WHYSTOMACHACIDISGOODFORYOU

WHYSTOMACHACIDISGOODFORYOU

NaturalRelieffromHeartburn,Indigestion,Reflux,andGERD

JonathanV.Wright,M.D.,andLaneLenard,Ph.D.

M.EVANS

Lanham·NewYork·Boulder·Toronto·Oxford

DISCLAIMER

Theideasandadviceinthisbookarebasedupontheexperienceandtrainingoftheauthorandthescientificinformationcurrentlyavailable.Thesuggestionsinthis book are definitely not meant to be a substitute for careful medicalevaluationandtreatmentbyaqualified,licensedhealthprofessional.Theauthorandpublisherdonotrecommendchangingoraddingmedicationorsupplementswithout consulting your personal physician. They specifically disclaim anyliabilityarisingdirectlyorindirectlyfromtheuseofthisbook.

formywifeHollyandwithspecialthankstoJunePerbohner,forherincrediblededicationtofindingandpreservingcopiesofhundredsofresearchpapersconcerningstomachacidanddiseasefromthe1800sonwardalso,

thankstoLaneLenard,Ph.D.,coauthorextraordinaireandJenniferMorganti,N.D.,forherlongtimeskillfulhelpinthelibraryanddeepestappreciationtothethousandsofindividualssufferingfromlowstomachacidwithwhomIhave

workedatTahomaClinic—withtheinformationgatheredfromyourexperiencescollectedandreportedinthisbook,many,manyotherswillfindhelpfortheir

ownhealthproblems

—JonathanV.Wright,M.D.

forPhyllisandKatyyoumakeitallworthwhile

—LaneLenard,Ph.D.

CONTENTS

PrefaceWhistlingPasttheGraveyardPrologueThe“GrayMan”Chapter1TheMythofAcidIndigestionChapter2WhyStomachAcidIsYourFriendChapter3HowtheUpperGITractWorks…BasicallyChapter4StarvingintheMidstofPlenty:HowGastricAcidLevels

AffectNutrientAbsorptionChapter5HowLowStomachAcidCanMakeYouSick:TheBacteria-

CancerConnectionChapter6HowLowStomachAcidCanMakeYouSick:Asthma,

RheumatoidArthritis,andOtherDiseasesChapter7TreatingHeartburnand“AcidIndigestion”theNatural

Way.Appendix1IsDepressiontheResultofanAminoAcidand

NeurotransmitterDeficiency?Appendix2AreOurFacesRed?AcneRosaceaandLowStomachAcidNotesIndex

PREFACE

WhistlingPasttheGraveyard

Stomachacidhaslittleornovaluetoourhealth.Wemaynotevenneedit fordigestion.Therefore,what’s theharm in turningoff theacidpumpswhenourgastricjuicesstarteruptingintoheartburnandacidindigestion?Ifitgetsridofthepainanddiscomfort,whynotturnthemofffortherestofourlives?Stomachacid?Whoneedsit?

Ifthissoundssilly,trynottolaughtoohard,becauseit’swhatmostdoctorsinthis country believe. The conventional medical establishment in the UnitedStates,thanksinlargeparttohundredsofmillionsofadvertising,research,and“educational” dollars spent by the pharmaceutical industry each year, haslearnedtofeartheevilstomachaciddragon.Howelsetoexplaintheirzealforpushingdragon-slayingacidsuppressorsonapublicconvinceditisdrowninginitsowninternally-producedacidbath?

Acid-suppressingdrugsareamorethanseven-billion-dollar-a-yearindustryin the United States. Yet, this unimaginably large franchise is built on aconvenientdeception:thatvirtuallyeliminatingacidfromthestomachcanonlybe good for us, and that itwill have no consequences today, or tomorrow, ortwenty or thirty years from now, when we’re still popping potent acid-suppressingpillstocontroloursymptomsof“hyperacidity.”

In thisbook,weemphasize someof the important—evenessential—rolesthat stomach acid plays in digestion. We describe how hydrochloric acid,secretedbyspecialcells in thestomach’s lining in reponse toameal, isakeyupstreamlinkinacomplexchainofeventsthatculminatesintheabsorptionofvital nutrients that make a long, healthy life possible. Break that chain—bysevering the acid link—and the downstream cascade of events required forproperdigestionandthecontinuinghealthofthegastrointestinal(GI)system—aswellastherestofthebody—willbeseverelyimpeded.

We also ask an important question: What diseases can emerge whenstomachacidsecretionistoolowfortoolong?Wewishtheforcesthatcontrol

conventionalmedicinewouldaskthisquestion,butforthemostpart,theyseemuninterested. The fact is they don’t really want to know the answer. There issimplytoomuchinvestedinthemythof“acidindigestion.”

Yet the consequences for our health of long-term acid reduction due todisease or aging (known as atrophic gastritis) have been well-known for thebetterpart of a century.What about long-termdrug-inducedacid-suppression?Based on very limited FDA approved trials, conventional medicine’spractitionersandpromotersfeelcomfortablepretendingthateverything’sgoingtobeallrightforpeopletakingacid-quenchingdrugslikePrilosec,Prevacid,andtheirevenmorepowerfulsuccessorsforten,twenty,orthirtyyearsorlonger—iftheylivethatlong!

We think that those who choose to believe this myth have their headsburiedfirmlyinthesand.Thesearepowerfuldrugsthatcauseprofoundchangesin the body’s chemistry and physiology at a key juncture in the digestiveprocess. They should not be taken casually. Yet the current trend, with thewidespread promotion of acid-blocking drugs for ordinary heartburn, ispromotingjustthat.

Whenitcomestoacidblockers,theconventionalmedicalestablishment—including groups like the American Medical Association (AMA)—NationalInstitutes of Health (NIH), the various specialty medical associations (e.g.,American College of Gastroenterology, ACG) and disease advocacy groups(e.g., International Foundation for Functional Gastrointestinal Disorders(IFFGD), not to mention the two most powerful groups of all, the globalpharmaceutical industryand its “in-house”enforcementagency, theU.S.Foodand Drug Administration (FDA)—are all whistling (in chorus) past thegraveyard.At our peril, they ignore decades of research clearly demonstratingthat lowstomachacid,whethercausedbydiseaseordrugs, is linkedtoawiderange of serious, chronic, so-called incurable diseases, some of which can befatal.

Justbecause“serious”problemshavenotappearedafteronlyafewyearsofdrug use, there’s no guarantee wewon’t start seeing them—and experiencingthem—inafewmoreyears.“Natural”atrophicgastritistypicallytakesdecadesto progress tomore serious conditions such as ulcer or stomach cancer.Whyshouldweexpectacid-blockingdrugstobeanydifferent?

Ifyouor someoneyou love suffers fromheartburnorother symptomsofgastricupset,weurgeyoutoignoretheconstantbarrageofadvertisingthatleadsmostpeople—includingmostdoctors—tobelievethattheonlywaytotreatthesedisorders is by suppressing acid secretion. More than a century’s worth ofscientificresearchconfirmsthatthissimplyisn’tso.Whathascometobecalled

—incorrectly—“acid indigestion” is almost always associated, not with toomuchstomachacid,butwithtoolittle.

In this book,we propose anatural program that inmany cases can cure“acidindigestion.”InsteadofdrugsthatmerelysuppresssymptomsbydisruptingnormalGIfunction,wetellyouhowtouseavarietyofsafe,natural,inexpensivesubstances that work with the body’s physiology—not against it—to restorehealthy gastric functioning, heal damaged tissues, prevent future disease, andperhapsextendyourlife.

PROLOGUE

The“GrayMan”

AtTahomaClinichewasknownasthe“GrayMan.”HegotthenicknameafterSue, the receptionist, and Barbara, the nurse, agreed that they’d never seenanyonewithhisskintones.Anyonecouldseeit.AlthoughhewasCaucasian,hisvisible skin was devoid of any pink tones. He scarcely had any brown hue.Instead, he was a peculiar whitish gray. I’ve not seen anyone with the samepigmentationbeforeorsince.

Thesixty-one-year-oldGrayManhadn’tcome inbecausehewas lookinggray, althoughhiswifehadmentioned it tohim“a timeor two.”Actually, heexplained, he didn’t have any symptoms or illnesses; he was just plain tired.Reallytired.

Further questioning turned up little but the fatigue. In the past, he’d hadchronicindigestionandintermittentbutpersistentheartburn.Henotedthatbothsymptoms had gone on for over twenty years, and that he’d taken “plenty ofthose Tums and Rolaids and other antacids” since his forties. However, hereported he hadn’t had any indigestion or heartburn problem at all since he’dstarted taking that “newprescription acid-blocker stuff, Tagamet,”which he’dbeentakingeverydaysinceitcameoutin1977.Bythetimeheappearedattheclinic,heguessedhe’dbeentakingthedrugeverydayforsevenyears.

“Youknowthatstomachsarenaturallydesignedtosecreteenoughacidtoturnevenlargemealsintotheequivalentofsoup?”Iasked.

“Yeah,Iknowthat,Iguess,butallmydoctorstoldmethatmyindigestionand heartburn were due to too much acid. It just made good sense to takesomethingthatwouldknockdowntheexcessacid,”hereplied.

“Didanyoneeveractuallymeasuretheamountofacidinyourstomach?”“No … but the symptoms sure have gone away since I started the

Tagamet.”“Andariverwilldryupifwestopalltherain.Maybethat’sanadvantage

foralittlewhileiftheriverhasbeenflooding,butwhathappensifwestoptherainpermanently?”

Hethoughtforamoment.“Permanently?”“Well,sevenyears,atleast.”“Quiteadrought.Nothing’llgrow,forsure.”“Right.Andifweshutoff,orneutralize,ourstomachs’naturalacidityfor

more than brief intervals, there’s bound to be consequences. First, we don’tbreakdownfoodsaswell,andmanynutrients—especiallyessentialaminoacids,certain minerals, and at least two B vitamins—aren’t as available as they’resupposedtobe.Sotheydon’tgetabsorbedintoourbloodstreams,andourcellsdon’tgetthenormalamountsofnutrientstheyneedtokeepthemgoing.

“Second,when that ‘acidified soup’ empties out of our stomachs into theupper part of the small intestine—the duodenum—it triggers the secretion ofhormonesthatinturnstimulatethepancreasandgallbladdertomake,orrelease,their own digestive secretions, including enzymes, bicarbonate, and bile.Without this ‘acid trigger,’ these hormones are underproduced, and thesubsequentstagesindigestiondon’tworkaswellasthey’resupposedto,either.Thismeansthatanotherwholegroupofnutrientsbecomeslessavailabletoourcells.”

“Soit’slikeacascadeofevents,”saidtheGrayMan,startingtocatchon.“Iftheacidityisn’tthere,thenotherpartsofdigestionaren’ttriggeredproperly,either.”

“Exactly,and theremaybemanyother ‘cascades’ in thedigestivestreamthatwestilldon’tknowaboutthatmightbeaffected.”

“NowonderI’mtired,”hesaid.“I’vebeenliterallydryingupa lotofmydigestionforyears.Whydidn’tanyonetellmeaboutthis?”

“Don’tknow.It’sallrightthereinthebasictextbooksformedicalstudents.But that’s not all. The same textbooks list a third consequence of low, or no,stomachacidproduction.Let’s think about it thisway:Whathappens if I addbacteriaorparasitestoanacidsolutioninatesttube?”

“Notsure,butI’dguessalotofthem’lldie.”“Right. They die. Textbooks of gastroenterology—the medical specialty

thatconcentratesonthedigestivesystem—actuallyrefertostomachacidasthe‘acid barrier’ to intestinal tract infection. Also, everyone knows that fartherdown,theintestinesarehometoawidevarietyofmicroorganisms—sometimescalled intestinal microflora (literally tiny plants)—which help with digestion,secreteafewimportantvitamins,andgenerallybehavethemselves.

“But if the acid-alkaline balance—technically called the ‘pH’—isn’t justright, then many of these ‘friendly’ microorganisms literally die out and arereplaced by not-so-friendly germs. At best, these unfriendly microorganismsaren’tashelpfultousasthefriendlyones.Atworst,someofthemmayexcrete

substancesthataretoxictoourownbodycells,whichareabsorbedandspreadallaroundourbodies.”

The Gray Man shifted uncomfortably in his chair. “So by keeping mystomach acid low to prevent heartburn, not only have I been semi-starvingmyself for the lastsevenyears,butalsoImaybeencouraging toxinsfrommyguttoentermysystem?”

“Afraidso.”“CouldthisbewhyI’vebeensotiredallthetime?”“Very likely. Let’s work on restoring your normal digestion as much as

possible. We’ll try to make up for all those years of malnutrition, and ifnecessarywe’lldosomethingrestoreyournormalgutflora.Thenwe’llseewhathappenswithyourfatigue.”

“IguessthefirstthingistostopthisTagamet.ButthenI’llhaveindigestionandheartburnalloveragain,won’tI?”

“There are natural ways we can try to stop indigestion and heartburnwithoutblockingstomachacid.”

“How?”“First,weneedtofindoutifyourstomachreallyismakingtoomuchacid.

Chances are very high—over 90 percent—that the real culprit is likelyunderproduction of stomach acid. Heartburn means that some of that smallamount of acid is turning up in thewrong place, causing the burning feeling.Let’swaituntilwedoatestortwo.”

Liketheoverwhelmingmajorityofpeoplewithindigestionandheartburn,theGrayMansoonfoundthatalthoughhehadbeensufferingfromheartburnforyears, his stomach had actually been underproducing acid all that time. Byreplacing the missing stomach acid with capsules containing betainehydrochloride (a safe, convenient, inexpensive source of stomach acid, orhydrochloricacid—HCl)and thedigestiveenzymepepsinwitheverymeal,hewas soon able to eliminate his symptoms. His program also includedreplacement digestive enzymes, intestinal flora normalizers (also calledprobiotics),andsupplementsofvariousaminoacids,vitamins,andmineralsthathehadnotbeenabsorbingproperlyduetohislowacidcondition.

Slowlybutsurely,hisgrayskincolor returned tonormal,healthy-lookingbrown and pink skin tones.His fatigue dissipated, too, replaced by increasingenergy. His wife also noted an improvement in his mood and attitude. Sixmonthslater,hedeclaredhimselfbacktonormal.

TheonlythingentirelyatypicalabouttheGrayMan’s—John’s—casewashisskincolor.Asnotedabove,I’veneverseenanythinglikeitbeforeorsince.Buttherestofhisstory—indigestionandheartburncausedbyunderproduction

of normal stomach acid—is absolutely typical. Since the 1970s, I’ve workedwithliterallythousandsofindividualswithoneoranothervariationofthesamestory—indigestionandheartburn,frequentlyaccompaniedbybloating,belching,gas, constipation, occasionally loose bowels—caused by a failure or partialfailure of normal stomach function. (Stomach overfunction, or excess acidproduction, is actually quite rare.) Most of these individuals had beencompounding their health problems by taking antacids or acid-blocking drugseitherontheirownorontheadviceofhealthcarepractitioners.

Inthepagesthatfollow,Dr.LenardandIexplainnormalstomachfunctionand what it does for us, and describe some of the many manifestations of“stomach failure.”We cover health problems commonly associatedwith poorstomachfunction.Wedescribeconventional treatmentsfor themythical illnessknownas“acidindigestion,”andthenthepreferrednaturalalternatives.

Asyou’llsoonfind,thisismorethanjustanotherbookaboutindigestion.Formanyofus,thisisalsoafor-realguidetoantiagingandlongevity:Howcanwe expect our cells and our whole bodies to “live long and well” if they’rechronicallymalnourished?

For others, we offer a little-known perspective on a variety of diseases,including depression, diabetes, osteoporosis, rheumatoid arthritis, lupus,ulcerativecolitis,acnerosacea,multiplesclerosis,childhoodasthma,andmanyothers,thatoftenimproveoncedigestivefunctionisnormalized.

Sowhyhaven’tmoreof usheard about this before?Here’s a small clue:Themarketforantacidsandacid-blockingdrugsamountstomorethan$7billionperyear.Theactualfactsaboutdigestivefailureareliterallydrownedintheseaofadvertisingandpatentmedicine(pharmaceutical)industry-sponsoredresearchdesigned to sustain the profits made from this superficial and profoundlymisguided“treatment”ofindigestion,heartburn,andaccompanyingsymptoms.

Forthetruestory,weinviteyoutoreadon!

CHAPTER1

TheMythofAcidIndigestion

Heartburn, indigestion, dyspepsia, and “acid indigestion” are extremelycommonafflictions.Thanksmostlytodietandlifestyle,andsometimesbecauseofgenetics,pregnancy,anatomy,orsimpleaging, itseemsthatsoonerorlater,almosteverybodygetsanupsetstomachinoneformoranother.Whohasn’tfelttheacuteburning in thebackof the throatandupperchestaftereatingcertainfoods?Whohasn’tpoppedaTumsorgulpeda“bicarb”toextinguishtheacidicflamesthatseemtoroarupfromthestomachduringaheartburnattack?

AGallup Poll found that 44 percent of the U.S. population suffers fromheartburnatleastonceamonth,and7percentexperienceitweekly.1Accordingto the National Institute of Diabetes and Kidney Digestive Diseases, sixtymillion people experience heartburn at least once a month and twenty-fivemillionfeeltheburneveryday.

Ifwe are to believewhatwe see in themedia, theAmericanpopulace isawash in indigestion-causingstomachacid.Wecan’twatchTV(especially theeveningnewscasts)without seeingdozensof slick commercials for expensive,high-tech drugs like Prilosec, Prevacid, Tagamet, Zantac, Pepcid, Axid, andothers, not tomentionmore traditional low-tech remedies likeTums,Rolaids,Maalox, and Alka-Seltzer. All of these products are designed to eliminateheartburnpainbyreducingtheamountofacidinthestomach.Theold-fashionedantacid remedies simplyneutralize anyacidpresent in the stomach, taking theacidic “bite” out of it, thus rendering it temporarily harmless. (One popularneutralizingantacidused toadvertise that it “soakedup47 times itsweight inexcess stomach acid.”) The more advanced drugs work by squelching theproduction of acid at its source. The drug most commonly prescribed forheartburn today, Prilosec, virtually eliminates acid in the stomach around theclock, a fact that is proudly promoted in the drug’s widespread consumer-oriented advertising. Prevacid, Aciphex, Protonix, and Nexium do about thesamething.

Themyth that underlies the conventional treatment of “acid indigestion,”

and the impliedmessage in all these commercials—although they rarely comerightoutandsayit—isthatheartburnhappensbecausewe’vegottoomuchacidinourstomachs.Asaresult,someofthatacidflowsback—orrefluxes—intotheesophagus,themusculartubethatcarriesfoodfromthebackofthemouthintothestomach.Sinceaciddoesnotbelongintheesophagus, itspresenceirritatesthedelicatetissuethatlinestheinsideofthetube.Heartburnpainisasymptomofthatirritation.Ifwe’vegotheartburnorothersymptomsofthemoreseriousdisorder,gastroesophageal refluxdisease (GERD), the commercialmessage isclear:“Thelessacidwehaveinourstomachs,thebetter.”Tomostphysicians,itis“commonknowledge”thatheartburnandothersymptomsofacidindigestionaresignsoftoomuchstomachacid.Torelievethepain,weneedmerelyreducethelevelofacid.Ifwebelievethis, itmakessensethatweshouldallbeusingthesepowerful acid-reducing treatments to relieveourheartburn.According tothemanufacturersoftheseproducts,long-termacidsuppressionisanadvantage,allowingustocontrolheartburn“aroundtheclock,”perhapswithasinglepill.

But aswe explain in this book, this kindof extremeheartburnprotectionmay come at a cost to health that is being ignored by the pharmaceuticalcompaniesthatpatentandprofitfromthesedrugs,andignoredbytheFoodandDrugAdministration (FDA),which collects truly enormous sumsofmoney to“approve”them.Mostimportantly,perhaps,thecosttohealthofthesedrugsisbeing ignoredby the thousandsofphysicianswhoprescribe them.Theyfail torecognize that the acid-suppression theory, which currently governs theconventionalmedicaltherapyof“acidindigestion,”isseriouslyflawedbecauseit isbasedon themyth that“acid indigestion,”heartburn,and itsmoreseriousconsequence, GERD, are the result of too much stomach acid. The facts sayotherwise.

Figure1-1.Contrarytopopularbelief,stomachacidsecretiontendstodeclinewithadvancingage.This

graphshowsmeanstomachacidsecretionfromtheseconddecadetotheeighthdecade.AdaptedfromK.Krentzetal.,1984.

Consider this conveniently overlooked observation: The incidence ofindigestion, “simple”heartburn, andGERD increaseswithage,while stomachacid levels generallydeclinewith age (seeFigure1-1). If toomuchacidwerecausing these problems, teenagers should have frequent heartburn, whileGrandmaandGrandpa shouldhavemuch less.Of course, as everyoneknows,exactlytheoppositeisgenerallytrue.

Weareledtobelievethatifwesimplyhaveotherfeelingsof indigestion,like“thatoverfull feeling,”withexcessgas,bloating,orbelching,butperhapsonlya littleheartburn, this is alsodue to“toomuchacid.” If this is true, thenanswerthisquestion:Whyistoomuchacidsoefficientatrefluxingbackintotheesophagusbutsoinefficientatactuallydigestingfood?

It issimplyamatterofcommonsense.Howmanyofuscanrunfasteratagefortythanatagetwenty?Howmanyhavebettervisionatfiftythanatthirty?Weallexperiencedeclininghormonelevelsaswegrowolder.Wecanthinkofliterallydozensofexamplesoffunctionsthatdeclinenaturallywithage,sowhyshouldtheoutputofacidbythestomachrunintheoppositedirection?Sciencehas confirmedwhat common sense tells us. Formost of this century,medicalresearchershaverepeatedlyandconsistentlydocumentedanage-relateddeclineinstomachacid.So,ifwehavelessandlessstomachacidastheyearsaddup,why do we get more and more heartburn and indigestion? And moreimportantly,whyarewetreatingthatheartburnandindigestionbytakingdrugsthatwringthelastfewdropsofacidoutofourstomachs?

