Dropping Acid: The Reflux Diet Cookbook & Cure | Blog

This blog is a companion to Dropping Acid and it allows us to continually publish new viagra pharmacy in india material.

The Missing Link

Almost all of these foods and beverages are acidic. Surprised?

Almost all of the above items are quite acidic, surprised?


Please note this post is an excerpt  from the book chapter “Reflux Science You Can Digest”

Why is reflux epidemic? Why is esophageal cancer one of cialis mail order uk the fastest growing cancers in America? Why do so many buy propecia international pharmacy people with reflux fail medical treatment? We believe that the answer is related to high levels buy amoxicillin without a perscription of dietary acid. How and when did this accutane generic cheap happen?

While the story of the reflux epidemic is going to focus on acid, we should point out that since the Second World War there have been four interrelated and unhealthy dietary trends: (1) increased saturated fat; (2) increased (low-glycemic index carbs) sugar; (3) increased preservatives, stabilizers, thickeners, artificial sweeteners; and (4) increased acidification of prepared foods and beverages.  From a historical perspective, here’s what happened.

Landmarks and Milestones in the American Diet

1886    Coca-Cola invented; Pepsi Cola invented in 1898

In 1886 Coca-Cola was invented by a pharmacist in Atlanta and Pepsi Cola two years purchase real name brand viagra later. These were fountain drinks and they weren’t actually bottled in the 20th century.  Coca-Cola really rose to prominence low cost brand viagra fast as an American drink during and then after the Second World War. While the components and ingredients have changed over the years, the drink bupropion from turkey (and beverages like Coke) have always been very acidic. The current pH (acidity) of Coca-Cola is 2.8, as acidic as stomach acid itself. Perhaps of interest; see article: The History of Soft Drinks Timeline

1919    American Bottlers of Carbonated Beverages formed

In 1919, the American Bottlers of Carbonated Beverages was formed.  The significance of this group wasn’t clear in 1919, but as you will see later on (with a couple name changes), it became a national lobby.

1952    First diet soda pop sold (Kirsch No-Cal Ginger Ale)

In 1952, the prednisone 20mg tablets first diet soda pop was sold. This represented a new potential market for the soda industry. That is it gave people something to drink that wasn’t fattening, but it also introduced a whole host of new additives and chemicals. In some cases, these diet drinks are/were more acidic than their non-dietary counterparts.

1955    McDonalds Corporation formed; fast-food is born

In 1955, Roy Kroc started the McDonalds Corporation.  Most baby boomers remember when they first encountered McDonalds.  For most of us, it was actually in the 60s.  Personally, the senior author (JK) recalls buying a hamburger in Dedham, MA for 13 cents in 1963.

1962    Instant foods become common in American homes

By 1962, instant foods were common in almost every American household, including things like instant milk, instant pudding, and other foods. Again this implied new ways of processing foods and some new ingredients. These products were essentially carryovers from WWII rations made palatable for the consumer (after the war, SPAM surpluses were sold to the general population). Incidentally, it was also about 1962 that the term “mystery meat” was coined.

1963    McDonalds begins marketing meals for families

This was a milestone for marketing and public relations, the idea that this type of fast food was appropriate for family; it was a paradigm shift.  That one could get an inexpensive meal outside of the home in a fast-food restaurant was new. Until this people looked at fast food as an inferior food, but through McDonald’s marketing, fast food became an acceptable part of the American diet. As a consequence, we began consuming more hamburgers, fries, and more saturated fat … and more soda pop, too.

1965    Canned soda first distributed in vending machines

Canned soda pop appears in vending machines.  Diet and regular and different flavors as well began popping up everywhere in 1965. This probably represents the greatest increase in soda consumption because now it was everywhere.  You didn’t have to buy it at a soda fountain or store, and it was available 24 hours a day 7 days a week.  After this, soda pop was available to anybody who had a dime and a nickel. Soda machines could just as well be at the library, golf course, in the hair salon, or in the workplace.

