee on cancer incidence rates in Ohio Amish. Cancer Causes Control
Speech, Voice, and Swallowing Disorders of the American 2010;21:69-75.Copyright of Annals of Otology, Rhinology & Laryngology is the property of Annals Publishing Company and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
You can also read