What’s so bad about depleting stomach acid? Lots. Unfortunately,conventionalmedicalwisdomrefuses torecognize this,whichsuits themakersofacid-depletingdrugsjustfine.Theproblemisthatmanyoftheadverseeffectsassociatedwith long-termsuppressionofstomachacidmay takeyearsorevendecadestodevelop.Atthesametime,clinicaltrialsofmostdrugs,whichmightexposetheseproblems,generallylastonlyafewmonths.Ayearisalongtimeinthe world of clinical trials, and the number of people who take these drugsduring these trials is relatively small. Once clinical trials end and a drug isapprovedbytheFDA,monitoringofadversesideeffects tendstoberelativelyhaphazard,usuallydependingondoctorstakingthetroubletofilereportstotheFDA. If a side effect is not immediately and obviously linked to stomach ordigestivefunction,itwillprobablynevergetreported.Regrettably,manyofthepotential accompaniments of long-term acid suppression, including asthma,allergies, skin disorders, rheumatoid arthritis, insomnia, osteoporosis,

gastrointestinal (GI) infection, depression, and many, many others, can takeyearsorevendecadestodevelop.Theywouldseemtohavenothingtodowithstomachacidand,therefore,wouldrarely,ifever,bereported.

GERD:TheSeriousSideofHeartburn

It wasn’t too long ago that heartburn was viewed as largely a nuisance,somethingwe joked about, put upwith, blamed onMother’s cooking. Today,heartburniswidelyseenbythemedicalprofessionastheprimarysymptomofapotentially dangerous medical condition known as gastroesophageal refluxdisease,orGERD.Thisshiftinattitudehasbeendriveninpartbynewresearchand partly by the availability (and marketing) of new drugs and surgicalprocedures.

GERDisnotreallyadisease,perse,butmorelikeasyndromeconsistingofoneormoreofthesedisorders:

• Damage to the esophageal lining that may or may not producesymptoms.

•Mildtosevereinflammationofthedelicateliningoftheesophagus.• Symptoms such as heartburn; belching; upset stomach, bloating/gas;sense of fullness, particularly when accompanied by chronic cough;regurgitation of stomach contents, hoarseness, wheezing or asthma,difficultyswallowing,orsorethroat.

When heartburn occurs regularly for months or years, it is said to bechronic. People with chronic heartburnmay have damage to their esophageallining(especiallythelowerendof theesophagus) thatbeginsasmildirritationbutmayendupwithscarring,constriction,ulceration,andultimately,inaverysmallpercentageofpeople,cancer.Thisiswhyintermittentorminorheartburnshouldneverbeallowedtobecomechronic.

AlthoughGERDoccursonlyinaminorityofpeoplewhohaveheartburn,given the potential danger of chronic heartburn, today’s acid-trumpingtreatments would seem to be among modern medicine’s more important, ifunderappreciated,marvels.GERDappearstohavemetitsmatchinthesepotentdrugs that not only relieve heartburn, but promise to protect us against moreserious,evenlife-threateningconditions.

It’s no wonder they have become among the best-selling drugs everproduced.Indigestion/heartburn/GERDisamultibillion-dollarcashcowforthe

pharmaceutical industry. In the United States alone, we spent more than $7billiononthemin1999.Prilosecaloneaccountedformorethanhalfofthat,$4billion,nearlydoublingitssalesfromthepreviousyear.2

IndigestionandHeartburnAreNotCausedbyTooMuchStomachAcid

Asyoumighthaveguessed,wethinkthere’ssomethingdreadfullywrongwiththis rosy financial picture.Wewonderwhy somuch of humanity is going tosuchgreatlengthstoriditselfofallthatannoyingstomachacid,whenveryfewofuseverconsistentlyhastoomuchacidinourstomachs,andwhen(exceptforafewrareconditions)heartburnishardlyeverassociatedwithtoomuchstomachacid.

Chronic heartburn sufferers often have their stomachs and esophagusesexaminedviax-raysandgastroscopes(fiberoptictubesthatallowthedoctortolook inside the stomach and even take pictures), but in my thirty years ofmedicalpractice,notonepersonwho’shadtheseproceduresdoneelsewherehasever told me that they have also had careful measurements made of theirstomachacidproduction!Whenweactuallymeasurestomachacidoutputundercareful, research-verified conditions, the overwhelming majority of heartburnsufferersarefoundtohavetoolittlestomachacidproduction.

Yes,youreadthatcorrectly.Heartburnalmostneversignalstoomuchacid,anditmayoftenbeassociatedwithtoolittle!

Thisisnosecret.Thisisawell-documented,butlittle-appreciated,medicalfact. Ithasbeenconfirmed in thescientific literaturerepeatedlyandfrequentlythroughoutthelastonehundredyears.

Thepharmaceuticalcompanies,whomakeallthosepotentacid-suppressingantiheartburnmedications,knowthatheartburnandGERDarenotcausedbytoomuch acid. Their researchers are very smart, and they read the scientificliterature.They arewell aware of the kinds of stomachs their drugs are goinginto. That’s why their ads almost never actually come out and state thatheartburnisaprovenresultof“toomuchacid.”Still,themessagecomesthroughloudandclear: If stomachacidcausesheartburn, then lessacidmustbebetterthanmore.

Logical as this sounds, though, it simply isn’t true! As we show in thisbook, for many people with heartburn and/or GERD, the best treatment mayactually be more acid, not less. If this sounds like throwing gasoline on

smoldering embers, that’s right, it does sound like it, but in fact, it’s not.Paradoxical as it seems, for the better part of a century, knowledgeablephysicians have successfully treated tens of thousands of people withindigestion,heartburn,andotherdiseasesrelatedtodeficientstomachacidwithnatural, inexpensive acid supplements (along with various other naturalremedies).Oncethetreatmentiscompleted,indigestionbecomeslargelyathingof thepast, and theirpatientsno longerneed to takepowerful, expensive, andpotentiallydangerous(overthelongterm)acid-suppressingdrugs.

Q:WhenIsaCausenotaCause?A:WhenIt“Causes”Heartburn.

Well,onemightask,ifheartburnisn’tcausedbytoomuchacid,thenwhatisitcausedby,andwhydothosedrugsseemtoworksowell?Afterall,itcertainlyappearsthatloweringstomachacidlevelsrelievesheartburnandhelpshealtheesophagealdamageassociatedwithGERD.

We do not deny that stomach acid causes the symptoms of heartburn(althoughnotnecessarilyotherformsofindigestion)andthatitisresponsibleformuchGERD-relateddamage.Weagreethatexposuretoacidcausestheburningfeeling of heartburn, and that chronic exposure to acid can causemore severeconditions such as reflux esophagitus and GERD. Our argument is with themistakenconceptthatittakes“toomuch”stomachacidtodothedamage.Evena small amount of acid in thewrong place (such as the esophagus) can causesymptomsandultimatelytissuedamage.(Afterall,weknowthatstomachacidmust be strong stuff, if it can help reduce even a tough beefsteak into theequivalentofbeefsoupinanhourorso.)

Norcanwedisagreewiththefactthatloweringtheacidityofthestomachoften does help relieve the symptoms of heartburn and reduce the damage ofGERD,albeittemporarily.Andyet,wefeelquitecomfortableinturningaroundandstating—withabsolutelynoequivocation—thatneitherheartburnnorGERDisreallycausedbytoomuchstomachacid.

Figure1-2.Heartburnhappenswhenasmallamountofstomachacidrefluxesupthroughttheloweresophagealsphincter(LES)valve,irritatingandinflamingthedelicateliningoftheesophagus.

Confused? You’re in good company. Most of the medical professionprefers toavoiddealingwith thisapparentparadox,aswell.But isacid takingtheheatforthe“crime,”whenitspresenceintheesophagusisreallytheresultofotherevents?

Asanyonefamiliarwiththerelevantscientificliteraturewillquicklyagree,heartburnandGERD(butnotnecessarilytheothersymptomsofindigestion)arenot primarily diseases of stomach acid. Rather they are usually diseases ofmuscle,specificallythemuscularvalve(orsphincter)thatguardsthelowerendoftheesophagus.Knownastheloweresophagealsphincter(LES),itnormallyopenswidetopermitswallowedfoodandliquidstopasseasilyintothestomach,but,exceptforbelchingandvomiting,thisistheonlytimetheLESisintendedtoopen.It’ssupposedtoshutdownsoonafterthefoodhaspassed,blockinganyacidicstomachjuicesfrommakingthereturntripuptheesophagus.IftheLESisworkingproperly,itdoesn’tmatterhowmuchacidwehaveinourstomachs.It’snotgoingtomakeitupintotheesophagus.Ontheotherhad,iftheLESisasleepattheswitch,evenasmallamountofacidcouldrefluxintotheesophagusundertherightconditions.

Scientists have found that when we have heartburn or GERD, the LESopensbrieflywhenit’snotsupposedto.Ifwe’vegotacid—oranythingelse—inourstomachs,sometimesevenalittlebit,andithappenstobeinthevicinityoftheLESwhenthevalvepopsopeninappropriately,wegetreflux(seeFigure1-2).Theprimarysymptomofreflux,ofcourse,isheartburn.Ifrefluxhappenstoofrequentlyandexposes theesophageal lining to toomuchacidover too longa

period,theliningcanbecomeirritatedorinflamed,aconditionknownasrefluxesophagitis.Onceanareahasbecomeinflamedorirritated,acid—anyamountofacid—willtendtoadvancethedestructiveprocess,ultimatelytoGERDandtheformationofulcersorworse.

Isanexcessofstomachacidtoblameinthisscenario?Hardly.Acid,afterall,isjustaliquid,preytogravityandthemuscularcontractionsofthestomachandesophagusanddestinedtopassivelyfinditsownlevel.

Itdoesn’tmatterhowmuchacidthereisinthestomach.AslongastheLESstaysclosed,wewon’tgetheartburnor reflux. (Remember, stomachsarebuiltfortheverypurposeofcontainingandworkingwithverystrongacid,acidthatisone-hundred-thousand times stronger than theacidityofourblood.) Insteadofpointingtheaccusingfingerat“excess”stomachacid,weshouldreallybeeye-ballingthatold,asleep-at-the-switchgatekeeper,LES.

ConventionalTreatmentsforHeartburnandGERD

Nearlyallcurrentlyavailableconventional treatmentsforheartburnandGERDaredesignedtoreducetheacidityofthegastricjuice.Mostoftheseproductscanbecategorizedaseitheracidneutralizersoracidsuppressors/acidblockers.

AcidNeutralizers

Theseclassicproducts,commonlyreferredtoasalkalis,relyonthefundamentalchemical fact of life that acids and alkalis (also called bases) neutralize, orcancel each other out (see “Acids, Bases, and pH” on page 29). The activeingredients are typically calcium, sodium, aluminum, ormagnesium salts thatcombinewith stomach acid (hydrochloric acid,HCl), to form a “neutral” salt.Sinceantacidsdonotaffectthesecretionofstomachacid,theirinfluenceonthegastricacid-basebalance(knownasthepH)istransient,lastingonlyuntilalltheantacidmoleculesareusedup.Inthemeantime,thestomachcontinuestosecreteHCl.

Antacidproductsareeasilyavailablewithoutaprescriptionandarewidelyregardedasextremelysafe.Foroccasionaluse,theycanbeusefulforreducingheartburnand,whenusedthisway,probablywillnotcauseanyharm.However,overuse, especiallywhen prolonged, can result in serious problems. Themostimportant adverse effect of acid neutralizers is known as the milk-alkalisyndrome,whichconsistsofexcesscalciumintheblood,anelevatedbloodpH

(alkalosis), and,most importantly,kidney failure.Milk-alkali syndrome resultsmost easily from the excessive consumption of milk (high calcium) plus anantacid over a long period of time, but it can also occur by taking excessivecalcium-basedacidneutralizersalone.

Inthedaysbeforeacid-blockingdrugs,thecombinationoflargeamountsofmilkandantacidswasaverycommonconventionaltreatmentforpepticulcers.Unfortunately,many of the peoplewho followed this dubiousmedical advicewoundupwithmilk-alkali syndrome.The incidenceof the syndromedroppedoffsharplywiththeintroductionoftheacidblockers.However,itisstartingtoriseagainaspeople,especiallyelderlywomen,takehighdosesofantacidsmadefromcalciumcarbonate(e.g.,Tums)asameansofsupplementingtheircalciumintakeinanattempttopreventthebone-wastingdiseaseosteoporosis.3–5(Aswedescribe inchapter4,calciumcarbonate isoneof theworstdietarysourcesofcalcium, because the calcium is so poorly absorbed, especiallywhen stomachacid secretion is low. Since calcium carbonate neutralizes HCl, it actuallyinhibitstheabsorptionofcalcium.)

Othertypesofantacidscontainthemetalaluminum.Althoughtheevidenceis far from conclusive, it is possible that aluminum may be involved in thedevelopmentofbraindementias,suchasAlzheimer’sdisease.Forsafety’ssake,it’s probably best to avoid the long-termuse of these products for this reasonalone.Commonlyavailableneutralizingantacidsinclude:

•Aluminumhydroxide+magnesiumcarbonate(Duracid)• Aluminum hydroxide + magnesium hydroxide + calcium carbonate(Tempo)

• Aluminum hydroxide + magnesium hydroxide (Maalox, Mylanta,Gelusil,Gaviscon)

•Aluminumhydroxide(Amphojel)•Aluminummagnesiumhydroxidesulfate(Riopan)•Calciumcarbonate+magnesiumcarbonate(Mi-AcidGelcaps,MylantaGelcaps,MylagenGelcaps)

•Calciumcarbonate+magnesiumhydroxide(Rolaids)•Calciumcarbonate(Tums)•Magnesiumhydroxide(milkofmagnesia• Sodium bicarbonate (“bicarb,” baking soda, Alka Seltzer*, BromoSeltzer)

Acid-Suppressors

Acidblockingdrugscomeintwobasicvarieties:histamineH2-receptorblockersandprotonpumpinhibitors.

HistamineH2-receptorblockers.Thesedrugs(alsocalledH2-blockers)reduceacidlevelsbythrowingaroadblockrightinthemiddleoftheprocessthatleadstoacid secretion.Asdescribed ingreaterdetail in chapter3,mostgastric acidsecretion is the end result of a process that begins with the hormone gastrinstimulatinghistamine-producingcells,whichinturnsignalacid-producingcellstosecreteHCl.Byblocking theactionofhistamine, themessagenevergets tothe acid-producing cells to secrete acid. These drugs can be very effective inturningoffmostoftheacidflowforhoursatatime.

Originally developed primarily to treat peptic ulcers, they came to bewidely used for relieving heartburn/GERD once it became clear that pepticulcerswere actually caused by the bacteriaHelicobacter pylori, not by excessacid.Astheirpatentsranout,therespectivepharmaceuticalcompanieshaveallbroughtoutlow-doseversionsoftheirdrugsfornonprescriptionsales.

Aswediscussthroughoutthisbook,thelong-term,continuoussuppressionof gastric acid secretion may have important adverse consequences for ourhealth,whichare largely ignoredbypractitionersofconventionalmedicine. Inaddition to these effects, these drugs all have well-documented adverse sideeffects,most ofwhich involveGI disturbances such as constipation, diarrhea,nausea, vomiting, and, yes, heartburn. Tagamet is particularly problematicbecauseitinteractswithsomanyotherdrugs,producingvariousadverseeffectsdependingontheotherdrug.Oneofthemostdisturbingofthesesideeffectsisaninterferencewiththemetabolismofthehormonesestradiol(themostpotentof the estrogens) and testosterone. In some men, this has resulted in breastenlargement and sexual dysfunction.6Currently availableH2-receptor blockersinclude:

•Cimetidine(Tagamet)•Ranitidine(Zantac)•Famotidine(Pepcid)•Nitazidine(Axid)

ProtonPumpInhibitors.Themechanisminsidecertaincells inthestomach’sliningthatactuallyproducesandsecretesHClisknownastheprotonpump.Themost potent of the acid-suppressing drugs block the action of this pumpmechanism,hencetheirname,protonpumpinhibitors(PPIs).Justoneofthese

pills iscapableof reducingstomachacidsecretionby90 to95percent for thebetter part of a day. Taking higher and/ormore frequent doses of PPIs, as isoften recommended for “intractable” heartburn or for treating peptic ulcers,producesastateofachlorhydria (virtuallynostomachacid). Inaddition to theconsequences of chronic acid-suppression, there are many serious concernsassociated with the use of PPIs. The most common adverse effects includediarrhea,skinreactions,andheadache,whichcansometimesbesevere.7–9Otheradverse effects, which occur less frequently, include impotence, breastenlargement,10andgout.11Aswediscussinsubsequentchapters,theseandotheradverseeffectsdirectlyrelatedtoprofoundsuppressionofgastricacidsecretionby these drugs are a major concern that is being completely ignored bypractitioners and supporters of conventional medicine. Currently availableprotonpumpinhibitorsinclude:

•Omeprazole(Prilosec)•Lansoprazole(Prevacid)•Rabeprazole(AcipHex)•Esomeprazole(Nexium)•Pantoprazole(Protonix)

MotilityEnhancers.Drugs known asmotility enhancers try to tighten up theLESandhustle food (andacid)outof the stomach faster.Thiswouldseem tomakealittlemorephysiologicalsenseintermsoftheactualcauseofheartburn,but these drugs have been limited by their unwanted side effects. The mostadvanced of these drugs, Propulsid, was pulled from the market by the FDAafter a few years of widespread clinical use showed that it was causing anunacceptable number of potentially fatal heart failures. As happens all toofrequently with new drugs, these problems were not apparent during clinicaltrialsofthedrug,buttheyshoweduponcethedrugwasreleasedtothegeneralpublicandmillionsofpeoplestartedusingit.

WhyDoAnti-AcidDrugsSeemtoWork?

Instead of strengthening the LES “dam” and helping it to perform its normalfunction, conventionalmedicine treats heartburn/GERD primarily bymoppingup asmuch of the acid “flood” as possible (with neutralizing antacids) or bydrying up the river of acid itself (with drugs like Zantac and Prilosec). In so

doing,theclinicaleffectsofthemalfunctioningLESareareminimized.

Acids,Bases,andpH

Acidsandbases(oralkalis)[Pronounced,AL-KUH-LIES]aretheyinandyangof the chemical world. Scientists measure the relative acidity-alkalinity of asubstancebyusing apH scale.ThepH scale ranges from0 (most acid) to 14(mostalkaline).ApHof7isconsideredneutral.

AcommonwaytomeasurepHisusingstripsoflitmusorpHpaper,whichare treated with a chemical that changes color depending on the relativeacidity/alkalinityof the substance it contacts.ElectronicpHmeters thatgive anumericalreadoutaretypicallyusedwhenarapid,precisereadingisrequired.

The HCl produced in the stomach has a pH of 0.8, which makes it anextremely potent acid. HCl is formed in the lining of the stomach by thecombinationofionsofhydrogen(H+)andchloride(Cl–).

Asimilarlypowerfulalkalinesubstance,likesodiumhydroxide(alsoknownaslye,orNaOH),hasapHapproaching14.Getthisstuffonyourhandsandyoucouldgetjustasbadaburnasifyou’dhandledpureHCl.BecauseNaOHissocorrosive, it is widely used to unclog bathroom and kitchen drains, selling asDranoandotherbrandnames.Anotherfamiliar,butmuchmorebenign,alkalinesubstanceissodiumbicarbonate,alsoknownasbakingsoda.

In general, our bodies tend to prefer chemicals more toward the neutralmiddle of the pH scale. Water, for example, has a pH of 7, squarely in themiddle.Bloodtendstobeslightlyalkaline(pH7.4).ThepHofthe“resting,”orbetween-meal,stomachusuallyrangesfrom1to3.

When we mix chemical opposites like acids and bases, they tend toneutralizeeachother.Let’ssaywemixtwopowerfulpHoppositeslikeHCland

NaOH.[Pleasedon’ttrythisathome!]TheresultingchemicalreactionproducesNaCl+H2O,betterknownastablesalt+water,orsaline,whichhasapHof7.

Oneoftheearliestmeanspeoplecameupwithtorelieveheartburnwastoswallowanalkalinesubstanceinordertoneutralizetheoffendingstomachacid.Ofcourse,wewouldn’twanttoswallowlye,butsodiumbicarbonateworksverywell,producingnotonlysaltwater,butalsothegascarbondioxide(CO2).TheCO2 can make us feel bloated and cause burping, as it fills the stomach andescapesbackuptheesophagus.

Tothedegreethattheyreducetheamountofacidavailabletoreflux,thesedrugs can temporarily relieve the symptoms of heartburn and also prevent thedamageassociatedwithGERD.Neutralizingantacids reducegastric (stomach)acidityonlymodestly,butusuallyenoughtorelieveheartburndiscomfortforanhouror two.Themorepotentacid-suppressingdrugs reduce theacidsecretionbyupto90percentormore,essentiallyeliminatingacidfromthestomachforuptotwenty-fourhoursorlonger.12

IfSymptomsDisappear,What’sSoBadAboutSuppressingStomachAcid?

Acid-neutralizing agents and acid-suppressing drugs minimize heartburnsymptoms, reduce the risks ofGERD, can help heal ulcers, and are generallyconsideredbyconventionalmedicinetobesafe.Doesit reallymatter that theysuppressstomachacidsomuch?What’stheharm?Webelieveitdoesmatter,forseveralimportantreasons:

• The drugs disrupt the natural gastrointestinal environment. Althoughwidely believed to be safe and well tolerated, acid-blocking drugs, bytheirverynature,induceprofoundchangesintheinternalenvironmentofthestomachand intestines.Decadesof researchhavedemonstrated thatchronicallylowlevelsofstomachacid(notnecessarilycausedbydrugs)canbeharmful in the long run, leading tomaldigestion,malabsorption,and malnutrition, which can predispose to a wide range of seriousailments.

•Thereliefanti-aciddrugsofferistransient.Heartburnstaysawayonlyaslongasacidlevelsstaysuppressed,andacidlevelsstaysuppressedonly

as long as we keep taking the drugs. If we stop taking them, we riskheartburn’sreturn,sometimeswithavengeance.It’snotuncommonforpeopletotakeacidblockers,andevenacidneutralizesdailyforyearsandyearsatatimeinordertoavoidarelapse.

• The drugs don’t cure heartburn, they only temporarily relieve thesymptoms.Likemanyofthe“wonderdrugs”thathavebecomeavailableinthisageofpharmaceutical-dominatedmedicine,neitheracid-blockingdrugs nor traditional neutralizing antacid products do anything to cureheartburnorGERD.Theyonlytemporarilysuppressthemajorsymptom—heartburn.SymptomsuppressionisthestandardtreatmentstrategyformostdiseasesinconventionalWesternmedicinetoday.Withthepossibleexception of antibiotics, very few drugs being marketed today canactuallycureanything.