1966    The National Soft Drink Association was formed

In 1966, the American Bottlers of Carbonated Beverages changed their name to the National Soft Drink Association (NSDA). Since then, the NSDA has become a powerful lobby that has often been successful in fighting consumer groups that have attempted to limit access to soda pop in places like public schools. In 2004, they again changed their name to the American Beverage Association (ABA). Last year, the ABA spent over $19 million on marketing, promotion and lobbying, employing 25 lobbyists at 7 different firms, a 1000% increase in spending from the previous election cycle.  Recently, their efforts have been able to defeat laws raising taxes on high-sugar drinks.   See: Lobbying: American Beverage Association. Only recently, have consumers begun to gain the upper hand; see Pepsi to pull high calorie drinks from schools around the world.

1967    High-fructose corn syrup was introduced

In the late 60s, high-fructose corn syrup was introduced.  Within two decades, it found its way into use in American soda products and sweetened beverages almost ubiquitously.  HFCS is more fattening and less expensive than sugar.  Since its introduction, the public’s consumption of it has grown to an equal level as cane and beat sugar.  It’s recently become a target in America’s battle against the obesity epidemic. In other words once this became an ingredient in soda, soda became more fattening and higher in low-glycemic sugar.  See table:  USDA Sweetener Timeline

1973    Title 21: Law was response to outbreak of botulism

In response to an outbreak of botulism, Congress passed Title 21, a law giving the Food and Drug Administration (FDA) the power to regulate canned and bottled goods that were crossing interstate lines.  Title 21 underwent major revisions and was expanded in 1979 with the creation of “Good Manufacturing Practices.” These practices specified specific food additives and acidity levels in pre-packaged food to discourage bacterial growth and reduce the likelihood of bacterial contamination in prepared foods and beverages.   The idea that acidification of the food supply might have adverse consequences was never considered in any of the documented discussion about food safety.  See full-text: Code of Regulations Title 21: Food Acids

1985    “New Coke” introduced with high-fructose syrup

The introduction of “New Coke” was meant with loud boos and great disdain by angry “Coke-aholics,” who complained that it was a syrupy drink without any kick.  At the time, the senior author (JK) knew that this was simply a rouse to substitute high-fructose syrup for sugar.  Indeed when Classic Coke was “returned” to the market and “New Coke” disappeared, high-fructose syrup had been successfully substituted for real sugar, completing one of the most brilliant cost-saving ploys in marketing history. It appears that the whole thing had been planned

1990    Nutrition Labeling and Information Act Passed

A significant movement in Congress that suggested consumers had a right to know what was in the food that they were consuming.  It was designed to help consumers make healthy choices about the food they purchased and also encourage manufacturers to produce more healthy products.  See article: The Nutrition Labeling and Information Act of 1990

2003    Report: Junk food Mote than 1/3 of American calories

By 2003, the obesity epidemic became national news and the focus was on saturated fat and low-glycemic sugar.  Meanwhile despite all labeling efforts, Americans continued to consume a large portion of their calories from “junk food.”  In 2009, the average annual sugar intake was 142 lbs, the average sodium intake per day was 4500 mg, and the average daily saturated fate intake was approximately 20 grams.

The FDA’s “Good Manufacturing Practices”

The acidification of food has long been used as a means to preserve food, but it wasn’t until the modern era that the process evolved to meet transnational needs.  In order to prevent and regulate bacterial growth on food traveling long distances to sit on a store shelf, the FDA implemented a system of “Good Manufacturing Practices” through Title 21 regulations. Title 21 does not regulate which acids and preservatives within a broad group are used, but it does require the pH to be below 4.6, a level that is low enough to discourage most bacteria.  In fact, Title 21 encourages acidification of foods and beverages to 4.0 in below:

“Acidified foods should be so manufactured, processed, and packaged that a finished equilibrium pH value  of 4.6 is achieved.  If the finished equilibrium pH is 4.0 or below, than the measurement of acidity of the final product may be made by any suitable method.” Title 21, 2002.

What this says is that the manufacturer only needs to use a pH meter, a very inexpensive device if their product is below pH 4.

Food and Drug Administration (FDA) Approved Food Additives

A corollary question when considering how FDA regulated food is acidified is wondering, what does the FDA allow to be used as food additives to achieve these lower pH levels?  As it turns out there are 373 substances that are FDA approved, referred to as GRAS “Generally recognized as safe” food additives.