•Thesedrugsmaybeeffectiveatremovingtheirritatingagent,butasfarasthecauseisconcerned,theycompletelymissthepoint.Wecanthinkofacid-blockingtreatmentlikedryinguptheriverafterafloodbutneverrepairing the faultydam that’s actuallycausing the flooding.Notehowgingerly the American College of Gastroenterology (ACG) treats theissue of “cure” (see below). Although they use the “c-word” ratherloosely, it’s clear that, from their conventional perspective, the only“real”cureisnotdrugsbutsurgery.*

•Wecanbecomedependent,oratleastreliant,onanti-aciddrugs.Theyworkonlyaslongaswekeeptakingthem.Stoppingtreatmentcommonlytriggers an acid “rebound,” which can be quenched only by—youguessedit—takingmoreacidsuppressingdrugs.Althoughthereboundistypicallyshort-lived,lastingacoupleofdaysatmost,howmanypeopleare willing to “tough it out” and endure the heartburn when they canquicklysquelchitbygettingbackontheiracidblocker?Whilethisisn’texactlyatrueaddiction,oncethiscyclegetsgoing,we’realmostasgoodas“hooked”onacidsuppression.

CanAnythingActuallyCureMyTroublingHeartburn?

WhattheAmericanCollegeofGastroenterologysays:

“In patients with mild heartburn, simple lifestyle changes may improve

symptoms. However, patients with more severe symptoms or esophagealdamage usually need either long-term medications or surgery to cure theirheartburn. Similar to the treatment of high blood pressure, medications forGERDcontrolthedisease,butareeffectiveonlywhentakenregularly.Forthosewho cannot achieve adequate symptom relief and healing through medicaltherapy,anti-reflux surgery offers the only potential for cure by strengtheningtheloweresophagealsphincter.”(Italicsadded.)

—PatientInformation

This strategy leavesmuch to be desired for peoplewith heartburn, but itworks great for the pharmaceutical companies. If the drugs actually curedheartburn/GERD,thecompanieswouldn’tmakenearlyasmuchmoneyastheydobysellingdrugsthatprovideonlytemporarysymptomaticrelief.

RepairingtheCauseofIndigestionandHeartburn,theNaturalWay

Amuchmoresensible—but lessprofitable—tactic is to treat therootcauseoftheproblem, repair it, andsendusonourway,heartburn-and indigestion-free,andunbeholdento thepharmaceuticalgodsPrilosec,Zantac, theircousins,andtheirdescendants.Curingadiseasemeanseliminatingthecauseoftheproblem.Whenadiseaseiscured,itdoesnotreturnoncethetreatmentishalted.Curingadiseasemeansremovingthereasonwedevelopedheartburninthefirstplace,notjustsuppressingitssymptoms.

With treatment that addresses thecause of the symptoms, indigestioncanalmost always be eliminated, and (as a consequence of addressing the cause),overall health improves.Given the right environment and enough time tohealitself, an irritated or injured LES often returns to its normal, healthy state,eliminatingheartburn.EventhemoresevereconditionofGERDcanoften(butnotalways)bebroughtundercontrolbythisapproachtotreatment.

All of this can be accomplished by proper diagnosis, elimination ofoffending agents, food allergies and sensitivities, toxins (including caffeine,nicotine, and alcohol), and then by taking a variety of natural substances,including(inalmostallcases)supplementsofstomachacid(HCl)itself.Appliedjudiciously at the appropriate times and accompanied by certain dietary andlifestyle modifications, these treatments can help return digestion to normal,

restore theGI environment to near normal conditions, eliminating indigestion,heartburn,andevenGERDforgood.

If this sounds suspiciously like the“c-word,” formanypeople it is.Oncetheirindigestionand/orheartburn/GERDisgone,it’sgone.Theymaynolongerneed to take some of their natural treatments again, let alone their Prilosec ortheirTums.However,peoplewhoarefoundbyactualtestingtohaveastomachacid deficiency (remember, they’re the overwhelming majority of those withindigestion) can benefit with better overall health by continuing to take acidsupplementswith theirmeals.Thisparticularbenign,natural solution involvesreplacingsomethingthebodyismissing.Itavoidsusingsyntheticchemicalsthebodyisill-equippedtohandle.

BeyondHeartburn:TreatingOtherDiseasesRelatedtoLowStomachAcid

Asaphysicianpracticingformorethanthirtyyears,I’veseentheharmthatlowstomachacidcandooveralongperiodoftime.Ihaveworkedwiththousandsofpatients who arrived at the Tahoma Clinic with diseases as disparate asrheumatoid arthritis, childhood asthma, type 1 diabetes, osteoporosis, chronicfatigue,depression,andmanyothersonlytofindthat theyallhadonethingincommon:theirstomachswereputtingoutaless-than-optimalamountofacid.Inmany cases, by restoring normal gastric function using safe, inexpensive acidsupplements; pepsin and other digestive enzymes; and amino acids, vitamins,minerals, and botanicals, we have been able to help them improve or eveneliminate their disease conditions. And we do this with almost no risk ofdangeroussideeffects.

Admittedly,theideathatheartburnandotherdiseasesmayberelatedtotoolittlestomachacidandcanbetreatedbyswallowingmoreacidfliesinthefaceof medicine as it is taught and practiced today. This wasn’t always the case.Hardly anyone pays any attention to the medical facts—many of themaccumulated during the 1920s, 1930s, and 1940s—showing that low stomachacidoccursdisproportionatelyinpeoplewithnumerousseriousdiseases.Thisisold science, but it is still good science, andmost of these findings are just asvalidtodayastheywerethen.However,nomatterwhattheirage,suchideasdonotfitcomfortablyintoconventionalmedicalwisdom,muchofitpropagatedbythe pharmaceutical companies in support of their valuable acid-suppressingdrugs. Themultibillion-dollar anti-acid franchise depends on the conventional

medicalwisdomstayingrightwhereitis.Yet, the truth is that correcting digestive malfunction can often yield

dramaticimprovementsinmanyofthesediseases.Remarkably,inchildrenwithasthma,itcanbepartofthecure.Inhundredsofcases,Ihavefoundthatmorethan 50 percent of children who come to me with asthma can have theirwheezing cured simply by normalizing their stomach acid and properlyadministeringvitaminB12,withnobronchodilatorsandnocorticosteroids.Thinkabout that:curingthewheezingofchildhoodasthma!There isnoconventionalpharmaceutical treatment for asthmaticwheezing on themarket that can evencomeclosetopermanentlyeliminatingthemostlife-threateningsymptomofthisdisease.

Thefactisthatthecorticosteroidsandbronchodilatorspeoplewithasthmacommonly take—often daily for their entire lives—do not and cannot cureasthma.Insteadofremovingthecauseof thedisease, theymerelysuppressthesymptoms.Andtomakemattersworse,theycanhaveserioussideeffects.

Thisisnotaprettypicture,butitisanaccuratedepictionofthewaymostdoctors treat childhood asthma today. Unfortunately, their treatment strategiesare basedon a fundamentalmisunderstandingof thenature ofmost childhoodasthma.*Thecauseofasthmainthesechildrenliesnotintheirairways,butintheir stomachs. Certainly, treating the symptoms (wheezing, bronchialinflammation)providesquicktemporaryrelief,but itdoesnothingtoeliminatethecause.Instead,itmayleavethechild“reliant”ondangerousandcostlydrugsuntiltheasthma“disappears”(asitoftendoes)atpuberty,orevenpossiblyforthe rest of his or her life. By treating the causes, the symptoms often resolvewithoutfurthertreatment,andtheydonotreturnaslongasstomachacidiskeptatanoptimumlevelandvitaminB12issupplied.Thisiswhywehavebeenableto cure the wheezing of half of all the children who come to our clinic withasthma.(Werealizethatchildrenwithasthmahavenotbeentakingtheantacidsor acid blockers we’ve been discussing. We mention this condition as anexample of one of themany diseases associatedwith inherently low levels ofstomachacidthatcanbeimprovedorcuredbyappropriateattentiontostomachfunction.)

It’sYourChoice

Ifyouhaveindigestionorheartburn,oradiseasefrequentlyassociatedwithlowstomach acid output and poor digestion, whichwould be preferable, treat the

cause or take adrug to suppress the indigestion andheartburn, and thenmoredrugsforeachothersymptom?Theanswerappearsobvious,yetit’sgoingtobealongtimebeforeconventionalmedicinegivesupitsantacid/acid-blockercashcow.

Fortunately,youdon’thave towaituntil theFDA, theAmericanMedicalAssociation, and the many other alphabet-soup agencies that control the“conventional wisdom” in medicine today (almost always following thepharmaceutical industry line) see the “error of their ways.” (Hint: It’s nevergoing tohappen,because there’s so littleprofit in thenatural—unpatentable—acid, vitamin, mineral, amino acid, herbal and other supplements that can beused toeliminateheartburn,and indigestionand to treat relateddiseases.)YoucouldgodowntoyourlocalhealthfoodstorerightnowandpurchaseeverythingyouneedforafractionofthecostoffillingaprescriptionforPrilosec,Prevacid,orotheracidsuppressor.

Before you do that, though,we suggest you read this book first, becauseyou’lllearnthat:

• Thepharmaceutical industry spendsbillions trying toconvinceus that“acid indigestion” comes from toomuch stomach acid, even though acasual readingof the scientific literatureon the subject reveals that theoppositeistrue.

•Asweage,stomachacidlevelsdonotincrease,aswewouldexpectfromthe increase in heartburn associatedwith age. In fact, formost people,acidsecretiondecreaseswithage.

• Overuse of neutralizing or buffering antacids, and ordinary use ofpowerful acid-suppressingdrugs, can inhibit the absorptionof essentialnutrients and impair the digestion of protein, minerals, and a fewvitamins.

• The resulting malnutrition can, over many years, lead to depression,osteoporosis, arthritis, and other chronic degenerative diseases thatreducethequalityofourlivesandmayultimatelyshortenourlifespans.

•Thebestwaytotreat“acidindigestion”isnotwithlessstomachacid,but(almostalways)withmore.

• Replacement acid in the form of safe, inexpensive substitutes forendogenous (internally produced) stomach acid, such as betainehydrochlorideandglutamicacidhydrochloride,enhancesdigestion,andcausesheartburn,indigestion,bloatingandgaseventuallytovanish.

• Theimproveddigestionandabsorptionofessentialnutrientsthatresultfromappropriateacidreplacement,combinedwithnaturalsupplemental

digestive enzymes and elimination of toxins and allergens, improveshealth and reduces the symptoms of a long list of diseases associatedwithlowstomachacidproduction.

• In many of us, correcting the naturally occurring, gradual “digestivefailure of aging” will help restore energy and improve health, thusextendinglife.

ANoteofCaution

Heartburn isusuallyabenigncondition,but ifyousuffer from it regularly formonths or even years at a time, it can be a sign of diseases such as reflux,esophagitis, esophageal ulcer orBarrett’s esophagus, a serious condition thatcanleadtoafatalformofcancer.Thus,wealwayssuggestthatthefirststepyoutake in treating your heartburn is to consult a physicianwho can rule out theserious diseases and who will then guide and support you in treating yourheartburn/GERDthenaturalway. In thefinalchapter in thisbook,we tellyouhow to find a knowledgeable physician who, when you utter the words“heartburn”or“indigestion”won’tautomaticallyreachforthePrilosec.

*AlkaSeltzeralsocontainsaspirin,whichdoesnothingtorelieveheartburnandmayirritatethestomachlining.

*Eventhe“curative”powersofantibioticsaredebatedbynaturalmedicinepractitioners.Continuing theclassic“Bechampvs.Pasteur”argumentofthenineteenthcentury,manyagreewithBechampthatinfectionis only a symptom of an underlying weakness or disorder of the immune system, which antibiotics donothingtocure.

*Thisfundamentalunderstandingof therootcauseofmostchildhoodasthmaisover300yearsold,and(despitemygrayhair)didn’toriginatewithme.Thevery firstEnglish-languagebookdevoted toasthma(Floyer, A Treatise of the Asthma, 1698) stated that “asthma is a winde arising in the stomache.” Seechapter6formoreaboutoriginsofasthmainthestomach.

CHAPTER2

WhyStomachAcidIsYourFriend

Amidst all the media noise about “acid indigestion” and too much stomachacid,itiseasytoforgetapainfullyobviousfact:Acidisinthestomachbecauseitissupposedtobethere.Acidisnotsomenuisancesubstancethestomachusestopunishusforenjoyingapepperonipizza.Acidplaysavarietyofvitalrolesinthedigestiveprocess.Withoutit,ourdigestivehealth—andourhealthingeneral—isdoomedtosuffer.Thischapterdiscussesafewofthemajorrolesstomachacidplays.

AcidPromotestheDigestionandAbsorptionofManyVitalNutrients

Nutrientssuchas thepeptideandaminoacidcomponentsofproteins,minerals(includingiron,copper,zinc,andcalcium),aswellasvitaminB12andfolicacid,alldependonadequatestomachacidfortheirdigestionandabsorption.StomachacidaccomplishesthisbyoptimizingthegastricpH(theacid/basebalance)andby triggering the action of the stomach’s own digestive enzyme, pepsin. If,becauseofinadequatestomachacid,ourbreakfasts,lunches,anddinnersaren’tbeingdigested,thenwecan’tabsorbtheamountofnutrientsfromthatfoodthatNatureintended.Howcanweexpecttostayhealthyifwehavechronicallypoornutrientabsorptionduetoincompletedigestion?

Breakingdownwholefoodintoitsnutrientcomponents thatcanbeeasilyabsorbed into the bloodstream is the raison d’être of digestion. In manyimportantways,ourstomachsinitiatethisprocess.Formanyessentialnutrients,thisbreakdownoccursatanoptimumrateonlywithinanarrowrangeofrelativeacidity.Ifthereistoolittleacid,thenormalchemicalreactionsrequiredtobreakdown and make nutrients ready for absorption may not occur at maximumefficiency. If this condition persists for an extended period of time, a state of

selectivemalnutritionmay result that can adversely affect various vital bodilyfunctions,manyof themwellbeyondthedigestivesystem.Over time, thiscananddoesleadtodiseasessuchasanemia,osteoporosis,cardiovasculardiseases,depression,andmanyothers. (Ournursesand techniciansarealwayssurprisedwhenawomanwhoisknowntohavethebonewastingdiseaseosteoporosis—due in part to poor calcium absorption—turns out to havenormal, rather thanlowstomachacid.)Attheotherextreme,toomuchacidcanliterallyeatawaythetissues of the digestive tract, contributing to ulcers.Aswe have said, though,truelong-termhyperacidityisveryrare.

AcidHelpsDigestProteinbyStimulatingPepsinProduction

Pepsinisanenzymethatisrequiredfortheoptimuminitialdigestionofprotein.During the ingestion of food, the secretion of stomach acid triggers theproductionofpepsin.Ifacidlevelsaredepressed,thensoarepepsinlevels.Asaresult, proteins don’t get broken down into their component amino acids andpeptides (two ormore linked amino acids). The resulting deficiency ofmanyessentialaminoacids,*includingphenylalanine,andtryptophan,aswellasthe“nonessential” amino acid tyrosine, may lead to chronic depression, anxiety,insomnia,andotherdisturbingordangerouslong-termdisorders.

At the same time, the proteins that escape digestion by pepsinmay findtheirway into the bloodstream, an event thatwould not normally happen in ahealthy GI tract. The body generally reacts with hostility to the presence of“foreign”proteinsinthebloodorothertissues.Theresultingimmuneresponseissimilartowhathappenswhenthebodymobilizesitspowerfuldefenses(e.g.,Tcells,Bcells, andantibodies) toeliminateaviralorbacterial infection. In thisway, inadequate digestion by our stomachs (as well as inadequate pancreaticfunction)cancontribute togradually increasing foodallergies.For reasonsnotcompletelyunderstood,althoughgeneticsareafactor,peoplewithautoimmunediseases such as lupus, rheumatoid arthritis, type 1 diabetes,Graves’ disease,and many others very frequently have low levels of stomach acid, poordigestion,andmanyfoodallergiesthatservetoaggravatetheirconditions.(Thepossible role of low stomach acid in autoimmune and related diseases isdiscussedingreaterdetailinchapter6.)

StomachAcidPreventsBacterialandFungal

Overgrowth

Here’s an extreme, but very revealing, incident: Decades ago, public healthofficials in India investigatedwhy some people in a village in themidst of acholeraepidemicdidn’tcontract thedisease,whileothersdid.Theyfound thatmany more of those who stayed healthy had normal levels of stomach acid,while thosewhodeveloped thediseaseusuallydidnot.Apparently, the strongstomachacidkilledthecholerabacteriabeforeitcould“colonize”(anddamage)theentiregastrointestinaltract.

Most bacteria cannot survive very long in a highly acidic environment.WhilebacteriaarefoundinabundanceinthelessacidicregionsoftheGItract—themouth,esophagus,smallintestine,andespeciallythelargeintestine(colon)—thestomachremainslargelysterileduetoitsnaturalacidity.

Astheacidbarrierbeginstobreakdown(ascanhappenaftertakingacid-blocking drugs or with certain common disease states), the stomach becomesvulnerable to bacterial invasion on two fronts. First, otherwise “friendly”bacteria that normally live comfortably in the small intestine (where theyhelpwithdigestion)findamorealkalinegastricenvironment less threatening.Theymay migrate up to the stomach, where they multiply and colonize the once-forbiddenterritory.

At the same time, common bacteria constantly—and unavoidably—enterthebodythroughthenoseandmouth.Ordinarily,theywouldquicklymeettheirmaker inapoolof stomachacid,butwhenstomachacid isdeficient,manyofthese microorganisms may live to multiply—and infect—another day. Mostbacteriathatenterbytheseroutesarerelativelybenign.Theymayinterferewiththe digestion of some nutrients, and they may cause symptoms like diarrhea,constipation, and stomach pain in some cases, but the disruption is rarelyserious. But some microorganisms, including Salmonella, certain extremelyvirulentstrainsofE.coli,andtheVibriocholeraenotedabove,cancauseseriousillness,evendeath,whenlowstomachacidallowsthemtogainabeachheadonthegastricshores.

The significance forourhealthof a strongacidbarrier in the stomach isdiscussedingreaterdetailinchapter4.

WhatHappensWhenStomachAcidLevelsGetTooLow?

Until relatively recently, physicians were concerned, not so much with theeffects ofhigh levels of stomach acid, butmorewith the long-term effects ofexcessivelylowlevels.Adeclineinacidsecretionwithadvancingagehasbeenwell documented.1 From the late nineteenth century to the mid-twentiethcentury,researchersregularlyreportedthatthenumberofpeoplewithanacidity(totalornear total absenceof stomachacid), alsoknownasachlorhydria, andlowacidity,alsocalledhypochlorhydria,increasedwithagefromalowofabout4 percent at age twenty to as much as 75 percent after age sixty. A 1941reviewerofstomachacidresearchobserved:

“Anacidityorachlorhydria ismore likely tobeevidenceofdiseaseofthe stomach than any other variation of gastric secretion… There is nodisease known capable of inducing true gastric hyperacidity* …Pathological deviations in acid andpepsin concentrationswere invariablyinthedirectionofdecrease.”2(Italicsaddedforemphasis.)

As recently as 1996, a British physician, reviewing age-related GIdisorders,notedthatstomachacidoutputcommonlydeclinesaspeopleage,dueto a loss of the cells that produce the acid. This condition is termed atrophicgastritis, or gastric atrophy. Moreover, a large portion of “normal,” healthypeopleaboveagesixty—withoutheartburn—haveatrophicgastritis.3

Atrophic gastritis is the major cause of “age-related” declining stomachacid levels.Manystudieshavedemonstrated thatpeoplewithatrophicgastritisare exceptionally vulnerable to a wide range of serious disorders that go farbeyondthestomachandesophagus.Theseinclude:

•Poorabsorptionofimportantvitamins,minerals,andaminoacids•Poordigestionofproteins•Allergies• Bronchial asthma in childhood (an obvious exception to “age-related”atrophicgastritis)

•Depression• Bacterial overgrowth in the stomach and small intestine, leading tosymptoms such as heartburn, “gas,” constipation, diarrhea, and anincreasedsusceptibilitytopotentiallyfatalinfectionssuchascholeraandSalmonella.

•Perniciousanemia•Stomachcancer

• Skin diseases, including forms of acne, dermatitis (itching, redness,swelling),eczema,andurticaria(hives)

•Gallbladderdisease(gallstones)•Rheumatoidarthritis•Lupuserythematosus•Grave’sdisease•Ulcerativecolitis•Chronichepatitis•Osteoporosis•Type1(insulin-dependent)diabetes•Acceleratedaging

FunctionalGastricAtrophy

Ifstomachacidissoimportant,andifchronicallylowlevelsofstomachacidcanmakeuschronicallysick,doesitmakeanysensetobetakingdrugswhosesolepurposeistotodepletestomachacidevenfurther?

Scientificstudieshavesofarbeenunabletoshowconclusivelythattakingacid-suppressing drugs contributes to the development of atrophic gastritis.However, there have been reports that taking Prilosec can sometimes lead toachlorhydriathatlastedmorethantwoyearsafterdiscontinuingthedrug.4

Even without destroying acid-producing cells in the stomach, acidsuppressingdrugscancreate a chronic state that amounts to functionalgastricatrophy.Inotherwords,boththediseaseandthedrugaccomplishthesamefeat:Theydrasticallyreducestomachaciditytofarbelownormal.

We know what can happen when stomach acid levels are depressed fordecades due to ordinary, garden-variety atrophic gastritis. But what happensafter decades of depressed stomach acid due to functional gastric atrophyinducedbydecadesofusingtoday’spowerfulacidsuppressors?Nobodyknowsforsure.Prilosechasbeenwidelyusedforonlyafewyears.Prevacid,Aciphex,Protonix,andNexiumareevennewer.Willwebeseeingariseintheoccurrenceofstomachcancer,arthritis,osteoporosis,orotherseriousdiseasesasthesedrugsbecome even more popular and people start entering their second and thirddecade of continuous drug-induced gastric hypoacidity? We think it’s verylikely, but to be “scientifically precise,” we must say that nobody knows forsure.Butwhytakethisriskatall?

*Someaminoacids(andothernutrients)aretermedessentialbecausethebodycannotmanufacturethemitself.Theymustbeobtainedfromexternalsourcessuchasfoodand/orsupplements.

*RarediseasessuchasZollinger-Ellisonsyndrome,whichareassociatedwithexcessstomachacid,wereunknownin1941.