In February 2010, the Government Accountability Office (GAO), a non-partisan group appointed by Congress to investigate federal agencies, published a scathing report entitled Food Safety: FDA Should Strengthen Its Oversight of Food Ingredients Determined to Be Generally Recognized as Safe (GRAS). The first paragraph of the report reads:

“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; indeed 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 all industry self-regulated as long as the food additives comply with the list of 373 approved GRAS (“Generally Recognized as Safe”) substances.  It is reasonable for a concerned consumer to assume self-regulation could mean no oversight.  This would be like asking tobacco manufacturers to tell us whether or not cigarette smoke was harmful or not.

Furthermore, no consideration is, was, or has ever been given to the potential downside of acidification. At least not until now. Amazing as it may seem throughout the entire scientific community and in the literature and published reports dealing with food safety and food additives there has never been an expressed concern about the possible adverse health consequences of acidification.  By the way, 13% of the GRAS substances are acids, including hydrochloric acid, and every item in the photo shown  at the front of this post has been acidified to pH 4.6 or less.  This is what many of us eat much of the time … ouch!

In an recent report published by the Ohio State Medical Center on the Amish in Ohio, it was found that the cancer rates among Amish adults was 60% of the age-adjusted cancer rates in Ohio.  For “tobacco-related” cancers, including pharynx, larynx, and esophagus, the Amish cancer rate was only 37% of the Ohio population. Although the authors never consider the possibility, we offer this interpretation:  Pharynx, larynx, and esophagus cancers are reflux-related cancers.  One possible explanation for the lower rates of those cancers in the Amish is that they don’t eat highly acidified and preservative-ridden food; in stead they consume mainly homegrown and home-made food.   See the complete study: Low cancer incidence rates in Ohio Amish

Connection between Reflux Disease and Acid in the Diet

We know you’re not scientists and we don’t want to overwhelm you with complicated science; however, cell biology holds the key to understanding the consequences of excessive dietary acid.

LPR is different than GERD in fundamental ways

It is important to remember that reflux causes many different symptoms and that heartburn and digestive symptoms like indigestion represent one group of symptom manifestations.  Believe it or not, “Silent Reflux,” which affects the voice box, throat, and lungs, is an even bigger problem than “indigestion” that everyone seems to know about.  If you look at the most common symptoms for which people see doctors in America other than injuries and pregnancies, cough, sore-throat, hoarseness, asthma, etc., all common symptoms of reflux.  Thus, it is important to recognize differences in the GERD pattern of reflux and silent reflux. By the way, classic reflux is called gastroesophageal reflux disease GERD, silent reflux is usually called laryngopharyngeal reflux (LPR). A thorough discussion of manifestations and mechanisms of GERD and LPR is beyond the scope of this blog, but suffice it to say what makes silent reflux silent is that when reflux occurs it does not stay in the esophagus long enough to produce problems there; however, it does cause problems above. For further information,  see the sample chapters “What You Eat May Be Eating you” and  “How Do I Know If I Have Reflux” on this website.

Tissue injury is caused by active pepsin (not acid)

One of the great surprises for most people when we talk about reflux disease is that it is not all about acid.  In the stomach there is a very important digestive enzyme called “pepsin,” in addition to the well-known acid.  Scientific studies have shown that pepsin actually causes the problem and that confusion results from the fact that pepsin requires acid to activate.  For further information about this particular bit of science, see the sample chapter “What You Eat May Be Eating You” on this website.

How pepsin causes problems

Research has shown that people who have reflux disease have pepsin in the tissue.  Furthermore once pepsin is in the tissue, it can be activated and re-activated by acid of any cause.  The pepsin molecule is very stable and once it is attached to tissue in the throat, esophagus, or elsewhere, it tends to remain for days or weeks.  In the past, it was believed that this pepsin was inactive above pH 4, but that is incorrect.  Scientific experiments have shown that pepsin remains active, although weakly, up until pH 6.  Furthermore, we know that tissue damage can occur in the throat at pH 5 or less.

The Reflux Diet works

As clinicians, we have been restricting acids such as soda pop and citrus in our reflux patients for years, and we have found that it has been an extremely important part of medical treatment. Within the past year, we have tested the strict two-weeks-with-no-acid “pepsin detox” diet in our patients.