CHAPTER3

HowtheUpperGITractWorks…Basically

Most of us have only a vague idea of how the digestive systemworks.Weknow,forexample,thatafterweputfoodintoourmouths,chewit,andswallowit, it passes into the stomach, and what’s left after digestion is completeeventuallypassesoutofthebodyintheformofabowelmovement.Wemightremember fromhighschoolscienceclasses that thegastrointestinal (GI) tract,wheredigestionoccurs,isessentiallyahollowtubethatbeginsatthemouthandendsattheanus.Althoughitisnamedafteritstwomostprominentfeatures,thestomach(gastro-)andtheintestines,theGItractactuallyconsistsofmanymorevitalstructures(seeFigure3-1).

Mostofusalsohaveageneralideathatwhatweeatnotonlycomesouttheother end,but also finds itsway into the restofourbodies,nourishingbones,muscles, nerves, blood, and every other organ, tissue, and cell. The familiarexpression,“Youarewhatyoueat,”isatleastpartlytrue.ThefoodweeatgetsconvertedintheGItractintosomethingthatquicklybecomesanintimatepartofourphysicalbeing.Everycellinthebodyiscomprisedofmaterialsthatbegantheirexistencesomewhereintheoutsideworld.

Figure3-1.Majororgansofthegastrointestinalsystem,aswellasthelungs,trachea(windpipe),anddiaphragm.

DigestionistheprocessbywhichfoodgetsbrokendownintheGItractbybothmechanicalandchemicalprocesses,sothatnutrientscanbeextractedfromthefood,absorbedintothebloodstream,anddistributedthroughoutthebodyforthemyriadpurposesinvolvedinkeepingusaliveandkicking.

Althoughweoftentakeitforgranted,digestioninvolvesahighlycomplexand well-coordinated interaction of many different acids, enzymes, alkalinesubstances,hormones,andotheritemstoonumeroustomention.Whentheseareproducedandreleasedinjusttherightamountsatjusttherighttimes,digestionproceeds unnoticed, in the background, perfectly. But if something upsets thebalance, say a deficiency in stomach acid, it can have profound health effectsthatmaymanifestasanupsetstomachorheartburn,butmayextendfarbeyondthestomachitself.

In this chapter, we focus on a small but extremely important part of thedigestivestorythattakesplaceintheregionsometimescalledtheupperGItract,whichincludesthemouth,esophagus,andstomach.TheupperGItractfunctionsasakindofstagingareaforthedigestivesystem.Itisherethatfoodisbrokeninto small,manageablepieces, softened, lubricated,and liquefied.At the sametime,proteins,aminoacids,minerals,andothernutrientsareextractedfromfoodand processed to make them optimally available for the subsequent steps indigestionandabsorptionthattakeplacelateron.Anydisruptionherewillbefelt

andmagnifiedfardownstream.Likemostotherprocessesinthebody,digestioncanbeextremelycomplex,butdon’tgetscared,we’lltrytokeepitsimple.

Figure3-2.Theactionofperistalsispropelsa“bolus"offoodfromthemouthtothestomach.TheLESremainscloseduntilthefoodapproachestheesopheageal-stomachjunction,atwhichpointitopensbriefly

toallowthefoodtopassthrough.

TheMouth

Digestionbeginsinthemouth,wheretheactofchewingbreaksdownthefoodintosmaller,moremanageablepiecesandmixesitwithsaliva.Saliva,whichisreleasedassoonasfoodentersthemouth(orevenatitssight,smell,orthought,for Pavlov fans),moistens the food and begins the process of breaking downstarches. Italsohelps lubricate thefoodso itcanpassmoreeasily through thenextlegofthejourney,theesophagus.

TheEsophagus

The esophagus is a muscular tube that begins in the back of the throat andmerges at its lower end with the upper part of the stomach. The esophagusconsistsbasicallyofasmoothinnertubelinedwithdelicateepithelialcells.Theinner tube is surrounded by layers of muscle tissue. When we swallow, theesophagealmusclereactsbyinitiatingarhythmicseriesofcontractions—calledperistalsis—that start at the topandwork theirwaydown toward the stomach(seeFigure3-2).Theeffectistopropelthefoodintothestomach.Forthosewholikestatistics,ittakesaboutsixtoeightsecondsforaswallowoffoodtotraversetheentirelengthoftheesophagusandenterthestomach.Thefoodproceedsatanaveragevelocityofaboutoneinchpersecond.

TheLES is thevalve thatguards the junctionbetween theesophagusandstomach.Asmentionedinchapter1,inorderforfoodtopassfromesophagustostomach, theLESmust relax. It does this quite readilywhen food reaches thelowerendof theesophagus,andit thenquicklytightensup,actingasabarrieragainst the contents of the stomach, which would otherwise reflux (literally,“flow back”) up into the esophagus. This barrier function is critical, becauseunlike the stomach, the delicate tissue that lines the inside of the esophaguscannot standup to theharshdigestive juicesnormallyandnaturallypresent inthestomach.

WhentheLESisinitsnormalrestingmode,withnoswallowingandlittleornofoodinthestomach,itsaveragepressureisabout20mmHg(millimetersof mercury). (This means a counterpressure of 20 mm Hg would have to beappliedtopryitopen.)About1.5to2.5secondsafterweswallow,LESpressuredrops(relaxes)andremains lowforsix toeightseconds.StomachcontractionsthatincreasepressureinthestomachcausetheLEStotightenuptoprotecttheesophagusagainstreflux.1

Figure3-3.Schematicrepresentationofthestomachshowingthemajorregionsandconnectingorgans.

The problem in heartburn/ reflux/GERD is hardly ever low resting LESpressure. Researchers have found that reflux usually occurs when little low-pressureblipscalledtransientLESrelaxations(TLESRs)causeLESpressuretofallbriefly.TLESRshavenothing todowithswallowing.For reasonsmedicalscience does not yet completely understand, they occur all by themselves atintervalsthatvaryfrompersontopersonandfromhourtohourwithinthesameperson.AndbecausemostrefluxeventsoccurduringTLESRs,peoplewhohavethem frequently also have a higher risk of developing reflux esophagitis orworse.2

TheStomach

The stomach is a large, muscular, bladderlike structure, perfectly suited tochurningaquantityofchewedandswallowedfood,mixingitwithpotentacids,enzymes, and other digestive juices, and blending these into a liquefiedmushcalledchyme.

The stomach is considered to have several major regions, including thecardia,fundus,body(corpus),antrum,andpylorus.Itconnectstotheesophagusat its upper end (cardia) and the duodenum at its lower end (pylorus). Theduodenumconnectsthestomachtothesmallintestine(seeFigure3-3).

Thestomachservesfourbasicfunctions:

• Storage reservoir. It stores swallowed food for a short time. Thisreservoirfunctionletsuseatasubstantialmealinarelativelyshorttimeandprocessitlater.

•Foodprocessing.Itliquefiesandgrindsthefood,mixingitwithvariousdigestivejuices.

• Nutrient extraction and digestion. It begins the extraction anddigestionofproteinsaswellasnumerousvitaminsandminerals.

• Transfer. When the appropriate consistency of stomach contents isreached, thestomachbegins feedingchyme through theduodenumintothe small intestine, where the major work of digestion and nutrientabsorptionbegins.

Theliningofthestomachconsistsofsixbasictypesofcells,eachofwhichsecretesoneormoreimportantsubstances:

•ParietalcellssecreteHCl,ahighlypotentacidthatparticipatesinmanyreactions and lowers the intragastric pH (acidity inside the stomach) totherangethatisoptimalfordigestionandabsorptionofnutrients.Aswenotedinchapter1,thecellularmechanismthatisprincipallyresponsiblefortheproductionofstomachacidisknownastheprotonpump.Drugsknown as proton pump inhibitors, turn off this pump, reducing acidsecretion by more than 90 percent. Parietal cells also secrete intrinsicfactor,whichisrequiredfortheabsorptionofvitaminB12.

• Chief cells secrete pepsinogens,which are convertedwith thehelpofHCLintotheprotein-bustingenzymepepsin.

•Gcellssecretegastrin,anextremelyimportantregulatoryhormonethatregulates the release of HCl from parietal cells and pepsinogens fromchief cells. Gastrin also stimulates stomach muscles to contract andpromotesthegrowthofthegastricmucosa(theliningofthestomach).

• Enterochromaffin-like (ECL) cells secrete histamine in response tostimulationbygastrin.

•Mucouscellssecretemucus,whichhelpslubricateandliquefythefood.Mucusalsohelpsprotectthestomachliningfromthecausticintragastricenvironment.

• D cells secrete somatostatin, a hormone that puts the brakes on foodprocessinginthestomachbyslowingtherateofgastrinsecretionastheintragastricpHfalls.

GastricAcidSecretion

Present scientific knowledge tells us that stomach acid secretion is under thecontrolofthreeseparatesubstances:acetylcholine,gastrin,andhistamine.

•Acetylcholine(ACh)isaneurotransmitter,ahormonelikesubstancethatcarriesinformationwithinthenervoussystemandbetweenthenerveandmusclecells.NeuralcontrolofacidsecretionviaAChmakesitpossibleforthestomachtostartsecretingacidatthesight,smell,oreventhoughtof food, as impulsesoriginating in thebrain trigger the releaseofAChontoparietalcells.

• Gastrin promotes HCl secretion by two routes: it directly stimulatesparietal cells, which respond by pumping out acid molecules. Moreimportantisgastrin’sabilitytostimulateECLcellstosecretehistamine.

•Histamine,inturn,stimulatesparietalcellstoreleaseHCl.Thelocationon the parietal cell where histamine binds is called the H2 receptor.Histamine action at theH2 receptor is the primary stimulus for gastricacid release. Drugs known as H2-receptor blockers, including Zantac,

Tagamet, Pepcid, and Axid, prevent gastrin from stimulating H2receptors,whichsignificantlyreducesacidreleaseintothestomach.

TheDigestiveCascade:WhatHappensWhenFoodEnterstheStomach?

When a swallow of food passes through the LES and enters the stomach, ittriggersahighlycoordinatedseriesofeventsdesignedtooptimizedigestion(seeFigure3-4):

•Thestomachliningstretchesabit.

• The stretching is sensed by nerve fibers that signal G cells to beginsecretinggastrin.

•Gastrinstimulatesparietalcellstoincreaseacidsecretionandrelease.Italso stimulates ECL cells to secrete histamine, which then stimulatesparietalcellstoincreaseacidsecretionandrelease.

•Parietalcellsalsoreleaseasubstanceknownasintrinsicfactor,whichisrequiredfortheabsorptionofvitaminB12.

Figure3-4.Thedigestivecascade.

• Gastrinalso triggers the releaseofpepsinogens fromchiefcells in thegastricmucosa.

•Pepsinogens,inthepresenceofsufficientHCl,areconvertedintopepsin,theprimarystomachenzymeresponsibleforbreakingdownproteinsintoaminoacids. (Theconversionofpepsinogen topepsinoccursoptimallywhen the pHof the stomach is 4 or less. If the pH should rise to 5 orhigher [less acidic], pepsinogens are inactivated, and no pepsin isformed.)

• Whileall this isgoingon,gastrinalso signals the stomachmuscles tobegin churning and grinding away, helping tomix the contents and tomovethemalong.Oncethestomach’scontents(chyme)havebeen“fullyacidified,” the processing of proteins and many other vitamins andmineralscanmoveaheadatanoptimalrate.

•Bythetimethechymereachesthelowerreachesofthestomach,thepHbegins to riseso that thedigestionandabsorptioncan takeplace in thesmall intestine. The acidity of the stomach is reduced in the lowerregions of the stomach—the antrum and pylorus. This occurs by twomainmechanisms.First,availableacidstimulatesDcells in theantrumtobeginsecretingthehormonesomatostatin.SomatostatinfeedsbacktoG cells to slow the production of gastrin. Less gastrin means lesshistamine and less acid secretion from parietal cells. Second, acidifiedchyme contacting the lining of the duodenum stimulates the release ofthehormonesecretin.

• Secretin, in turn, signals the pancreas (a large gland best known forsecretingthehormoneinsulin)toreleaseavarietyofdigestiveenzymesaswellas ionsofbicarbonate.Bicarbonateproducedbythepancreas isactually the same as the “bicarb” that (i.e., sodium bicar bonate, orbaking soda) that people have long used to relieve heartburn byneutralizingstomachacid(raisingthepH).

•Thehormonecholecystokinin(CCK)isreleasedinthesmallintestineatthesametimeassecretin.Ittravelstothegallbladder,whereitstimulatesthe release of bile—essential for the proper digestion of fats—into thesmallintestine.

This has been a highly simplified description of a vastly more complexprocess.Nevertheless, it serves tomake five extremely important points aboutacidandGIfunction:

1.TheseessentialdigestivefunctionscanoccuronlywithinaverynarrowrangeofpH,andthatrangeshiftsdependingonthestageofdigestion.

2. “Blocking” or “neutralizing” stomach acid interrupts the normaldigestivecascadeatacrucialjuncture.Itremovesthe“acidtrigger”thatmakes virtually every subsequent event in the sequence possible.Reducing acid means less pepsinogen, less pepsin, less secretin, lessCCK,lesspancreaticenzymes,andlessbile.

3. With less acid to feedback and turn downgastrin production, gastrinlevelssoar.Aswediscussbelow, theexcessivelyhigh levelsofgastrinhavebeenlinkedtoaformofstomachcancer.

4. Since the absorption ofmany vitamins,minerals, proteins, and aminoacids occurs only within a narrow range of pH, disrupting the gastricdigestiveenvironmentbyreducingacidity(raisingpH)adverselyaffectstheprocessingandabsorptionofmanyofthesenutrients.

5.Consequently,evenifweeatanexcellentdiet,ifstomachacidlevelsarevery low, we may be unknowingly partially starving ourselves. Notsurprisingly,nutritionaldeficienciesareacommonfindinginpeoplewithlong-standingatrophicgastritisaswellas inpeople takingcertainacid-suppressingdrugs(seechapter4.)

PumpingAcidwithGastrin

HCl is secreted by parietal cells, which are located in the gastric mucosa,primarily in the fundusandbodyof thestomach (seeFigure3-3).Thisacid ismolecularlyidenticaltotheHClthatcomesinthoseheavyglassbottleswiththeglass stoppers in high school chem lab. It is the same stuff as muriatic acid,whichhaslongbeenusedforheavy-dutycleaningandotherindustrialpurposes.Itisverystrongstuff.Duringtheperiodsbetweenmeals,relativelylittleacidissecreted,but it isenoughtokeepthepHof the lumen(or insidecavity)of thestomach between pH1 and pH3.However, once food enters the stomach (or

evenfollowingthesight,smell,taste,orthoughtoffood),acidsecretionbeginstoincrease,reachingitsmaximalratewithinabouttwohours.Acidlevelsreturntotheirpremealbaselinebyfourtofivehoursafterthebeginningofameal.

TheamountofHClinthestomachatanyonetimeislargelycontrolledbythe hormone gastrin, which is released from G cells located in the stomachlining, or mucosa. As the intragastric pH rises above 3 (less acidic), G cellsbegintosecretemoregastrin,whichtriggersparietalcells tostartpumpingoutmoreHClintothestomach.TherisingacidtidelowersthepH,signalingtheGcellstoslowtheirsecretionofgastrin,whichslowstheflowofacid,andsoon.In the absence of food, this balanced feedback system keeps the “resting" pHsomewherebetween1and3inmostpeople.3

Foodupsetsthebalance,becausemostfoodshavepHssomewherearound“neutral”(pH7).SofoodenteringthestomachautomaticallyraisesthepHinthesurroundingfundusandbody,kickinggastrin-HClsecretionintoahighergear.AslongasthepHstaysabove3,gastrinwillcontinuetostimulateparietalcellstopumpacid.AsthepHdropsbackintothe2–3range,Gcellsslowtheirreleaseofgastrin.InadditiontothepHstimulus,G-cellsalsoreleasegastrininresponsetocertainfoodconstituents,includingpeptides,aminoacids,calcium,aswellascertainelementsincoffee,wine,andbeer.

Gastrin also stimulates acid release indirectly by signaling ECL cells tosecretehistamine.Thehistamine, in turn,binds toH2 receptors, turningon theacidreleasepumps.

In addition to its secretory functions, gastrin also controls the muscularactionsofthestomach,referredtoasgastricmotility.Musclecontractionspropelthe stomach contents back and forth, mixing them completely, and at theappropriatetime,propellingthemoutofthestomachandintotheduodenumandsmallintestine.Gastrinreducesstomachmotility,whichslowsgastricemptying.

Inhibitinggastricmotilityhelpsthestomachholdandprocessalargemeal.Other factors that influence the rateofgastricemptying include thevolumeofcontents (motility increases as volume increases), pH (lower, pH slowsemptying), and composition of themeal (liquids empty faster than solids; fatsdelayemptying).

TheDangersofDisruptingtheGastrin-AcidBalance

The stomach is very happy as long as the acid-gastrin feedback system humsalong smoothly. It starts to act upwhen the secretion of gastrin, acid, or both

goestoofaruportoofardownfortoolong.When acid secretion is too low, the “resting” pH rises higher than the

normal gastric pH, 1–3.The elevated pH sends awake-up call to theG cells,which start spewing outmore gastrin to prod the parietal acid pumps toworkharder.Acid secretionmay appear normal, because theG cells areworking alittlehardertomakeupthedeficit,butgastrinlevelsarehigherthantheyshouldbe. Above-normal gastrin secretion is termed hypergastrinemia, and it is apotentiallyseriousconditionthatcanleadtogastricadenocarcinoma—aformofstomachcancer.4Thisisdiscussedindetailinchapter5.

Hypergastrinemia typically occurs in people with atrophic gastritis(atrophied,thinned,underfunctionalornonfunctionalstomachlining)orinthosewhotakepowerfulacid-blockingdrugsforlongperiodsoftime.Theamountofgastrin in play at any one time is a direct reflection of the current level ofstomach acid. Insufficient acid levels (pH greater than 3) in gastric atrophytriggerhighergastrin levelsas thebodytries tocompensatefor lossofacidity.Takingastandard20-mgdailydoseofPrilosectypicallyresultsinuptoathree-tofourfoldincreaseingastrinlevels.5Inpeoplewhoseheartburn/GERDfailstorespondtothestandarddose,long-termtreatmentwithdosesashighas40or60mghasproducedgastrinlevelsasmuchastenfoldabovenormal.6-17

WhyDoesn’ttheStomachDigestItself?

With all that potent acid floating around the stomach, the question inevitablyarises,whydoesn’tthestomachdigestitself?Howisthethin,delicateliningofthestomachprotectedwhiletheequallydelicateliningoftheesophagusisnot?

In fact, the protection afforded the stomach lining is as simple as it iseffective.Itconsistsprimarilyoftwosubstances:mucusandbicarbonate,whicharesecretedbycellsintheepitheliallining(topcelllayer)itself.

Mucusisaclearfluidthatservestolubricateandprotectdelicateepithelialtissue throughout the GI and other respiratory systems. Gastric mucus is notmuchdifferent fromthe fluid that runsoutofournoseswhenwehaveacold.Consisting largelyofwater (95percent)andasmallportionofasugar-proteinsubstancecalledaglycoprotein(5percent),ithasaslighdygel-likequalitythathelps it stick to the epithelial lining and serve as a physical buffer againststomachacidandotherdigestivejuices.

Bicarbonate is alkaline and very effective at neutralizing potent acids.Bicarbonateionsaresecretedbycellsintheliningofthestomachandduodenum

in response to contact with acid. Coating the gastric epithelium, along withmucus, theyneutralizeanyacid theycome incontactwith.Soeffective is thismucus-bicarbonatebarrier thatwhen thepHis2 (veryacidic) in the lumen,orcavity,ofthestomach,thepHatthestomach’sliningapproaches7,orneutral.

Theesophagusisstrictlyatransportorgan,notadigestiveorgan.Aciddoesnotbelongintheesophagus,becausetherearenocellsintheesophagealliningto secreteprotectivemucusorbicarbonate.Theesophagus isnot totally at themercy of refluxing acid, though. It gets someprotection from saliva,which isslighdyalkaline.Thus,swallowingsalivanotonlyhelpswashrefluxingacidoutoftheesophagus,italsoneutralizesittoacertaindegree.Atthesametime,acidintheesophagustriggersaseriesofwavelikeperistalticcontractionsdesignedtosendtheacidbacktothestomachwhereitbelongs.

An intact protective barrier in the stomach is essential to health.Inflammation(gastritis)orulcersmayoccurinregionsofthestomachwherethebarrierhasbeenbreached.Likeheartburn,ulcerswere,formanyyears,thoughtto be caused by too much acid. In fact, gastric ulcers often occur in peoplewhose acid levels are low. It is now widely accepted that most ulcers areinitiatedbyadisruptionintheprotectivebarrier,mostfrequentlycausedbythebacteriaHelicobacter pylori but also by certain drugs (e.g., aspirin and othernonsterioidal anti-inflammatory drugs, NSAIDs), which are exploited bystomachacid.

HiatalHernia

Thechestcavityandabdomenareseparatedbyalargesheetofmusclecalledthediaphragm. Above the diaphragm lie the heart and lungs. Below it lie thestomach, pancreas, liver, gallbladder, intestines, and the rest of the digestiveorgans. The esophagus passes through the diaphragm via an opening called ahiatus.It isnotuncommonforaportionof thestomachtoprotrudethoughthehiatus into the chest cavity. This condition is known as a hiatal (or hiatus)hernia(seeFigure3-5).

Figure3-5.Schematicdiagramofhiatalhernia.

Itisestimatedthatasmanyas25percentofpeopleaged50yearsandolderhaveahiatalhernia.Theseherniasaremore likely tooccur inpeoplewhoareoverweight or pregnant.Normally, the LES alignswith the diaphragm,whichhelps keep the valve closed except when it is supposed to open following aswallow. However, when there is a hiatal hernia, the LES rises above thediaphragm,which helpsweaken the valve and increase the chances of reflux.Also, the acidic gastric juice may accumulate in the herniated portion of thestomachandflowbackintotheesophagus.Hiatalherniaswereoncebelievedtobetheprimarycauseofheartburn.Itisknowntoday,though,thattheyareonlyone factor.Most hiatal hernias,while troublesome, do not require any specialattention. However, large ones can cause serious problems and may requiresurgery.

CHAPTER4

StarvingintheMidstofPlenty:

HowStomachAcidLevelsAffectNutrientAbsorption

Elaine and TomMacDonald walked into my office, Tom guiding Elaine asunobtrusivelyashecould.Heshowedherachair,andtheybothsatdown.

“As you may have guessed, I’m not seeing as well as I’d like,” Elainebegan.“Myeyedoctor tellsme it’smaculardegeneration inbotheyes, thoughtheleftisworsethantheright.I’vebeentakingthosevitaminsthateyedoctorsarestartingtorecommendthesedays,but theydon’tseemtobehelpingatall,andmyvisionisslowlygettingworse.”

“We’ve heard you have a treatment that can help macular degenerationsometimes,”Tomsaid.“We’rehopingit’snottolatetohelpElaine.”

“Asitisnow,IcanreadaninterstatehighwaysignifI’mstandingrightinfrontofit,”Elainesaid.“Andthat’swithmyglasseson.IwasateacherbeforeIretired,andIsomissbeingabletoreadmybooksandnewspapers.”

“Ofcourse,shecan’tdriveanywhereeither,”Tomadded.“How’syourhealthotherwise?”Iasked.“AsfarasIcantell,it’sOK.Idon’thavetheenergyI’dlike,butthenI’m

sixty-seven,soIguessthat’stobeexpected,”Elaineresponded.“Nootherbothersomesymptoms?”“NonethatIcanthinkof.”I asked about her health history, family health history, diet, and exercise.

Thenwewent to an examination room for a physical exam.All appearedOKuntilwegottoherfingers.Hernailsbentveryeasily.

“Excuseme,butyourfingernailsaren’tverystrong,arethey?”“They’vebeenthatwayallmylife.Neverhavebeenabletogrownicenails

likesomewomendo.Mine, theycrack,peel,chip…I tookgallonsofgelatinwhenIwasyounger,butitneverhelped.ThelastfewyearsI’vebeentakingalotofcalcium,ithelpsalittle.They’restrongerforawhile,butthenbadagain.

Can’treallyputittogetherwithanything.”“Doyougetcrampsinyourlegs?”“Yes.”“Howoften?”“Oh,twoorthreetimesaweek,especiallyatnight,butoccasionallywhen

I’vebeendoingalotofwalking.Butthere’snothingunusualaboutthat,isthere?Tomgetsthem,too,andsodosomeofourfriends.Wethoughtitjustwentwithourtimeoflife,likethisgrayhair.“Shetouchedherhead.

“You’reright, thoseofuspast fiftydogetmore legcramps thanyoungerpeople,butthosecrampsaren’taninevitablepartofaging.They’reacorrectablemalfunction.”

Imadeafewnotes.Wefinishedherexamandwentbacktomyoffice.“What shall I do first aboutmyeyes?”Elaine asked. “I’manxious toget

startedrightaway.”“First,haveyourstomachtested…”“Mystomach?Howwillthathelpmyeyes?”“Aswegetolder,anincreasingnumberofsymptomsandhealthproblems

need to be approached by checking the stomach and the rest of the digestionfirst.Bythe timewe’resixty,at leasthalfofuswhohavesymptomsorhealthproblems have problems with digestion and nutrient assimilation. The legcramps that you and many past-fifty people have are usually a symptom ofinadequate digestion and assimilation of calcium, magnesium, potassium, andotherminerals.”

“In your particular case, it’s likely you’ve had digestion/assimilationproblems for years. If we don’t patch up these problems as best we can, wewon’t have asmuch of a chance to help your eyes, since all the nutrients oureyesneedenterourbodiesthroughthedigestivetract.”

“Maybethat’swhythesevitaminstheeyedoctorgavemearen’tworking?”“Likelythat’spartofit,buttheydon’thaveallthenecessarynutrients,and

thefewtheydocontainareinverysmallquantities.”“WhydoyouthinkI’vehaddigestionproblemsforyears?Idon’thaveany

digestivesymptoms,asfarasIcantell.”“Yourfingernails.Alargemajorityofwomenwhohavecracking,peeling,

chippingfingernailsalsohavepoorstomachanddigestivefunction.”“Really? You’re saying I could have had glamorous fingernails all these

yearshadIonlyknown?”“Don’tknowaboutglamorous,butatleastalotstronger.Butgettingback

to tests … along with the stomach test, we need to check further on yourdigestion through a stool analysis, looking atmineral levels, amino acids, and

hormones,particularlytestosterone.”“So far, I think I understand checkingmy digestion and theminerals…

eventhesevitaminsyousayareweak…butaminoacids?Testosterone?”“Aminoacidsarethebuildingblocksofprotein.Ifwehopetorebuildcells

andtissues,weneedtomakesureaminoacidsareadequate.Yourshaveahigherprobabilityofbeinglow—”

“Becauseofpoordigestionandassimilation.”“Exactly.”“But what about testosterone?” Tom asked. “What does that have to do

witheyes?”“It’scertainlynotthemostimportantfactor,butvisionissoimportantthat

wewant to cover all the bases right away. Testosterone is themost powerfulanabolicsteroidthatourbodiesmakenaturally.Anabolicsteroidsdomuchmorethan stimulate the growth of muscles. They stimulate repair and regrowth ofmanydamagedbodytissues.I’veobservedthatcorrectingunusuallylowlevelsoftestosteronecanhelptissuerepairineithersex.”

“HowlongwillittaketogetthetestsdonesoIcangetstarted?”“The tests are important, but I recommend you start treatment today or

tomorrow,assoonasyourtestsareturnedin.Overtheyears,I’vefoundthatifwe give key nutrients intravenously, particularly zinc and selenium, twiceweekly,wemakemuchfasterprogress.Wemakesurethequantitiesaresafe,ofcourse,butalsosufficienttodothejob.”

“Justzincandselenium?”“Thosearethemostimportantminerals,butwemakesuretobackthemup

withavarietyofmineralsandothernutrients.And,ofcourse,I’llaskyoutostartwithoralsupplementation,too.”

“Butwhataboutdigestingandassimilatingthemproperly?”“Your stomach test will be completed and the results known today; the

remainingtestsonyourdigestionwillbecompletedinjusttwoorthreedays.”“Whatabouttherestofthetests?Shouldn’twewaitforthem?”Tomasked.“We’lladjustoraddtowhatwe’redoingassoonastheybecomeavailable,

but sinceweknowmanyof themajor itemsof importance,wecan start themrightaway.”

“Howoftendoesthiswork?”Elaineasked.“Noteverytime,butdefinitelymorethanhalfthetime.”“HowlongbeforeIknowonewayoranother?”“In my experience, if we use the IVs, digestive aids, all the oral

supplements, and hormones, if necessary, you can see … literally … resultsstarting in four to six weeks. If there’s been no improvement in six to eight

weeks,thenit’snotlikelythisallwillhelp.”“Ihopeitworksforme.InadditiontotheIVs,whatsupplementsshouldI

take?”“Very,verylikelythelistwillstartwithbetainehydrochloridewithpepsin

withmeals, to replacewhat your stomach likely isn’t doing—secreting acid—andpancreaticenzymesaftermeals.Together, theseshouldrestorea largepartofweakdigestivefunction.

“We’ve already covered zinc and selenium, two of the most importantminerals.VitaminE and taurine are very important, too.Bilberry and ginkgo,herbal medications, contain flavonoids and other substances important to theretina.VitaminA,copper—”

“Holdon,”Elainesaid.“Ican’trememberallofthis.”“Youdon’tneedto.Thereareseveral‘combinationformulas’availablein

naturalfoodstoresthatcontainmostoralloftheseingredients.“IVs,digestiveaids,acombinationformulawiththenutrientsyou’verecommended…anythingelse?”Tomasked.

“The tests will tell us if amino acids, testosterone, and possibly otherhormonesareadvisable.”

“WhenIstartseeingresults,howlongwillIneedtocontinuehavingIVs?”Elaineasked.“Icertainlycan’tgetthosedoneforyearsandyears.”

“You won’t need to. Remember, much of the problem is due to poordigestion and assimilation, and you’ll be taking care of that so oralsupplementationhasabetterchancetodothejob.Butjustfor‘insurance,’whenthe IVs are discontinued, we’ll ask you to use some of the key nutrientsdissolvedinDMSO,whichgetstheminthroughtheskin.Butdon’tworryaboutthatnow,we’llcoveritwhenthetimecomes.

“Also, please remember that this treatment doesn’twork every time. I’veobservedittoworkinamajorityofcases;unfortunately,that’snotone-hundredpercent.”

“Atleastallthesenutrientswon’thurtme,”Elainesaid.“Andwe’llpraythatElaine’sinthatmajority,”Tomsaid.“Pleasedo!That’llhelp,too.”In four weeks, Elaine’s vision started to improve. After eight months of

treatment,shereportedthatinsteadofjustbeingabletoreadinterstatehighwaysigns, she could read books and newspapers again. She’s continued hertreatment,andfiveyearslaterhasmaintainedhervisionatthatlevel.*

…

Let’ssayweeatthemosthighlynutritiousdietimaginable,containingjust

the rightamountsofeveryvitamin,mineral,protein, fiber,andothernutrients.Butlet’salsosaywehaveatrophicgastritisorwetakeanacidblocker,orboth.Thankstotheresultinglackofstomachacid,wemaystillwindupwithseriousnutritional deficiencies. The reason can be summed up in one word:“absorption.”

The reasonwehaveanesophagus,anda stomach,and intestines, and therestoftheGIsystemistodigestnutrientsofallsortsandthenabsorbthemintoour bodies. As we discussed in chapter 3, the processes of digestion andabsorption depend on the close coordination of a large number of hormones,enzymes,acids,mucus,andotherdigestivejuices.Whenworkingnormally,thissystem is so perfectly tuned that acid, pepsin, gastrin, bicarbonate, andmanyothersubstancesallgetsecretedatjusttherighttimesinjusttherightamountstoproduce just therightpHtoprepare thefoodforoptimaldigestionand thenabsorptionofeveryavailablenutrient.

Themostcommonthingthatgoeswronginthestomachisalossofacid-producing cells, which is accompanied by a fall off in acid production. Thisdisease, known as atrophic gastritis (or gastric atrophy), increases with age,affectingmorethan30percentofpeopleovertheageofsixty.1

AsstomachpHrises (remember,higherpH ismorealkaline, lowerpH ismore acid) in people with atrophic gastritis, the complex and finely tuneddigestiveandabsorptiveprocessesgetthrownoutofbalance.Asaresult,manyaminoacids,vitamins,minerals,andothernutrientsdestinedfortransportacrosstheintestinalliningandintothebloodstreamliterally“misstheboat”andwindupexitingthebodyinthefeces.

As if “natural” atrophicgastritiswerenotbadenough,millionsofpeopletoday gulp down antacids and powerful acid-suppressing drugs to furthersquelchthefreeflowofacidsothatonlyatrickleremains.Whatisthisdoingtotheirnutrientabsorption?Decadesofscientificresearchhavedemonstratedthatlow stomach acid, whether occurring naturally (i.e., atrophic gastritis) oriatrogenically(medicine’seuphemismfor“causedbythedoctor”),shouldbeanimportantconcernbecauseof itspotentiallydestructiveeffectson thenutritiveprocess. We could be eating the richest, most balanced, most nutritious dietpossible,butifourstomachacidsecretionistoolow,wemaybemissingoutonmuch of the nourishment ourselves and instead nourishing the bacteria in ourseptictanksormunicipalsewagetreatmentplants!

In this chapter,we describe how some key vitamins,minerals, and othernutrients get processed in the stomach to make them available for use in thebody.We also showwhat happens to them—and to us—when the intragastricpHstartstorise.

Iron

Among its numerous vital functions in the body, iron is needed to formhemoglobin, theoxygen-carryingpigment that turns redbloodcells red. In theabsenceofsufficientdietaryirontomatchthatusedupbythebody,thediseasecalled iron-deficiencyanemiadevelops.Chronicanemiameans that thebody’stissues are starved for oxygen. It can sap muscle strength and drain stamina,leaving us feeling weak and tired. Sometimes anemia is signaled by palemembraneson the insideof theeyelids,and/orpaleoralmembranes,butoftenit’sdiscoveredonlybyabloodtest.

Although there had been anecdotal reports for decades, the connectionbetween stomach acid and iron deficiency anemia first started getting noticed“scientifically” during the 1930s. In one report, deficient stomach acid,described as either achlorhydria (complete absence of stomach acid) orhypochlorhydria (mild tosevere lossof stomachacid),was found inelevenofthirteenchildrenwithanemia.Inthreeofthesixchildrenwithachlorhydria,andfiveofthesevenwithhypochlorhydria,thecauseoftheanemiawasdeterminedto be deficient iron absorption.2 In another study reported thirty years later,thirty-fiveofforty-fourpeople(80percent)withchroniciron-deficiencyanemiawere found to have belownormal acid secretion.3 Iron-deficiency anemia is awell-knownconsequenceofsurgicalprocedures that remove the regionsof thestomachwhereacidisproduced(fundusandbody).4

Whether or not iron gets absorbed depends to a large degree on thechemicalformittakes.Invariousstudies,ferroussalts(e.g.,ferroussulfate)andferricsalts(e.g.,ferricchloride)haveoftenbeengiventoexperimentalanimalsorhuman“guineapigs”withvariouslevelsofstomachpH.Theyhavegenerallyfoundthattheabsorptionofferriciron(butnotferrousiron)iscloselyrelatedtopH;thelowerthepH(moreacidic),thebettertheirongetsabsorbed.Thereasonissimple.Inorderforirontogetabsorbedintheduodenumandsmallintestine,ithastobedissolvedinaliquidmedium(i.e.,stomachjuice).FerricironhasnotroublestayinginsolutionaslongasthepHislessthan5.ButoncethepHgetsabove5, as it can inpeoplewhohaveatrophicgastritis and/orwho take acid-suppressingdrugs, ferric ironstarts to falloutof solution—toprecipitate—andform an insoluble iron salt.When this iron passes through the duodenum andsmallintestine,insteadofgettingabsorbedintothebloodstreamwhereitcandosomegood,itpassesthrough—likeanexpresstrainthroughalocalstation—on

itswaytothecolonandultimateexcretion.Bycontrast,ferroussaltsremainsolublethroughamuchwiderrangeofpH,

extendingtoneutral(7)orslightlyabove(alkaline).Thus,theamountofacidinthestomachhaslittleornoeffectontheabsorptionofironfromaferroussalt.5

Thetypeoffoodtheironcomesfromalsomakesabigdifferenceintermsofabsorption.Acommonsourceofahighlybioavailablesourceofiron—knownashemeiron—ismeat.Likeferrouschloride,hemeironremainssolubleevenifthepHrisesabove7. Ifweeata lotofmeat,weabsorb lotsof ironnomatterhowmuchacidourstomachsmightbesecreting.However,ironthatcomesfrom“nonheme”sources,suchasgrainsandvegetables,aswellasthatwhichcomesfrom iron “fortification” of some foods, is usuallymuch harder to absorb, fortwomainreasons.First,itmustbereleasedfromitsfibrouscarrier,andsecond,itmustbedissolved.

Thesecret ingredient in thisdual reaction,ofcourse, isHCl.Gastricacidfirstbreaksthechemicalbondsthatholdtheironmolecules,freeingthemfromthe food, and then it converts them from insoluble ferric salts tomore solubleferroussalts.AsgastricpHrises, though,absorptionof“vegetarian iron”falls.Laboratory research using test-tube procedures have shown that virtually allfiber-boundirongetsabsorbedonlywhenthegastricpHislessthan4.0.6

ASouthAfrican study explored the relationship between iron and pHbyextracting samples of gastric juice from peoplewhowere known to be eithernormal or iron deficient.7 After adding the gastric juice samples to pieces ofbread containing a known amount of “nonheme” iron, the investigatorsmeasuredtheabilityofeachsampletoextracttheironinthebreadanddissolveit. The results were very clear.When the pH of the sample was less than 2,gastricjuicehadlittletroubledissolvingtheiron.WhenthepHwashigherthan2,though,theabilityofgastricjuicetosolubilizetheironwassharplycurtailed.

In the second phase of the study, the researchers gave pieces of iron-fortified bread (now containing a radioactive isotope “tracer” of iron) to thesame people, but this time for them to eat. A while later they measured theamount of radioactive iron absorbed by the test subjects’ bodies. In this “reallife” situation, iron absorption correlated quite well with the ability of eachsubject’s gastric juice to dissolve the iron in the earlier, test-tubephaseof theexperiment. The better the juice was at dissolving the iron in a test tube, thebetter the ironwasabsorbedby theGI tractsofactual livingpeople.Basedonthoseresults,theresearchersconcludedthatstomachpHwas“theonlyfactoringastricjuiceofimportanceinmodifyingtheabsorptionofnonhemeiron.”7

Figure4-1.ReplacingHClimprovesironabsorptioninpeoplewithanemiaandlowstomachacidlevels.Iron(ferricchloride)wasdissolvedeitherinwaterorHCl.Onaverage,morethan300percentmoreiron

dissolvedinacidwasabsorbedcomparedwithirondissolvedinwater.AdaptedfromPJJacobsetal.,1963.

Giventheseresults,itcomesasnosurprisethatwhensupplementaryHClisgiven to people with anemia and low stomach acid, their iron absorptionimproves and their anemia disappears. This was demonstrated in a study inwhich people with anemia and very low stomach acid levels were given iron(ferricchloride)dissolved inwaterononedayandHClonanother.Themeanrate of absorption on “acid days” was 9.2 percent, compared with only 2.2percenton“waterdays”(seeFigure4-1).8

Whydoesn’tironprecipitateoutofsolutiononceitreachestheduodenumand small intestine, where the environment becomes less acidic than thestomach? The reason is that, while iron remains in solution in the acidicstomach,itcombineswithcertainmoleculesknownas ligands,whichcanhelpthe iron remain dissolved even after the pH rises to 7 and above. Commonligands include ascorbic acid (vitamin C), proteins, amino acids, and sugars.Thisexplainswhy takingvitaminCwithan ironsupplementcan improve ironabsorption.However, inorder for these ligands to combinewith iron, the ironmustfirstbedissolvedinanacidicsolution.9

AntacidsandIron

Bytakingneutralizingantacidsoracid-suppressingdrugs,wemaybeinterferingwithnormalironabsorption.Swedishresearchersfoundthataliquidneutralizingantacid (similar to Maalox) containing aluminum hydroxide, magnesium

hydroxide, and magnesium carbonate significantly reduced the absorption ofiron supplements containing either ferrous carbonate, ferrous fumarate, orferroussulfate.Theabsorptionofferroussulfatewasreducedby38percentandthe fumarate by 31 percent. The ferrous carbonate was completely insolublewhentakenwiththeantacid.10

In another study, U.S. researchers compared iron absorption when ironsupplements (ferrous sulfate) were taken with either aluminumhydroxide/magnesiumhydroxide(e.g.,MaaloxII,Mylanta),sodiumbicarbonate("bicarb"), or calcium carbonate (e.g., Tums). The results showed that theMaalox IIhad littleornoeffecton ironabsorption,but theother twoantacidsprofoundlyinhibitedabsorption.Sodiumbicarbonatereducedironabsorptionby50percent,andcalciumbicarbonateby67percent(seeFigure4-2).11

Notethattheseantacidstudiesemployedferroussalts,whicharecommonlyusedinironsupplementsandwhicharenormallyeasilyabsorbable,evenwhenpHrisesintothealkalinerange.Whythendidtheseantacidshavesuchmarkedeffectonironabsorption?ItappearsthatthiseffecthadlesstodowithpHandmore todowith the formationof insoluble salts (e.g., ferric carbonate)by thecombinationoftheantacidwiththeironcompound.

Figure4-2.Reductioninironabsorptionassociatedwithantaciduse.Ironlevelsinplasmaweremeasuredtwohoursaftertakinganironsupplement(ferroussulfate)withorwithoutanantacid.Boththeantacids

tested,sodiumbicarbonateandcalciumcarbonate,sharplyreducedironabsorption,whilealuminum/magnesiumhydroxidehadlittleeffect.AdaptedfromO’Neil-CuttingandCrosby,1986.

These experiments do not ask or answer the question, “Howdoes simplyreducingstomachacidityaffecttheabsorptionofironfromfood?”Thisquestionwas investigated in a study inwhich normal volunteers ate “testmeals” (e.g.,

hamburger,Frenchfries,vanillamilkshake)containingaknownamountofironafter taking the acid-suppressing drug Tagamet. The results showed a highlysignificant, 28 percent decrease in iron absorption when the subjects took astandarddoseofTagamet(300mg).Increasingthedoseto600mgand900mgresultedinevengreaterdecreasesof42percentand65percent,respectively(seeFigure4-3).12

Figure4-3.Reductioninironabsorptionintestsubjectstakingtheacid-suppressingdrugTagamet.AsthedoseofTagametincreased,theabsorptionofirondeclinedby42percent(600mg)and65percent(900

mg).

Calcium

Calciumisanextremelyimportantmineralthatthebodyusestomakebonesandteethstrong,amonghundreds,ifnotthousands,ofotherfunctions.Forexample,calciumionsarealsoessentialformanydifferentmetabolicandotherreactions,includingthetransmissionofnerveimpulsesinthebrainandthecontractionandrelaxationofmuscles,suchas those thatmaketheheartbeat.Lossofcalcium,fromeitherpoornutritionorage-associatedcauses,canleavebonesthin,brittle,andeasilybroken,aconditionknownasosteoporosis.

Figure4-4.Acidreplacementimprovescalciumabsorption.ReplacementofmissingHClinoneachlorhydricpatientwithbetazoleHClimprovedcalciumabsorptionbyafactorof10.Source:Ivanovichet

al.,1967.

The importance of stomach acid for the absorption of calcium was firstnotedinthe1960satatimewhenhighdosesofcalciumcarbonate(e.g.,Tums)wereoneoftheprincipalmedicaltreatmentsforpepticulcers.Concernedaboutthepossibilityofexcesscalciumabsorption,onegroupofresearchersnotedthatsome ulcer patientswere barely absorbing any calcium at all—just 2 percent.Lookingcloser, theyfoundthat thesepeoplehadverylittlestomachacid; theirmeangastricpHwas6.5.However,whentheygaveoneofthesepeopleanHClsupplement(betazolehydrochloride), lowering thepHto1,calciumabsorptionrosefive-foldto10percent(seeFigure4-4).13

AlthoughTumsarenolongerthetreatmentofchoiceforgastriculcers,inrecent years, calcium “fortification” of foods has become a major obsessionamong food manufacturers wishing to ride the wave of “calcium awareness”presented in the media. (Calcium is currently one of only a small handful ofvitaminormineralsupplementsendorsedbytheFDA.)Yet,wecanconsumeallthe calcium-enriched foods, calciumsupplements, andTumswewant and stillwindupwithacalciumdeficiency,ifwehavelowstomachacidduetoatrophicgastritis or acid-suppression heartburn “therapy.”Aswith iron, the amount ofcalciumthatgetsabsorbeddependstoa largedegreeonboththesourceof thecalcium and the pH of the stomach contents. One very common source ofcalcium,calciumcarbonate,usuallyderivedfromoystershellsor limestone, isoftenusedincalciumsupplementsandantacids(e.g.,Tums).Arethesereallyagoodsourceofcalcium?Well,itdepends.