In a recent pilot study, the authors put twenty patients with recalcitrant reflux — still having symptoms of hoarseness, cough, and sore throat on twice-daily proton pump inhibitors like omeprzole, pantaprazole, and lansoprazole with an H2-antagonist at night (ranitidine 300 mg. q.h.s.) — on “pepsin detox,” a strict acid-free diet with nothing below pH 5, and found a statistically significant improvement in the patients’ symptoms and laryngeal findings.  These data will be presented at the annual scientific meeting of the American Broncho-Esophagological Association in Las Vegas on Wednesday, April 28th.

Summary and Conclusions

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 big 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 sited 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 a huge public health issue. Yes, we are worried about the implications of all this,  aren’t you?


Amin MR, Postma GN, Johnson P, Digges N, Koufman JA.  Proton pump inhibitor resistance in the treatment of laryngopharyngeal reflux. Otolaryngol Head Neck Surg 125:374-378, 2001

Amin MR, Postma GN, Setzen M, Koufman JA. Transnasal Esophagoscopy: A Position Statement from the American Bronchoesophagological Association (ABEA). Otolaryngol Head Neck Surg 138:411-13, 2008

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 110:1099-1108, 2001

Belafsky PC, Postma GN, Koufman JA.  Transnasal esophagoscopy (TNE). Otolaryngol Head Neck Surg 125: 588-589, 2001.

Belafsky PC, Postma GN, Koufman JA. The association between laryngeal pseudosulcus and laryngopharyngeal reflux.  Oto Head Neck Surg; 126:649-652, 2002.

Belafsky PC, Postma GN, Reulbach TR, Holland BW, Koufman JA.  Muscle tension dysphonia as a sign

Belafsky PC, Postma GN, Amin MR, Koufman JA. Symptoms and findings of laryngopharyngeal reflux. Ear Nose Throat J. 81: 10-3, 2002.

Belafsky PC, Postma GN, Daniels E, Koufman JA. Transnasal esophagoscopy. Otolaryngol Head Neck Surg;125:588-589;2001.

Belafsky PC, Postma GN, Koufman KA.  Laryngopharyngeal reflux symptoms improve before changes in physical findings.  Laryngoscope 111: 979-981, 2001.

Belafsky PC, Postma GN, Koufman JA.  The validity and reliability of the reflux finding score (RFS).  Laryngoscope  111:1313-1317, 2001.

Belafsky PC, Postma GN, Koufman JA.  Validity and reliability of the reflux symptom index (RSI). J Voice 16:274-277, 2002.

Birchall MA, Bailey M, Gutowska-Owsiak D, Johnston N. Inman CF, Stokes CR, Postma G, Pazmary L. Koufman JA, Phillips A, Rees LE. Immunologic response of the laryngeal mucosa to extraesophageal reflux. Ann Otol Rhinol Laryngol. 117:891-5, 2008.

Blot WJ, McLaughlin JK.  The changing epidemiology of esophageal cancer. Semin Oncol. 26(5 Supple 15): 2-8, 1999.

Brown, LM, Devesa, S, and Chow, W.  Incidence of Andenocarcinoma of the Esophagus among white Americans by sex, stage, and age.  J Natl Cancer Inst 100(16): 1184-1187, 2008.

Carrau RL, Khidr A, Gold KF, Crawley JA, Hillson EM, Koufman JA, Pashos CL. Validation of a quality-of life instrument for laryngopharyngeal reflux. Arch Otolaryngol Head Neck Surg 131:315-20, 2005.

Cohen JT, Bach KK, Postma GN, Koufman JA. Clinical manifestations of laryngopharyngeal reflux. Ear Nose Throat J. 81:14-23, 2002

Duke SG, Postma GN, McGuirt Jr. WF, Ririe D, Averill DB, Koufman JA.  Laryngospasm and diaphragmatic arrest in the immature canine after laryngeal acid exposure: a possible model for sudden infant death syndrome (SIDS).  Ann Otol Rhinol Laryngol 110:729-733, 2001.

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

Halum SL, Postma GN, Bates DD, Koufman JA. Incongruence between histologic and endoscopic diagnoses of Barrett’s esophagus using transnasal esophagoscopy. Laryngoscope. 116:303-6, 2006.

Gill GA, Johnston N, Buda A, Pignatelli M, Pearson J, Dettmar PW, and Koufman J. Laryngeal epithelial defenses against laryngopharyngeal reflux (LPR): investigations of pepsin, carbonic anhydrase III, pepsin, and the inflammatory response.  Ann Otol Rhinol Laryngol 114:913-21, 2005.