CalciumcarbonatereactswithHCltoneutralizetheacidandformcalciumchloride,which is a highly soluble salt, that gets easily absorbed in the smallintestine shortly after it leaves the stomach—in solution. The problem withcalciumcarbonateasasourceofcalcium,though,isthattheamountweabsorbisadirectfunctionoftheamountofacidpresentinourstomachs.Ifapersonhasatrophicgastritisand/ortakesanacid-suppressingdrug,calciumabsorptionfromcalciumcarbonatewillbemarkedlycurtailed.(Abettersourceofsupplementalcalciumiscalciumcitrateorcalciummalatewhichismoresoluble,evenwhenacidsecretionislow.)

Otherresearchhasconfirmedtheneedforadequateacidsecretiontoabsorbcalciumfromcalciumcarbonate,butonestudy14 showedthatabsorptioncouldbeenhancedinpeoplewithachlorhydriabytakingthesupplementalongwithamealcomposedofeggs,toast,orangejuice,andcoffee.ThemechanismforthisimprovedabsorptionmayhavebeendemonstratedbyProfessorHarveyCarroll,who experimentally combined calcium carbonate with orange juice (a richsourceofcitricacid)anddemonstratedsignificantformationofcalciumcitrate,15notedaboveasamuchmoreabsorbablesourceofcalcium.

As with iron, the absorption of calcium is a twofold process: first,extracting the calcium from its fibrous (vegetarian) carrier, thengetting it intosolution. Laboratory studies using calcium-containing corn bran and soy hullfibershavefoundthattheupperpHlimitforsignificantcalciumabsorptionwas4.5.16Mostantacidtreatmentsandacid-blockingdrugsaremorethancapableofraisingthegastricpHto5orhigher.Thus,itwouldseemlikelythatusingthesedrugsshouldreducecalciumabsorption.Surprisingly,though,theonlystudytoexamine this issue failed to find any effect of Tagamet treatment (whichproducedagastricpHof4.9to5.5)oncalciumabsorptioninhealthyyoungtestsubjects.17 However, this study has been criticized due to the methodologyemployed,anditsresultsandconclusion—thatTagametdoesnotaffectcalciumabsorption—remain doubtful in light of other studies showing that low acidlevelsinhibitcalciumabsorption.18

Given the importance of calcium absorption for health, onemight expectthat the pharmaceutical companies that make and market drugs that nearlyeliminate acid from the stomachwould be interested in finding outwhat theirdrugs do to calcium absorption.But alas, aside from the one studymentionedabove,noothershaveeverbeenpublished.It’seasytounderstandwhy.Aslongasnooneismakingabigfussaboutnutrientabsorption,andnoone(i.e.,publicdemandortheFDA)isforcingthepharmaceuticalcompaniestodotherelevantstudies,they’drathernotknow.

FolicAcid

Folicacid(folate)isaBvitaminthat,amongotheruses,isvitalforkeepingthecardiovascular system healthy by helping to reduce levels of the amino acidhomocysteine,andforpreventingcertainbirthdefects(e.g.,spinabifida).Folatelevels tend to decline with advancing age, leading to a rise in homocysteinelevels thathasbeen linked toan increased riskof cardiovasculardisease.Thismaypartlyexplainwhy theriskofcardiovasculardisease increasesasweage.Adequate folic acid intake (400–800 micrograms/day) easily prevents theseproblems,butfewpeopleingestenoughofthevitaminintheirnormaldiet.Tomakemattersworse,lowstomachacidlevels,suchasthosethatoccuringastricatrophy, can interfere with folate absorption by raising the pH in the smallintestine.WhenfolicacidisgiventoachlorhydricpatientsalongwithsomeHCl,absorptionofthevitaminincreasesby54percent.19

However, the issue of folate absorption in chronic low acid states iscomplicated by the paradoxical fact that elderly peoplewith atrophic gastritisusuallyhavenormalor even elevated folate levels in their bloodstreams.Howcanthisbe?

It appears that Nature has built in a safety mechanism to prevent folatedeficiencies,although thisdevicecanbea two-edgedsword.Aswediscuss inchapter5,lowgastricacidsecretionresultsinanovergrowthofbacteriawithintheconfinesofthestomach,whicharenormallynearlysterile.Researchershavefoundthatthesehordesofinvadingbacteriaactuallyproducefolatethemselves,thushelpingtomakeupthedeficiencycausedbylowacidlevels.

Whilethesebacteriamaybeperformingaserviceinthecaseoffolicacid,bacterial overgrowth is also associated with deficiencies in other nutrients,which the microorganisms actually “steal” from the body and use forthemselves. Bacterial overgrowth also raises the risk of bacterial infectionsleading to discomfort (e.g., diarrhea, flatulence) and even death from seriousbacterialdiseases (e.g., salmonella,dysentery,cholera).All thingsbeingequal,the best way to maintain normal folate levels is to keep the stomach acidflowing,andeatadietrichinfolicacidand/orfolicacidsupplementsratherthanrelyingonabnormalovergrowthofintestinalgerms!

HowAcidSuppressionAffectsFolateAbsorption

One good way to reduce folate absorption is to take neutralizing antacids or

acid-suppressing drugs. A study by researchers from the U.S. Department ofAgriculture (USDA) compared folate absorption in thirty normal, healthymenandwomenaged fifty-fiveandolder,who tookeitherMylanta II,Tagamet,orZantac following ameal containing200μgof folic acid.20BothTagamet andZantacsignificantlyraisedtheintragastricpHfromabout1to2beforetreatmentto5.5to6.5after,respectively.(NoposttreatmentpHvalueswerereportedforthe Mylanta II-treated group.) Folate absorption was reduced in all threetreatmentgroups,althoughthereductionintheZantacgroupwasnotstatisticallysignificant (see Figure 4-5).21 The overall reduction in folate absorption wasabout16percent.Although16percentlessfolateisprobablynotenoughtoharmanotherwisehealthyperson, itmightadverselyaffect thehealthofmanyotherpeople,includingthosewhotakemultipleantacidsforweeks,months,oryearsatatime;haveseriousatrophicgastritis,oreatadietlowinfolatecontent.

Figure4-5.Reductioninfolicacidabsorptionassociatedwithneutralizingantacidsandacid-suppressingdrugs.Healthytestsubjectsconsumedatestmealcontaining200mgoffolicacidandtookeitherMylanta

II,Tagamet,orZantac.P<0.001.AdaptedfromRusselletal.,1998.

Keepinmindthatchronicallylowfolatelevelsareassociatedwithelevatedhomocysteine levels, which are in turn associated with atherosclerosis and anincreased riskofcardiovasculardisease.Given these facts, itdoesn’t seem toofarfetchedtospeculatethatchronicallylowstomachacidcouldincreasetheriskof suffering a heart attack or stroke some day. It’s highly doubtful that anypharmaceuticalcompanyisdoingseriousresearchtoexplorethatpossibility.

VitaminB12

WeneedvitaminB12(cobalamin)fornormalnerveactivityandbrainfunction.Among its other important uses, vitamin B12, in combination with folate andvitaminB6,helpskeephomocysteinelevelsundercontrol.LowlevelsofvitaminB12 can leave us feeling dull, tired, and depressed. In children, low stomachacidity along with poor absorption of vitamin B12 has been linked to theoccurrenceofasthma(seechapter6.)

Vitamin B12 typically enters the body bound to food proteins, almostexclusively animal-derived foods, includingmeat, eggs, anddairyproducts. InorderforustoabsorbvitaminB12,thevitaminmoleculesmustfirstbeseparatedfromthisproteinwith thehelpofstomachacidandpepsin.Oncefree,vitaminB12 quickly combineswith anotherkindofproteinbinder,whichoriginates inthe salivary glands, stomach, liver, pancreas, and other GI organs. As the re-bound vitamin B12 enters the small intestine (where the pH has risen to nearneutral), enzymes from the pancreas (pancreatic proteases) break the vitaminfreeagainsoitcannowcombinewithasubstancewiththeratherprosaicnameintrinsicfactor.

Intrinsic factor is secretedbyparietal cells in the stomach, the samecellsthat produce and release HCl. The vitamin B12-intrinsic factor complex thentravelsalmosttheentirelengthofthesmallintestinetotheterminalileum.Hereitbindstospecificreceptorsandisquicklyabsorbedintothebloodstream.22

Figure4-6.SevereatrophicgastritisreducesvitaminB12absorption.VitaminB12levelsweremeasuredinelderlypeoplewithlowstomachacidpepsin,andintrinsicfactorduetoatrophicgastritis.Source:

Krasinski,1986

Looking back on this sequence of events, it’s easy to see how an acid

deficiency can disrupt vitamin B12 absorption. If vitamin B12 does not getdissociatedfromitsfoodproteinbinder in thestomachbyHClandpepsin, thechainisbrokenalmostbeforeitbegins,andnoneoftheothersubsequenteventscanoccur.

Vitamin B12 deficiencies tend to occur most often in elderly people,especially those who have atrophic gastritis (remember this occurs frequentlywhenwe’re older).Whengastric acid secretion is low in older people, pepsinproduction is also reduced. Moreover, the loss of parietal cells in atrophicgastritisalsomeansthatlessintrinsicfactorisproduced.Thus,whenapieceofmeat or fish is eaten, thevitaminB12 stays lockedonto its protein carrier andnevergetsabsorbed.

Inonestudy,32percentofagroupof359peopleagedsixtytoninety-nineyearswas found to have atrophic gastritis.VitaminB12 levels in participants’bodieswerecloselyrelated to theextentof theirdisease. In thosewithmild tomoderate gastritis, only 8.5 percent had a vitamin B12 deficiency. However,whenatrophicgastritiswas severe,more than50percenthad lowvitaminB12(seeFigure4-6).23

Low stomach acid also affects vitamin B12 absorption indirectly byencouraging bacterial overgrowth in the stomach. While these bacteria havebeenknowntoreturn thefavorbyproducingmorefolateandvitaminB6, theyare not so forthcoming with vitamin B12. In fact, they may steal it away forthemselves. Some use it to nourish their own cells, while others simplyinactivateitsoitcan’tdoanyoneanygood.

PerniciousAnemia

“Pernicious”anemiaisaseriousvitaminB12deficiencythatcanoccurinpeoplewith severe atrophic gastritis, resulting in the loss of HCl, pepsin, and,especially,intrinsicfactor.ItgetsitsnamebecausepeoplecommonlydiedfromitinthedaysbeforethediscoveryofvitaminB12.

Whatdistinguishesperniciousanemiafromgarden-varietyatrophicgastritisis its severity. In severe pernicious anemia, the damage to parietal cells is soextensive that they lose their ability to secrete intrinsic factor aswell asHCl.Withoutintrinsicfactor,eveniftherewereenoughacid,vitaminB12couldneverget absorbed down in the southern end of the small intestine. If itmisses thisstop along the digestion express, the next stop is the colon and excretion.

Pernicious anemia this bad can be treated only with vitamin B12 injections,whichworkverywell. (Theydon’t cure thebasicproblem,which is completefailure of stomach function, but they domake up the deficit of vitamin B12.)Perniciousanemiacanalsooccurwhenatrophicgastritisislessextensive,duetotherelativelackofacidandpepsin,thefirststepinthedigestion-absorptionofvitaminB12.Peoplewiththemilderformsofperniciousanemiamayalsobenefitfrom B12 injections, but they should first try HCl/pepsin supplementation torestoretheirstomachacidlevels.

HowAcid-BlockingDrugsAffectVitaminB12

Absorption

By suppressing the secretion of HCl, pepsin, and intrinsic factor, acid-suppressingdrugsarequitecapableofcausingavitaminB12deficiency.Inonestudy, administration ofTagamet to twelve duodenal ulcer patients resulted insignificantmalabsorptionofprotein-boundvitaminB12.Interestingly,crystallinevitaminB12,whichisnotboundtoprotein,waseasilyabsorbed.Thissuggeststhat malabsorption in this case occurs due to the lack of sufficient acid andpepsintoreleasethevitaminB12fromitsproteincarrier.24

SeveralstudiesshowthatPrilosectreatmentcaninterferewithvitaminB12absorption.AgroupofUSDAresearchers fromTuftsUniversitycompared theabsorption of protein-bound vitamin B12 in a group of elderly people withnormalstomachacid,agroupwithlowacidduetoatrophicgastritis,andagrouptaking Prilosec.25 They found that significantly less B12 was absorbed by thePrilosec and atrophic gastritis groups, compared with the group with normalstomach acid (see Figure 4-7).26 In other words, Prilosec produces a state offunctional atrophic gastritis inwhich vitaminB12 absorption is inhibited.Lowacid and pepsin levels in both conditions, inhibited the release of the protein-boundvitamin.However,whentheB12wastakenwithasmallamountofdiluteHCl, absorption shot up dramatically in both the normal control and Prilosecgroups.The small response toHCl theatrophicgastritisgroupmayhavebeenduetothelackofintrinsicfactororpepsinintheseindividuals.

Figure4-7.PrilosecinhibitsvitaminB12absorption;HClrestoresit.Elderlytestsubjectsconsumedprotein-boundvitaminB12.ThosetakingPrilosecandthosewithatrophicgastritisabsorbedsignificantly

lessvitaminthannormalcontrols.AdministrationofvitaminB12+HClresultedinasubstantialimprovementinabsorptioninboththenormalandPrilosecgroups.AdaptedfromJRSaltzmanetal.,1994.

Inanotherstudy,Prilosec(20or40mg)wastestedinagroupoftenhealthymenaged twenty-two to fifty-fiveyears.Stomachacid levelsdeclined tonear-zero,parallelingadramaticdeclineinvitaminB12absorption.27

Thesewereshort-termstudies,butwhathappenswhenpeopletakePrilosecandsimilardrugsdailyformonthsoryearsata time?There is little long-termdata evaluatingvitaminB12 levels inpeople taking thesedrugs.However,onereviewfoundthat,despitetheinhibitionofabsorption,levelstendtostayfairlynormalforthefirstthreetofouryearsofuse,perhapsduetolargestoresofthevitamin.After four years of treatment, though, vitaminB12 levels do begin todecline.28 We should also point out again that most of these studies wereconductedinhealthymenandwomen.WhenwestartoutwithlowvitaminB12levelsduetoatrophicgastritisorpoordiet,theadditionaldecreasesuperimposedby Prilosec or other drugsmay be just enough to tip the balance into seriousvitaminmalnutrition.

ReversingaVitaminB12Deficiency

It is possible to improve vitamin B12 absorption in people with low stomachacid. In one study, five people with hypochlorhydria and a vitamin B12deficiency were treated with supplements of HCl, pepsin, intrinsic factor, or

somecombinationofthese—simplyreplacingwhatwasmissing.Infouroutoffive,B12absorptionwassignificantlyimproved.29

Zinc

Themineralzinctakespartinmanymetabolicprocessesrelatedtokeepingcellmembranesstable,formingnewbone,immunedefense,nightvision,andtissuegrowth.Only three studies have evaluated the relationship betweengastric pHand absorption of dietary zinc. Of these, two suggest that stomach acid isnecessary, while the third found little or no connection. The negative findingcame from a study that has been criticized because of a variety ofmethodologicalerrorsthatbringtheresultsintoseriousquestion.30

In a much better controlled trial, Tagamet treatment reduced zincabsorptionbyabout50percent.31AnotherstudyfoundthatPepcid,whichraisedtheintragastricpHtoover5,hadthesameeffect.Theresearchersalsofoundthatzinc sulfate is better absorbed at high pH than zinc oxide.32While this studyimplies that zinc sulfate is preferable to zinc oxide as a supplement forindividuals who have atrophic gastritis or take acid-suppressing drugs, fifteenyearsofclinicalexperiencebasedontheknownbiochemistryofzincabsorptioninhumanshasshown that thebest-absorbed formof supplementalzinc iszincpicolinate.

DoesAntacidUseCauseBlindness?

Macular degeneration is the leading cause of irreversible vision loss in theUnitedStatesassociatedwithadvancingage.AccordingtoarecentreportfromtheongoingAge-RelatedEyeDiseaseStudy(AREDS),itappearsthatoneofthemost important risk factors for a subgroup of individuals with “dry” maculardegeneration (those characterized by “geographic atrophy”) is the use ofantacids.

Exactlyhowantacidusemayleadtomaculardegenerationisuncertain,butitisknownthatregularantaciduseproducesmaldigestion/malabsorptionofzincand other nutrients just as age-related hypochlorhydria/atrophic gastritis does.Other studies have linked low levels of zinc to the development of maculardegeneration.

Thus,by inhibiting the absorptionof zinc, long-termuseof antacidsmayleadtomaculardegenerationandlossofvision.

Source: Age-Related Eye Disease Study Group. Risk factors associated withage-relatedmaculardegeneration,Ophthalmology.2000:107:2224–2232.

OtherNutrients

Likefolate,vitaminB6absorptionnormallyrequiresanacidpHinthestomach.Nevertheless, vitamin B6 deficiencies are uncommon in elderly people withatrophicgastritis.Againitappearsthatbacterialovergrowthmaybemakingupthedifference.Therehasbeenverylimitedsystematicresearchontheabsorptionofothernutrients,butthereisgoodreasontobelievethatlowacidlevelsmightalsoaffect levelsofvitaminAandvitaminE, thiamin (vitaminB1), riboflavin(vitamin B2), and niacin (vitamin B3). Theoretically, the absorption of anynutrientthatisboundtoprotein(aswellasproteinsthemselves;seebelow)willbeinhibited.33

HowLowStomachAcidMayCauseDepression

Mention this possibility to most conventional, pharmaceutically orientedphysiciansandpsychiatrists,andthey’llprobablylaughinyourfaceandtellyouyou’ve been reading too many of those “alternative medicine” books. “JusthandmetheProzac,ifyouplease.”Butthefallowingcaseisonlyone(althoughcertainlythemostcolorful)ofliterallyhundredsI’veencountered.*

“I’mseventy-sixthisyear,andmywifeTheresaherethinksI’mlosingit,”saidVincentParnelli.“Iwasjustpassingitoff,butnowIthinkshe’sright.Lastweek,Idroveoffandlefttheboatatthelaunchforthesecondtimeinamonth…with thedog in it, too.Had thefish in thecar,don’tknowhowI thought Icaught’em.Hadtodriveallthewaybacktogettheboatandthedog…”

Theresareachedovertopathisarm.“You’renot‘losingit,’dear.You’vejustbeenalittlemoreabsent-mindedtheselastcoupleofyears.”

“Theresa’salwaysputtingagood faceon things,”hesaid, smilingather.“ButifIcan’tevenremembertheboatandthedog,‘losingit’ismoreaccurate.

AfterIdidthat,IdecidedtohaveagoodlookathowI’mdoing.Theresa’sbeentryingtogetmetocomeinhereforthelastfiveyears,andhereIam.”

Imadeanote.“Besidesyourmemory,haveyounoticedanythingelseaboutyourhealththatdoesn’tseemright?”

“I askedTheresa to come along so she could tell youwhat she’s seeing.LikeIsaid,I’vebeenpassingthingsoff,probablytoomuch.”Heturnedtohiswife.

“Well…,” she hesitated. “Vinnie’s beenmore forgetful for several yearsnow.Imean,weallarenowandagain,butit’sbeenmorethanthat.I’vebeenfinding a lotmore socks in the refrigerator, car keys in the laundry, unmailedletters in the car, things like that. To begin with, I just took care of it, but Istopped,becauseIwantedhimtonotice,too.Whenhedidn’t,Iwassurprised,soI started pointing things out… but until he forgot the boat and dog twice, itdidn’tmakeanydifference.”

“Anythingelse?”Shelookedatherhusband.“Vinnie,I’mnotbeingcritical,it’sbecausethe

doctorasked…”Thistime,hereachedoverandtouchedherarm.“It’sOK,Iwantyoutotell

thedoctoreverything,I’dprobablyforgetmostofitanyway…”“That’sanotherthing,doctor,Vinnie’sjustbeenmore‘down’thelasttwo

orthreeyears.Iwouldn’tcall itdepressedexactly.He’snot justsittingaroundstaringatthewalloranything,buthe’snotsmilingorlaughingthewayhehasinthepast.”

“With the politicians we got now, it’s enough to depress anyone,” Mr.Parnellisaid.

“It’smorethanjustpoliticians.YoucouldevenlaughatRoosevelt,Vinnie.“Sheturnedtomeandsmiled.“We’vebeenmarriedalongtime.”

“Roosevelt, that fascist, totally violated our Constitution … but when Ireallythinkaboutit,Theresa’sright,Ihaven’tseenasmuchthat’sseemedveryfunnyinthelastfewyears.Maybeit’sbecauseI’mnotsleepingaswellasIdidwhenIwasyounger.”

“Thattoo,doctor,”Mrs.Parnellisaid.“Iwasreadingaboutdepression,justin case, you know, and it said that insomnia and sleeplessness are ‘classicsymptoms’ofdepression.Isthattrue?”

“Dependsonyourpointofview.Depression, insomnia, and forgetfulnesscouldallbesymptomsofsomethingelse,too,”Ianswered.“I’llexplainlateron.Anyothersymptomsorthingsyou’venoticed?”

“Let’s see,” Mrs. Parnelli said. “More forgetful, depressed, not sleepingwell…andmaybetiringmoreeasilythanusual.Whatdoyouthink,Vinnie?”

“I was just blaming it on being older, I am seventy-six, but Theresaremindedmeaboutmyfather.Hewaszippingarounddoingthingsuntilhewasoverninety.EspeciallywhenItrytoworkhard,choppingwoodorwhatever,Igettiredoutandmymusclesjustphysicallygetmoretired.LikeIsaid,Ijustputitdowntoageandnotsleepingsogood,butwiththisforgetfulthing…”

We finished Mr. Parnelli’s health history, and went to the examinationroom.EverythingappearedrelativelyOKuntilwegottocheckinghisstomachandabdomen.

“Quiteabitofgassiness,”Iremarked.“That’s beenwithme for years.Most ofmy friends, too. Sometimeswe

evencallourselvesthe‘gassygrandpas.’Couldbeworse.AfewyearsbeforeIretired I had a bad stretch of heartburn. Doctor told me no ulcer, just takeantacids,it’dpass,anditdid.”

“With this, your symptoms are forming a fairly typical pattern.” Mr.Parnelli sat up abruptly. “What’s a lot of belching and gas got to do withforgettingtheboatandthedog?”hedemanded.

“Now,Vinnie, let the doctor finish, I’m sure he’ll tell us,”Mrs. Parnellisoothed.Mr.Parnelli lookeddoubtful,but laybackdown,andwe finishedhisexam.

“Sowhatdiseaseareyoufindinginwhateverpatternyou’retalkingabout?”Mr.Parnelliasked.Heputhisshirtonandsatdown,armscrossed.

“Nodisease,justafrequentlyoccurringpatternofwear-and-tear,”Ireplied.“Wearandtear?IsthatjustapolitewayoftellingmeI’mjustgettingolder

likeIthought,nothingIcando?”“We’reallgettingolder,butifwepayattention,there’salotwecandoto

stayhealthyatthesametime.Pleaseremember,whatI’mgoingtoexplainisjusta theoryuntilwedosome testsand trysome treatments,but this samepatternhappenstosomanyofus…”

“Gas,belching,andforgettingthedogmakingapattern.Wait’llItellthistoBill…”

“Vinnie…”“OK,Theresa,I’llbegoodandlisten.”“Aswegetolder,”Iexplained,”manyofuslosedigestivecapacity,some

of us sooner than others. By age sixty, at least half of us have significantdigestive slowdown. Usually, our stomachs aren’t making as much acid andpepsin aswhenwewere younger, so our food, especially the protein, isn’t aswell-digestedasitmightbe.Andinefficientdigestionisveryoftenaccompaniedbyconsiderablegas.It’sverylikelythatthe‘stretchofheartburn’andincreasinggasyouhadbeforeyouretiredwasasignalofprogressivestomachfailure.”

“So ifmy stomachwasmaking less acid andpepsin thannecessary,whydidthedoctortellmetotakeantacids?”

Isighed.“Habit,lackofunderstanding,inadequatetesting…reallyhardtosay.Butwhenwecarefullytestpeopleoveragefortywho’rehavingheartburn,indigestion,andgas,over90percentof the timewe find inadequateacid (andpresumably pepsin) production by the stomach. Hydrochloric acid and pepsinsupplementationrelievesthesymptoms,furtherprovingthepoint.That’slikelypartofwhatyou’llneed…butlet’sgetbacktoforgettingthedog.

“Hydrochloricacidandpepsinarewhatthestomachusestodigestprotein.The ultimate products of protein digestion are called amino acids and shortchains of amino acids are called ‘peptides.’ When we test people who haveseriously inadequate stomach function, or who’ve had inadequate stomachfunctionforalongtime,weusuallyfindapatternoflowerthanaveragetomuchlowerthanaverageaminoacidsinthebloodstream.Now,mostneurotransmittersaremadefromaminoacids—”

“Neurotransmitters?”“You remember,Vinnie, Iwas telling you neurotransmitters are the little

moleculesthebraincellsuseforsendingmessagestoeachother?”Mrs.Parnellisaid. “So if Vinnie’s stomach isn’t working right, he might not have beendigestingenoughprotein intoaminoacids forhisbrain touse tomakeenoughneurotransmitters,sohemightgetforgetful?”

“Exactly.Itcouldalsoaccountforalotofhissleeplessnessandinsomnia.Thoseveryoftengetalotbetterwhenwegetpeopleontherightcombinationofaminoacids.”

“Isn’tmusclemadeoutofaminoacids,too?”Mrs.Parnelliasked.“Allproteinsare,andmuscleismostlyprotein.”“So ifmystomachdoesn’twork right,and I’mnotgettingenoughamino

acids, then my muscles might get weak, too?” Mr. Parnelli leaned forward,uncrossed his arms, and looked much more interested. “Let’s see … gas,belching,poordigestion,lowaminoacids,weakmuscles,lowneurotransmitters,sleeplessness,insomnia,depression…andforgettingtheboatanddog.Damn!Itallmakessenseafterall!”

Ismiled.“Oneofthecommonpatternsaswegetolder,ifwe’renotcareful.Thereareafewmoredetails,too.Ifthedigestionisn’tworkingwell,injectionsofvitaminB12andotherBvitaminscanbeveryhelpfulforthefunctionofthebrainandnervoussystem,andcanbeespeciallyhelpfulagainstfatigue.Overtheyears,manypeoplewith poor stomach function have toldme that intravenousinjections of essentialminerals are very helpful in restoring strength, stamina,

andendurance.“Also, the large majority of us at age seventy-six are quite low on the

hormoneDHEA, andmany of usmen are low in testosterone. Supplementingwith small quantities of one or both of these hormones in identical-to-naturalform can be very useful, even reinvigorating, and can help to rebuild healthytissueallaroundthebody.Mostpeoplenoticeimprovementinmentalfunction,too.”

“SowhendoIgetstartedonallthisstuff?”“Remember, this is all just theory until we get the right tests done. But

giventheoverallpattern,testswillprobablyshowthathydrochloricacid-pepsinreplacement, amino acids, B12 injections, essential minerals, DHEA, andpossiblytestosteronewillbetheitemsrecommended.”

“SoImaynotbe‘losingit.’I’mjustlowonthingsthatbelonginmybodyanyway. It’smore likepatchingand repairinganoldhouse than treatingsomedisease.”

“Right.”Mr. and Mrs. Parnelli began to get up, but she sat down with another

question. “Aren’t there some vitamins and herbs that can help memory anddepression,too,doctor?”

“Sure. Ginkgo, acetyl-L-carnitine, and phosphatidylserine all haveimpressive studies done showing their ability to improve memory anddepression,especiallywhenwe’reolder.Let’swaittoseehowMr.Parnellidoesonthe‘homerepair’itemsfirst,andthenconsiderusingoneormoreofthose.”

As expected, Mr. Parnelli’s tests disclosed weak digestive function, lowamino acids, many low minerals, and low DHEA. With the help of theappropriate amino acids, vitamin B12 injections (with other B vitamins),minerals, DHEA, and digestive correction, his memory, low-grade depressionandothersymptomsweremuchimprovedwithineightmonths.Atthatpointweaddedinginkgobothtotrytosharpenmemoryfurther,aswellasforitsactioninimprovingsmallbloodvesselcirculationanderectilefunction.Oneyearlater,Mrs.Parnellitoldmetherehadbeennomoresocksintherefrigerator,only“theoccasionalmemory lapse like the rest of us,” andVinnie hadn’t forgotten theboatorthedogsince.

…

Whiletheevidenceislargely“anecdotal”andcircumstantialatthispoint,itisatleasttheoreticallypossiblethathavingadvancedatrophicgastritisortakingacid-suppressingorotherdrugsdailyformonthsoryearsatatimecouldleavea

personfeelingclinicallydepressed.Theimmediatereasonisalackofabsorbtionofadequateamountsoftheessentialaminoacidstryptophanandphenylalanine,andthe“nonessential”butimportantaminoacidtyrosine,andverylikelyothers.The body uses these three amino acids for the production of theneurotransmittersserotoninandnorepinephrine(aka,noradrenaline).

Figure4-8.Proteindigestion(hydrolysis)occursbestwhenthepHislessthan2.5.TheresultsofthisstudyshowthatatnormalgastricpH(lessthan2.5),75percentofproteinishydrolyzed,comparedwithonly25

percentwhenthepHishigh(greaterthan5).AdaptedfromMaltby,1934.

Deficiencies in these neurotransmitters are closely associated withdepression and other emotional disorders. Drugs like Prozac, Zoloft, Serzone,andothersareused to relievedepressionbecause theyraise the levelsof theseneurotransmitters.TheaminoacidsthemselvesarederivedfromdietaryproteinsthatarebrokenapartbytheactionsofHClandpepsininthestomach.

HCI,Pepsin,andProteinDigestion

Protein is digested (hydrolyzed) in the stomach to produce amino acids andpeptides(twoormoreaminoacidslinkedtogether)bytheactionsofpepsin.ThisactionoccursbestwhenthepHisbetween1and2.AsthegastricpHclimbs,therateofhydrolysisdeclines.34AsshowninFigure4-8,whenthegastricpHislessthan2.5 (within thenormal range),75percentofprotein (beef) ishydrolyzed,compared with only 25 percent when the pH is high (greater than 5). Acid-suppressingdrugstypicallyraisetheintragastricpHto5orhigher.

Normaldigestionofproteinresultsinthereleaseofessentialaminoacids,including phenylalanine, tryptophan, valine, and leucine, as well as

“nonessential”butimportantaminoacidssuchastyrosineandarginine.Thereislittle direct evidence that hypochlorhydria or achlorhydria, whether due toatrophicgastritis or acid-suppressingdrugs, inhibits the absorptionof essentialamino acids. However, there is considerable circumstantial evidence. In onestudy,peoplewhohadhadpartoftheirstomachssurgicallyremoved(resultingin less acid secretion), absorbed less protein than a control groupwithnormalstomachs.35

Bacterialovergrowthduetochronicallylowacidlevelscanalsogetintheway of normal amino acid absorption. As we noted earlier with vitamin B12,somebacteriamayhijacktheaminoacidsfortheirownuse,possiblyproducingtoxicbyproductsintheprocess.36-37

Duringtheearlyyearsofthetwentiethcentury,therewereisolatedreportsthat certain products of bacterial metabolism of amino acids could cause asyndrome that resembled what may now be diagnosed as clinical depression.Symptoms included excessive fatigue, reduced ability to concentrate, andinsomnia (in people), and somnolence and lack of interest in the externalenvironment(inmonkeys).38

Amorelikelyconnection,aswementionedabove,maybethedeficitinatleasttwoneurotransmitters,serotoninandnorepinephrine,andtheiraminoacidprecursors, tryptophan, phenylalanine, and tyrosine. Numerous reports haveconfirmed that a large reduction in plasma tryptophan levels can result indepression, especially if the individual is prone to depression due to geneticmakeuporfamilyhistory.39–45

Canlowstomachacidmakeusdepressed?AlthoughI’vefoundthis tobetrue formany individuals, there are no “controlled studies,” so “scientifically”speaking,at thispoint, thepossibility remainsnothingmore thanan intriguinghypothesis.46 However, should it be borne out by systematic research, it maymean that, for some people at least, treatment for their depressionmay be assimple as taking HCl supplements, accompanied by amino acids and other“missing”nutrients.

The subject of low stomach acid, amino acids, neurotransmitters anddepressionissoimportantthatWe’veincludedaseparatediscussioninappendixI.

ForWomen,LowStomachAcidOftenCauses“Lousy”FingernailsorHairLoss

Inaway,womenwithlowstomachacidareoften“lucky”todeveloponeoftwo“signs” thatmenwith the same problem rarely encounter: cracking, chipping,peeling,and“layering”fingernails,oroverall(notlocalized)headhairloss.(It’srare to have both poor-quality fingernails and hair loss occur in the samewoman.)

Didwe say “lucky”?Rapidly thinninghair, or nails only a cosmetologistcouldlove?Lucky,becausewomenwith theseproblemsknowsomething’s thematter and sometimes are also lucky enough to find nutritionally orientedphysicianswhowillhelpthesesymptomstodiagnoseandcorrectorcompensatefor the underlying cause: poor stomach function. “Patching up—the stomachproblemhelpsnotonly thehair lossand the“lousy” fingernails,but theentirebody’snutritionaswell!

Wemenaren’t“lucky”enough todevelop these telltalesymptoms,sowecontinuetosuffertheconsequencesofpoorstomachfunction.

WhyHighFiberandLowStomachAcidDon’tMix

Dietary fiber includesmanydifferent substances found inplant cellwalls.Foryears,we have been told (and rightfully so) to eatmore fiber for a variety ofpreventiveandtherapeuticpurposes.Dietaryfiberappearstobecomeevenmoreimportant aswe age, since itmay be involved not only in promoting healthybowelactivity,butalsoinpreventingcoloncancerandcardiovasculardiseasebyhelping to reduce cholesterol levels. Thus, elderly people, in particular, areencouragedtoeatfoodscontaininglotsoffiber.

Butfiberalsohasalittle-knowndarksideasfarasnutritionisconcerned.Fiber can bindwith nutrients and actually remove them from the body beforetheyhavechance togetabsorbed.This isespecially likely tooccuras thatoldgastric pH starts to rise, as it often doeswith advancing age or as a result oftakingacid-suppressingdrugs,or, increasingly,both.Bynowyouknowwherethis is going: Eating a high-fiber diet on a low-acid stomach drives many ofthesevaluablenutrientsfromtheGIsystemdirectlyintothatmunicipalsewagetreatmentplant.

Here’showitworks insimplifiedway:Both fiber itselfandaconstituentcalledphyticacid orphytate, are extremelyeffective at “lockingonto”dietaryminerals. Phytic acid, which comes from many grains, cereals, and seeds,combineswith numerousminerals, including zinc, copper, nickel,manganese,

iron,andcalcium.The solubility of thesemineral-phytate complexes depends on a complex

interactionamonganumberoffactors, includingthepHvalueandthespecificmineral(s) involved, among others. In general, mineral-phytate complexes aresoluble—andtherefore,absorbable—onlyatlowpH(usuallylessthan3).Test-tubestudies,forexample,showthatzincandcopperphytatesstarttodropoutofsolutionwhen the pH gets into the 3 to 4.5 range, and solubility continues todeclineasthepHrises.Thesamethinghappenswithiron,zinc,copper,andtheothers, although the pH levels may vary. It also happens with protein, whichrequiresacidandpepsinfordigestion.

And just to complicatematters, if there’s enough calcium ormagnesiumpresent,astheyprecipitateoutofsolution,theytakesomeoftheothermineralsoutwiththem,thusmagnifyingtheloss.47

Themain reason this nutrient theft doesn’t go on all the time is that thenormallylowgastricpHpreventsitbykeepingthevariousmineral-phytate/fibercomplexesinsolution.However,whenthepHstartstoriseabove3to4,5,6,or7, themineralsbegin toprecipitateout in the formof insoluble,unabsorbable,and,therefore,unusablecompounds.

Whatdoesthismeanforusfibereaters?Itmeansthatifwedoalltherightthings—eatahigh-fiber,low-meatdietandmaybethrowinsomeextracalcium(forstrongbones)—buthaveatrophicgastritisortakeanacid-blockingdrug,orboth,wemaybestarvingourselvesofnumerousvitalnutrients.

The leading scientific voicewarning about this potential loss of nutrientshas been Elaine T. Champagne, PhD, a researcher with the USDA.48-50 Sheargues that the incomplete digestion of protein-mineral-phytate complexes,combined with the incomplete digestion of protein due to inadequate pepsinactivity,couldbe“themostimportantconsequencesofraisedstomachpHvaluesonmineralnutriturefromhigh-fiberfoods.”Dr.ChampagnewarnsthatelderlypeoplewhohaveelevatedstomachpHvaluesandwhoregularlyconsumedietsthatarehigh infiberandphytateandlowinanimalprotein“maybeat riskofsuffering from mineral impairment.”37 Of course, the risk of excess dietarymineral loss is similar every time we take Prilosec, Tagamet, Zantac, Tums,Rolaids,orotheracid-blocking/antacidtreatmentandtheneatmealscontainingdietaryfiber.

ResearchandClinicalObservation

Sofar,We’vewrittenabouttheclinicalresearchthatexistsconcerningnutrientabsorptionandnaturallyoccurringordrug-inducedlowlevelsofstomachacid.We’ve noted research concerning iron, calcium, folate, vitaminB12, zinc, andaminoacids.We’vealsomentionedthelesseningofnutrientabsorptionbroughtabout by the combination of low stomach acidity and dietary fiber. But whataboutalltheothernutrients:carotenoids;otherBvitamins;vitaminsA,C,D,E,K; essential fatty acids; flavonoids;magnesium; copper; chromium; selenium;manganese;biotin;andmanyothers?

Recallthatinchapter3,wedescribedthe“digestivecascade,”theseriesofevents triggeredbyfullyacidifiedmeals.This“cascade” includesacid-inducedhormone release triggering the secretion of bile and pancreatic enzymes.Withoutthe“acidtrigger,”therestofthe“cascade”doesn’tworkaswelleither,and thesecretionofbicarbonateandenzymes(trypsin,chymotrypsin,amylase,lipase,elastase,protease,andothers)bythepancreasandbileandbilesaltsbythe gallbladder aren’t stimulated properly. Absorption of many of the othernutrients noted above can be impaired, even though stomach acid and pepsinmay not be directly responsible for their digestion and absorption. In a way,then,normalstomachfunctionislikethefirstdominoinarow:Ifitdoesn’tfallasitshould,therestwon’teither.

In more than thirty years of medical practice, twenty-eight of themnutritionally oriented, I’ve observed improvement in the absorption of nearlyeverynutrientwhenpoorstomachfunctionisimproved.Whileit’struethatthemost frequently affected nutrients include all of the essential minerals exceptsodium and potassium, and all of the essential amino acids, any one or anycombinationoftheothernutrientscanalsobeinvolved.

What’spresentedinthischapterismostoftheresearchthatcouldbefoundthrough extensive library andonline searching.Sowhere’s the research on alltheothernutrients?Thesadfactisthatithasn’tbeendoneyet,eventhoughthisissaidtobe“themostmodernscientificera.”It’snotlikelythatpatentmedicine(pharmaceutical)companieswithafinancialinterestinacidblockersorantacidswill fund studies on the adverse effects of their money-making drugs andtreatments, especially if the adverse effects escape immediate notice.Government grants and the large majority of foundation grants are usuallymotivatedbywhat’strendyandpopularinmainstreammedicine.Sothemoneyfor“hard”researchusuallyisn’tthere.

Alloftheproblemsassociatedwithlowstomachacid(ofwhatevercause)wereapparentwithinmyfirst tenyearsofmedicalpractice.Butsincemuchofthe “hard research”hadn’tbeendone, I thought it best towait formanymore

yearsofclinicalobservationbeforejoiningDr.Lenardinwritingthisbook.

*ReprintedfromDr.JonathanVWright’sNutritionandHealingnewsletter,AgoraSouthLLC,Baltimore,Maryland,21201(410)223–2611

*ReprintedfromDr.JonathanVWright’sNutrition&Healingnewsletter,AgoraSouthLLC,Baltimore,Maryland,21201(410)–223–2611.

CHAPTER5

HowLowStomachAcidCanMakeYouSick:

TheBacteria-CancerConnection

We try not to think about it, but the mouth, esophagus, and intestines arevirtual bacterial cities, containingmore than four-hundred different species ofmicroscopic bugs.1 But a healthy stomach, which lies directly between theesophagusandthebeginningoftheintestines,isnormallyanoasisofsterility,ornear sterility.Thismicrobe-freebuffer zoneexistsbecauseofone simple fact:stomach acid kills bacteria. “The low pH of the intragastric environmentconstitutes one of the major non-specific defense mechanisms of the body,”wroteoneresearcher.2

The gastric acid barrier guards two gateways simultaneously. Mostswallowedorinhaledbacteriaplaynoroleindigestionandwouldconstituteanunwelcomealienpresenceamidsttheflourishingnaturalmicrobialecologythatisessentialfordigestionintheintestines.Thus,stomachacidinterceptsbacteriathatenterthroughthegatewayofthenoseandmouthandkillsthembeforetheycanpassintotheintestine.Bythesametoken,intestinalbugshavenobusinessfarthernorth,wheretheycanonlycausetrouble.Theacidbarrier(atermtakendirectlyfrommedicaltextbooks)keepsthesebacteriafrommigratingupthroughtheduodenumandpylorusandputtingdownrootsinthestomachlining.

Althoughsomebacteriacanusuallybefoundinahealthystomach,thevastmajority turnout tobe recentarrivals.When thepH is3or lower, thenormalbetween-meal “resting” level, bacteria don’t last more than fifteen minutes(perhaps a little longer if the pHgets up to 4). Ifwewere to completely stopswallowing for fifteenminutes ormore, our stomachswould rapidly revert totheirnaturallysterileornear-sterilestate.

AsthepHrisesto5ormore,though,manybacterialspeciesavoidtheacidtreatmentandbegintothrive.Withoutregularacidbathstodrivethemout,thestomach can become a quite hospitable locale for bacterial colonization. It’s

dark, it’s warm, it’s moist, and it’s often full of nutrients.3 Acid-suppressingdrugsroutinelydrivetheintragastricpHover5.Fortunately,mostofthebacteriaweingestwon’tkillus,at leastnotrightaway.Butsomeof themwill.Peoplewho have a gastric pH high enough to promote bacterial growth may bevulnerabletoseriousbacterialinfectionssuchasSalmonella,cholera,dysentery,typhoid, and tuberculosis,2 not to mention garden-variety heartburn, diarrhea,constipation, bloating, flatulence, or other common symptoms of dyspepsia(“upsetstomach”).

Theevidenceisunmistakable.TheriskofSalmonellainfectionismorethanthreefold inpeoplewhohavehad stomach surgery that inhibits acid secretion,and it rises in direct proportion to the degree that the operation reduces acid-secreting capacity.4 In a 1970w cholera outbreak in Israel, one-fourth of thetwenty-five people who came down with the disease had had prior stomachsurgery.SixteenofthepatientshadnofreestomachacidatallandameanpHof6.4.Thosepeoplewiththeleaststomachacid(achlorhydria)hadthemostseverecholera.5

Inastudyofthirty-sevenBangladeshiswithcholera,sixteenhaddeficientstomachacid.Whenresearcherssampledgastricjuicefromthesesixteenpeopleand put these samples into test-tubes with the cholera-causing bacteria, V.cholerae,theyfailedtokillthebug.6

Infact,though,V.choleraeisexceptionallyvulnerabletoalowpH.7Thus,whenthestomachpHisnormal(i.e.,3orless),theriskofdevelopingcholeraoranyotherinfectiousintestinaldisease,evenifwehappentodrinksometaintedwater, is much lower. As noted above, the concept of the “acid barrier togastrointestinal disease” has been firmly established in medical textbooks formany,manydecades.

Muchthatwehavesaidaboutcholera isalso trueofSalmonella, typhoid,andnearlyallbugsthatmightinfectourintestines.The“acidbarrier”isn’t100percent effective (even children and teenagers with “maximum-strength”stomach acid can get intestinal infections), but it definitely lowers our risk ofgastroentericinfection.Elderlypeople,whoaremorelikelytohavelowstomachacid due to decades of progressing atrophic gastritis, have been found to beparticularlypronetoSalmonellainfection.8

Anti-acidDrugsCanMakeUsVulnerabletoInfection

OnereasondiseaseslikeSalmonella,cholera,typhoid,anddysenterycanbesodevastating in poor countries is that malnutrition leaves the stomach lininginflamed (gastritis) and acid secretion dangerously impaired. But even in themidstofplenty,wemaybeleavingourselvesvulnerabletoseriousbacterialGIinfectionssimplybyfollowing“doctor’sorders,”thatis,bytakingantacidsandacidsuppressors.