Knight J, Lively MO, Johnston N, Dettmar PW, and Koufman JA.  Sensitive pepsin immunoassay for detection of  laryngopharyngeal reflux. Laryngoscope 115:1473-8, 2005.

Johnson PE, Koufman JA, Nowak LJ, Belafsky PC, Postma GN.  Ambulatory 24-hour double-probe pH monitoring: the importance of manometry.  Laryngoscope 111: 1970-1975, 2001.

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 112:481-491, 2003.

Johnston N, Knight J, Dettmar PW, Lively MO, Koufman J. Pepsin and carbonic anhydrase isoenzyme III as diagnostic markers for laryngopharyngeal reflux disease. Laryngoscope 114:2129-34, 2004.

Johnston N, Dettmar PW, Lively MO, and Koufman JA.  Effect of pepsin on laryngeal stress protein (Sep70, Sep53, and Hsp70) response: role in laryngopharyngeal reflux disease.  Ann Otol Rhinol Laryngol 115:47-58, 2006.

Johnston N and Koufman JA.  What are the compared mechanisms of cellular defense in the esophagus and at the laryngeal level?  The duodenogastroesophageal reflux.  125 questions and 125 answers (Proceedings from the World Organization for Specialized Studies on Diseases of the Esophagus, Paris, France, September 2003).  R. Giuli and C Scarpignato Eds. 15-23, 2006.

Johnston N, Dettmar PW, Lively MO, and Koufman J.  Effect of pepsin on laryngeal stress protein (Sep70, Sep53, and Hsp70) response: role in laryngopharyngeal reflux disease.  Ann Otol Rhinol Laryngol. 115:47-58, 2006.

Johnston N, Dettmar PW, Bishwokarma B, Lively MO, Koufman JA. Activity/stability of human pepsin: implications for reflux attributed laryngeal disease. Laryngoscope. 117:1036-9, 2007.

Johnston N, Dettmar PW, Lively MO, Postma GN, Belafsky PC, Birchall M, Koufman J. Effect of pepsin on laryngeal stress protein (Sep70, Sep53, and Hsp70) response: Role in laryngopharyngeal reflux disease.  Ann Otol Rhinol Laryngol 115:47-58, 2005.

Koufman JA, Wiener GJ, Wu WC, Castell DO.  Reflux laryngitis and its sequelae:  the diagnostic role of 24-hour pH monitoring.  J Voice 2:78-89, 1988.

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 101 (Suppl. 53):1-78, 1991

Koufman JA, Burke AJ. The etiology and pathogenesis of laryngeal carcinoma.  Oto Clin N A 30:1-19, 1997.

Koufman JA, Amin M, Panetti M.  Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders. Otolaryngol Head Neck Surg  123:385-388, 2000.

Koufman JA, Aviv JE, Casiano RR, Shaw GY.  Position statement of the American Academy of Otolaryngology-Head and Neck Surgery on laryngopharyngeal reflux. Otolaryngol Head Neck Surg 127:32-35, 2002.

Koufman JA. Laryngopharyngeal reflux is different from classic gastroesophageal reflux disease. Ear Nose Throat J. 81:7-9 2002.

Koufman JA, Belafsky PC, Daniel E, Bach KK, Postma GN.  Prevalence of esophagitis in patients with pH-documented laryngopharyngeal reflux.  Laryngoscope 112:1606-1609, 2002.

Koufman JA, Block C. Differential Diagnosis of Paradoxical Vocal Fold Movement. American Journal of Speech and Hearing. 17:327-34, 2008.

Knight J, Lively MO, Johnston N, Dettmar PW, and Koufman JA.  Sensitive pepsin immunoassay for detection of  laryngopharyngeal reflux. Laryngoscope 115:1473-8, 2005.

Little JP, Matthews BL, Glock MS, Koufman JA, Reboussin DM, Loughlin CJ, McGuirt Jr. WF.  Extraesophageal pediatric reflux: 24-hour double-probe pH monitoring of 222 children.  Ann Otol Rhinol Laryngol Suppl 169: 1-16, 1997.

Loughlin CJ, Koufman JA. Paroxysmal laryngospasm secondary to gastroesophageal reflux. Laryngoscope 106:1502-1505, 1996.

Loughlin CJ, Koufman JA, Averill DB, Cummins MM, Yong-Jae K, Little JP, Miller Jr. IJ, Meredith W. Acid-induced laryngospasm in a canine model. Laryngoscope  106:1506-1509, 1996.

Postma GN, Cohen JT, Belafsky PC, Halum SL, Gupta SK, Bach KK, Koufman JA. Transnasal esophagoscopy revisited (over 700 consecutive cases). Laryngoscope 115:321-3, 2005.

Postma GN, Tomek MS, Belafsky PC, Koufman JA.  Esophageal motor function in laryngopharyngeal reflux is superior to that of classic gastroesophageal reflux disease. Ann Otol Rhinol Laryngol  110:1114-1116, 2001.

Rees CJ, Halum SL, Wijewickrama RC, Koufman JA, Postma GN. Patient tolerance of in-office pulsed dye laser treatments to the upper aerodigestive tract. Otolaryngol Head Neck Surg. 134:1023-7, 2006.

Rees LE, Pazmany L, Gutowska-Owsiak D, Inman CF, Phillips A, Stokes CR, Johnston N, Koufman JA, Postma G, Bailey M, Birchall MA. The mucosal immune response to laryngopharyngeal reflux. Am J Respir Crit Care Med. 177:1187-93, 2008.

Reavis, K, Morris, C, Deepak, G, Hunter, J and Jobe, B. Laryngopharyngeal reflux symptoms better predict the presence of esophageal adenocarcinoma than typica gastroesophageal reflux symptoms.  Ann Surg. 239(6): 849-858, 2004.

Reulbach TR, Belafsky PC, Blalock PD, Koufman JA, Postma GN.  Occult laryngeal   pathology in a community-based cohort. Otolaryngol Head Neck Surg 124:448- 450, 2001.

Smoak BR, Koufman JA.  Effects of gum chewing on pharyngeal and esophageal pH.  Ann Otol Rhinol Laryngol  110:1117-1119, 2001.

Weiner GJ, Koufman JA, Wu WC, Cooper JB, Richter JE, Castell DO.  Chronic hoarseness secondary to gastroesophageal reflux disease:  Documentation with 24-H ambulatory pH monitoring. The Amer J of Gastroenterol 84:12, 1989.

Westcott CJ, Hopkins MB, Bach KK, Postma, GN, Belafsky, PC, Koufman, JA. Fundoplication for laryngopharyngeal reflux. J American College of Surgeons 199:23-30, 2004.

FOOD SAFETY: FDA Should Strengthen Its Oversight of Food Ingredients Determined to Be Generally Recognized as Safe (GRAS). United States Government Accountability Office Congressional Report.  February 2010.  Retrieved 2010-3-17.

Westman J, Ferketich A, Kauffman R, et al.  Amish Cancer Rates in Ohio. Ohio State Medical Center.  September 2009.  Retrieved 2010-3-17.

CFR – Code of Federal Regulations: Title 21. U.S. Food and Drug Administration (FD. April 2009.  Retrieved 2010-3-17.


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  1. I really do appreicate of some one of the things that you mention is about the egg veggie omelet & how to prepare it.I did’nt know that to get rid of some of the egg.I always throw away the thick white part anyway because high in cholesterol.I have been diagnoised for 4 years that I have acid reflux.I a m takink nexiums.But I would like to try another methods besides taking pills all the time.I am glad that something has come up & I will be more than happy to try something better.Please keep me posted

  2. I am really confused about what to eat when you have LPR. I have two diets and they contradict each other. HELP. I need a list of do’s and don’t’s.

  3. Your findings sure sound convincing and show a new perspective. I suffer from GERD and my doctors point it towards a malfunction of the LES, (abnormal relaxations) and not the acid. But you seem to blame it on the acid and pepsin. So are you also saying that the abnormal relaxations of the LES don’t cause acid reflux and esophgeal damage or are your findings majorly focused on LPR?

    Also, to add that many studies have shown that the rate of LES relaxations in healthy people and patients with GERD dont have any difference but that the GERD patients experience more acid relfux than normal people.


    So does the problem lie in the acid and not LES? Please advise.


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