As far back as 1885, the pioneering German bacteriologist Robert Kochfound he could promote cholera infections in guinea pigs simply by feedingthem a dose of bicarbonate (which neutralizes normal stomach acid) prior toinfectingthemwiththeV.cholerae.9Thisworksinpeopleaswell.Almostone-hundredyearslater,astudyshowedthathealthyhumanvolunteer“guineapigs”couldalsoincreasetheirriskofcholerainfectionbyfirsttakingadoseofsodiumbicarbonate.10 (Even thoughcholeragets themost researchattentionasoneofthemost serious infectious gastrointestinal diseases, please remember that thisdiscussion applies to every potential gastrointestinal infection, including the“mutant”E.coliOH157,thedeadlymeat-contaminantorganismthatappearstobearesultofroutinelyfeedingantibioticstoanimals.)Onewaythatdoctorsmayliterally be killing people is by promoting bacterial infections with acid-suppressingdrugs. Ithasbecomecommonpractice inhospitals today to freelydispensedrugs likePrilosec andZantac to very sickpatients, such as those inintensive care. The aim is to make them more comfortable (if they haveheartburnor esophageal reflux) and toprevent “stressulcers” from forming inthestomach.*

Nodoubt,thedoctorswhoprescribethesedrugshavethebestofintentions,buttheevidencesuggeststhattheir“approved”treatmentpromotespneumonia*development ina significantnumberof theirpatients. “Nosocomial” (hospital-caused) pneumonia—a bacterial infection of the lungs—is a huge problem inhospitals today, accounting for 17 percent of hospital-acquired infections. Itincreaseslengthofstayinthehospital,helpssendhealthcarecoststhroughtheroof, and kills 50 percent of people who develop the disease while on amechanicalventilator.11

In thevastmajorityof casesofhospital-acquiredpneumonia, thebacteriathatinfectthelungsoriginatedeepdownintheGItract.Withnormalacidlevelsin the stomach, there is little riskofbacteria from the intestinesworking theirway up into the lungs. However, reduced stomach acid that may accompanycritical illness, combined with drug-induced acid suppression and/orneutralization,canraisegastricpHtolevelsthatencouragebacterialovergrowthandmigration.

How do the bacteria get from the gut to the lungs? Small amounts ofbacteria-laden gastric contents may get aspirated (inhaled) during episodes ofreflux.Also,inseriouslyillpeople,tubesplacedintotheairways,nose,mouth,andstomachcanallserveassuperhighwaysfordisease-causingorganisms.

Lots of research demonstrates that the risk of nosocomial pneumonia incriticallyillpeopleissignificantlylowerwhentheyaretreated,notwithanacidsuppressor, but with a mucosal protective agent (sucralfate) that coats themucosal lining but does not alter gastric pH. In a study published in theNewEnglandJournalofMedicine,patientsonmechanicalventilationwererandomlydividedintotwogroups.OnegrouptookeitheranH2-receptor-blockingdrug,aneutralizingantacid,orboth,whiletheothergrouptookjustsucralfate.Therateofpneumoniawas twice ashigh in the acid suppressor/neutralizer group as inthe sucralfate group. The acid-sup-pressed people were also 60 percent morelikelytodiefrompneumonia.12

“Stealing”Nutrients

In the previous chapter, we described how low acid directly inhibits theabsorption of many vitamins, minerals, proteins, and amino acids. Bacterialovergrowthduetolowstomachacidcanalsorobusofvitalnutrientsinavarietyofotherways:13

•StealingvitaminB12.SomebacteriacapturefreevitaminB12orvitaminB12-proteincomplexes.Othersproduce“falsevitaminB12” (technicallytermed “vitamin B12 analog” ), which competes with its regularcounterpart for absorption, effectively diluting the actual vitamin B12.These analogs can also interfere with certain forms of vitamin B12testing,creatingafalseimpressionof“normal”levels.

• Blocking fat absorption. Fat malabsorption can occur when certainbacteriainthestomachbreakdownbilesalts(deconjugation)beforetheyhaveachancetometabolizethefat.

• Carbohydrate malabsorption. A number of mechanisms have beenproposed to explain how bacteria in the stomach interfere with theabsorptionofsugarsandothercarbohydrates.

•Waterandnutrientloss.BacterialovergrowthintheupperGItractcanpromote excessive loss of water and nutrients by causing chronicdiarrhea.

HowtoFillYourStomachwithGerms

Acid-suppressing drugs promote bacterial overgrowth, a fact that has beendocumented in numerous studies of people being treated for either GERD orduodenalulcer.14–25

Inonerecenttrial,thirtypeoplewithGERDweretreatedwithhighdosesofPrilosec (40 mg/day) for at least three months. A control group included tenGERDpatientsnottakinganyacidsuppressorsatthetime.Whentheresearcherstooksamplesofstomachjuicefromallthesubjects,theyfoundthatelevenofthethirty Prilosec-treated people had developed bacterial overgrowth, comparedwith one of the ten people in the control group (see Figure 5-1). Bacterialovergrowth in the Prilosec group also interfered with bile acid metabolism.26Bile acids,which are produced in the liver and stored in the gall bladder, arerequiredfornormalfatdigestion.

Aswenotedearlier, ithasbeenknown formore thanacentury thathighintragastricpHpermitsbacteriatogrowinthenormallysterilestomach.Long-term use of Prilosec, one of the most potent acid-suppressing agents everdeveloped,reducesthesecretionofHCltonearzero,resultinginastateofnear-achlorhydria and a kind of “functional atrophic gastritis.” Here is what theofficial,FDA-“approved”PrilosecProductInformationstatesabouttheriskofbacterialovergrowth:

As do other agents that elevate intragastric pH, omeprazole [Prilosec]administeredfor14daysinhealthysubjectsproducedasignificantincreasein the intragastric concentrations of viable bacteria. The pattern of thebacterial specieswasunchanged from thatcommonly found in saliva.Allchangesresolvedwithinthreedaysofstoppingtreatment.27

What’s curious about this statement is the way it downplays thesignificanceofwhatisclearlyanimportantsideeffect.ThestatementbeginsbypointingoutthatPrilosecisnottheonlyguiltypartyhere,since“…otheragentsthatelevategastricpH”alsocausebacterialovergrowth.Theimplicationseemsto be that this makes it all right. Of course, this is nonsense. If bacterial

overgrowth is an undesirable and potentially dangerous condition, then that’swhatitis.Tosuggestthatit’snotsuchabadthingiflotsofdifferentdrugsalsocauseitisself-servingandmisleading.

Thestatementreflectstheresultsofaratherlimited(fourteen-day)clinicaltrial in “healthy subjects,” that is, people without heartburn or other seriousdisease.Unfortunately,mostpeoplewith indigestion,heartburn,orGERDtakePrilosecforalotlongerthanfourteendays.Theymaytakeitdailyformonthsoryears or even decades, because if they stop taking it, their indigestion andheartburnwill almost certainly return. (Lestwe forget, Prilosec does not cureanything;itjusttemporarilysuppressessymptoms.)Moreover,peoplewhotakePrilosec in “real life” are probably not going to be as healthy as the paidvolunteers in this controlled clinical trial. Theywill likely have long-standingindigestion and/or reflux causing heartburn andmay have atrophic gastritis orotherseriousGIdisorders.Theymayalsobetakingotherdrugs,theirdietmaybedeficient in some importantnutrients, and theymaybe less able to tolerateanyaddedacidsuppression.

Figure5-1.GERDpatientstreatedwithPrilosec(40mg/day)forover3monthsshowedsignificantlymorebacterialovergrowththanacontrolgroupofGERDpatientswhowerenottakingacid-suppressingdrugs.

AdaptedfromTheisenetal.,2000.

ThePrilosecstatementalsopointsoutthatmostofthebugsfoundgrowinginthestomachcomefromthemouth(saliva),asiftosay,“Howbadcouldtheybe?” In fact (just ask your dentist), the normal, healthymouth containsmorethan four-hundred different species of bacteria, amounting to billions andbillionsofmicroorganisms.Asonedental researcherobserved,“Inonemouth,the number of bacteria can easily exceed the numbers of people who live onEarth.”28More importantly, aswehavediscussed, some types of bacteria that

enterthestomachviathenoseormouthcouldcauseserious,evenfatal,illness.Whetherbacteriaarebenignordangerousdependsnotjustonthenatureofthebugs themselves, but alsoonwhere they are located.Bacteria from themouth(and the intestines) are supposed to be killed by acid when they enter thestomach.Allowing them to live in the stomach creates an unnatural conditionwith proven consequences for our health. The skin ofmost people is literallycovered with bacteria called Staphylococcus aureus.We get along quite wellwithStaph.aureus as longas it stayson the skin.But should it getunder theskin,or,worse,intothebloodstream,Staph.aureuscanbedeadly.

The Prilosec statement concludes by pointing out that bacterial growthceaseswithin3daysafter stopping thedrug.That iscertainlygoodnews.Theproblem,of course, is that theway acid suppressors are promoted, prescribed,andusedtoday,peopledon’tstoptakingthemafterthreedays.Theyoftentakethem daily for months or years at a time, creating a chronic state ofhypochlorhydriaorachlorhydria.

Helicobacterpylori:TheBugThatBeatstheAcidTestWhile most bacteria are doomed to extinction once they encounter the acidicenvironmentofanormalstomach,thereisone,calledHelicobacterpylori, thathas found a way to live a long and happy life in the land of the low pH.Unfortunately, once established in the stomach,H. pylori becomes a seriousthreattoourhealthandlongevityforanumberofreasons:

•H.pyloriispresentlythoughttobetheleadingcauseofatrophicgastritis,accountingfor80percentto100percentofcases.29

• H. pylori also causes the vast majority of gastric* (80 percent) andduodenal(95percent)ulcers.30

• H. pylori has been linked to two forms of stomach cancer:adenocarcinoma and lymphoma. According to results of largeepidemiologicstudiesfrombothEuropeandtheUnitedStates,H.pyloriinfection increases the risk of gastric carcinoma by 600 percent and isresponsiblefor50percentofallcasesofadenocarcinoma.31–32

H. pylori protects itself from HCl in the stomach by a mechanism thatmimics the way the stomach lining protects itself. The bacteria secrete anenzymethat results in theformationofammoniaandcarbondioxide,which in

turn combine with water to produce ammonium bicarbonate. Bicarbonatemolecules,ofcourse,makeexcellentacidneutralizes.ThismeansthatH.pylori,bathingsafelyinitsself-madeneutralizingshield,isfreetothriveandburrowitscorkscrewlike body through themucosal layer and into the gastric epithelium,where it is protected not just from stomach acid but from antibiotic drugs aswell.

Exactly how H. pylori damages the stomach lining is still underinvestigation. Its damage can be diffuse (gastritis) or localized (ulcers).Dependingonthelocationofthegastritisitcauses,H.pyloriinfectioncanresultin true hyperacidity (hyperchlorhydria) or a loss of stomach acid(hypochlorhydriaor achlorhydria).WhenH.pylori infection is confined to theantrumofthestomach,theregionwheremostofthegastrin-producingcellsarelocated, it stimulates these G cells to work overtime making and secretinggastrin. The excess gastrin circulates in the blood, and when it reaches theparietalcells,locatedfarthernorthinthebodyandfundus,itprodsthemtoturnontheacidspigotsfullblast.All thisextraacid,helpedalongbyanH.pylori-mediated reduction in bicarbonate production in the duodenum, is the primaryirritant (but not the cause) in duodenal ulcers. The acid degrades the gastricmucosallayerlaidbarebyH.pylori.Theresultinglong-termirritationcanleadto localizedopen sores calledduodenalulcers.Duodenalulcers areoneof thefewGIdisordersactuallyassociatedwithexcessstomachacid,orhyperacidity.(Noticewesay“associatedwith”andnot“causedby.”That’sbecausethecauseofboththeulcerationandtheexcessacidityisH.pyloriitself.)

DoYouHave“BowelBreath”?

Fromtimetotime,I’mconsultedatTahomaClinicbyindividualswhomention(usuallyreluctantly)thatoneoftheirsymptomsis“verybadbreath,”“incrediblybadbreath,”orinonememorableinstance,“bowelbreath,”thatwon’tgoawaywithbrushing, flossing,ormouthwash.Bynow, chances aregood that you’veguessed where “bowel breath” comes from. That’s right: all those germs,uninhibited by stomach acid, making their happy home in the stomach andlettingtheworldknowbytheirodor!

Most of the time, H. pylori sets up shop in the centrally located body(corpus) of the stomach. When this happens, a whole different pattern ofpathology emerges. The resulting inflammation—atrophic gastritis—inhibits

normal acid secretion from the parietal cells located there.Localized irritationmaydevelopintopepticulcers,evenasacidlevelsfall.OnceanareaisdamagedbyH.pylori,itdoesn’ttakemuchacidtomakethingsworse.Prolongedatrophicgastritisandhypochlorhydriaorachlorhydriacaneventuallydevelopintogastriccancer (see below). Thus, while acid suppression has long been a majortreatment—sometimestheonlytreatment—forbothduodenalandgastriculcers,highacidlevelsareseenonlywithduodenalulcers.Gastriculcersoccurdespitelowacidsecretion.Ifthistreatmentdoesn’tworkverywell,it’snothardtoseewhy.

UlcersandAcidSuppression

Thispictureofpepticulcers is actuallya relatively recentdiscovery.Until the1980s,conventionalmedicineconsideredulcerstobearesultofstressorotherfactors,whichallowed“excess”stomachacidtocause the lesion.AlthoughH.pyloriwas known to inhabit the stomach (calledCampylobacter pylori at thattime),fewsuspectedthatithadanythingtodowithulcers.

Initstime-(dis)honoredfashion,though,thepatentmedicineindustrytookoff after stomach acid as the “cause” of GI ulcers. Acid-suppressing drugs—from Tagamet to Prilosec—were initially developed to treat ulcers. Althoughtheycouldoftenrelievesomeoftheulcerpainanddiscomfortandperhapshelpslow their progression, the drugs could never “cure” ulcers, for the obviousreason that acid doesn’t cause them.Peoplewith ulcerswho took these drugsneededtotakethemforever,becauseassoonastheystoppedtakingthem,theirulcers would almost certainly flare up again. (Also in the 1980s, research inEngland demonstrated that an inexpensive licorice compound actually healedulcersaswellasTagamet,andpreventedulcerrecurrenceevenbetter…butitwasn’t patentable, so only people who visited natural food stores were everinformedaboutit.Seechapter7formoreaboutthehealingpowerof licorice.)Therealbreakthroughagainstulcerscameintheearly1980swhenanAustralianmedical researcher, BarryMarshall,M.D., began presenting evidence that theactualcauseofulcerswasH.pylori.Withbillionsinvestedinacid-suppressingdrugs,conventionalmedicinewantednothingtodowithMarshall’sdiscoveries,andforthebetterpartofadecade,theyignoredandridiculedthem.(Wherehavewe heard that refrain before?) Eventually, though, theweight of the evidencebecametoomuchtoignore,andH.pyloriinfectionwasfinallyacknowledgedastheprimarycauseofpepticulcers.

WhyH.pyloriandPrilosecDon’tMix

During the early1990s, the focusofulcer treatmentbegan to shift away fromacidsuppressionandtowardH.pylorieradication,usuallywithantibioticdrugs.(There’s an effective, inexpensive, and much safer natural treatment for H.pylori,too.Moreaboutthisinchapter7.)Nevertheless,acidsuppression,usuallywith Prilosec, is still widely prescribed as an adjunct to antibiotics, thepresumptionbeingthatreducedacidsecretionpermitsmorerapidhealing.

Prilosec also remains the most widely prescribed drug for treatingheartburn, indigestion, and relateddisorders.This, of course, is a vastly larger“market” for the drug than peptic ulcers everwere. The fact remains, though,thatmanypeoplewithsymptomsof“acidindigestion”haveH.pyloriinfectionseventhoughtheydonothaveulcers.Unfortunately,thepracticeofgivingacidsuppressors topeoplewithH.pylori infectionnotonlyprovidesnotherapeuticbenefit (Prilosecdoesnotkill or inhibit thebacteria), but it canactuallymakethingsmuch,muchworse.

TherealityisthatreducingstomachacidmakeslifesignificantlyeasierforH. pylori and, therefore, significantly more dangerous for us. Several studieshave shown that gastritis (inflammation) and epithelial lesions in the body(corpus) of the stomach increases when people infected with H. pylori takePrilosecorotheracid-suppressingdrugs.33–39

ThedangersofmixingPrilosecandH.pyloriwerebroughtclearlyhomeina 1996 article published in the New England Journal of Medicine. Theresearchers, from Sweden and the Netherlands, followed (for a mean of fiveyears)twogroupsofpeoplewhowerebeingtreatedforrefluxesophagitis.Onegroup took Prilosec (20–40 mg/day) and the other underwent a surgicalprocedurecalledfundoplication,whichrepairstheLESbutdoesnotinvolveacidsuppression.Among thosepeoplewhohaddocumentedH.pylori infections atthe start of the study andwhowere treatedwith Prilosec, the rate of atrophicgastritisincreasedfrom59percentatthebeginningoftreatmentto81percentbytheendofthestudy(seeFigure5-2).40Itisworthnotingthat,amongthosewhohadnoatrophicgastritisat thestartof thestudy,30percentof thosewhotookPrilosec laterdeveloped it.Bycontrast, just4percentof the surgically treatedgroupdevelopedatrophicgastritis.

Figure5-2.Developmentofatrophicgastritisinpeople,withorwithoutH.pyloriinfection,whoweretreatedforrefluxesophagitiswithPrilosecandwhohadnoatrophicgastritisatbaseline.AdaptedfromEJ

Kuipersetal.,1996.

AdvancingtheCancerClock

Let’sthinkaboutallthisforamoment.Atrophicgastritisisamajorriskfactorfor stomach cancer (as well as a host of other diseases related to acidsuppression).H.pyloriistheleadingcauseofatrophicgastritis.Takinganacid-suppressoron topofanH.pylori infectionmakes thebacteriaanevengreaterthreat to cause atrophic gastritis.Would it be toomuch to suggest, then, thattakinganacidsuppressorwithH.pyloriinthegutincreasesourriskofstomachcancer?Wethinknot.Giventhisknowledge,itwouldbesafetosaythatthesedrugs should be classed as carcinogen-facilitators under these conditions.Prescribing thesedrugswithout,at thevery least, testingpatients forH.pyloriwouldappear toborderonmedicalmalpractice.Howmanydoctorsare testingtheirpatientsforH.pyloribeforereachingfortheirprescriptionpadatthefirstsignofheartburn?Preciousfew,wecanbesure.

AlthoughtheDutch/Swedishstudyappearedinoneoftheleadingmedicaljournals in theworld, it seems to have caused barely a ripple. In an editorialaccompanyingthearticle,JulieParsonnet,M.D.,ofStanfordUniversityMedicalSchool,writes:“Inprinciple,current[acid-suppressingdrug]therapiesmightbeadvancingthecancerclockbyconvertingrelativelybenigngastricinflammationintoamoredestructive,premalignantprocess.”Sheaddsthatwhiletherewasnoconvincing evidence that drug-induced acid suppression increases the risk ofgastriccancer,“thelong-termuseofacid-inhibitingtherapyinpatientswithH.pyloriinfectionshouldbeviewedwithsomecaution”41(emphasisadded).Note

thatDr.Parsonnetwrotethesewordsin1996,justayearbeforethewidespreadpromotion of Prilosec for treating common heartburn began. Despite thesecautions, the official Prescribing Information for Prilosec and other acidsuppressorsoffersnotevenahintthatphysiciansortheirpatientsmightwanttothinkaboutH.pyloribeforeusingthesedrugs.

Figure5-3.Theulcer-cancerparadox.Havingduodenalulcers(andexcessgastricHCI)appearstoprecludegastriccancer,whilehavinggastriculcers(andanHCldeficiency)increasestherisk.AdaptedfromL-E

Hanssonetal.,1996.

Evenmore frightening is the fact thatmillions of people are now takingacid suppression into their own hands by using over-the-counter versions ofZantac,Pepcid,Axid,andTagametwithoutevengoingtothedoctor.Thus,theyvirtuallyeliminateanychanceofdiscoveringanH.pyloriinfection.Weshuddertothinkaheadwhendecadesofacidsuppressionbegintobearfruitintheformofanepidemicofstomachcancer.

HowAcidSuppressionRaisestheCancerRisk

Thereisaparadoxthatbaffledmedicineearlyinthenineteenthcentury.Thatiswhenitwasfirstnoticedthatpeoplewhohavegastriculcerstendtogetstomachcancer, while those with duodenal ulcers do not. Once the role ofH. pyloriinfectioninduodenalandgastriculcersandatrophicgastritiswasdiscoveredinthe1980sand1990s,theparadoxtookonanotherdimension:H.pyloricouldbethecausativeagent in eitherduodenalulcersorgastric cancer,buthardlyeverbothat thesametime.Ontheotherhand,gastriculcersandgastriccancercanoccursimultaneously.Themostrecentconfirmationofthisparadoxwasawell-

controlled U.S.-Swedish study that found twice the expected rate of gastriccancer in people who had gastric ulcers but 40 percent less than expected inthosewithduodenalulcers(seeFigure5-3).42

Howcan this be?The likely answer lies in—youguessed it—gastric pH.Remember we mentioned earlier that duodenal ulcers were associated withhyperacidity,whilegastriculcersoccurinanenvironmentofhypochlorhydriaorachlorhydria.AlowgastricpH(rememberlowpH=highacidity)isthenormalstateofaffairsforthestomachandcouldnotbecarcinogenic,evenifacidlevelswereexcessive. (If thatwere thecase, thehumanspecieswouldhavediedouteonsago.Ontheotherhand,anelevatedpH—anunnaturalconditionassociatedwith disease (e.g.,H. pylori infection, atrophic gastritis)—is an important riskfactorforgastriccarcinoma.

There appear to be at least two major mechanisms by whichhypochlorhydriaandachlorhydriaelevatetheriskofstomachcancer:byraisinggastrinlevels(hypergastrinemia),andbypromotingbacterialovergrowth.

HypergastrinemiaSpeedsUpMucosalCellGrowth

Hypergastrinemia (high gastrin levels in the blood) typically occurs in peoplewithatrophicgastritisorinthosewhotakeacid-blockingdrugsforlongperiodsoftime.Theamountofgastrininplayatanyonetimeisadirectreflectionofthecurrentlevelofstomachacid.Lowacidlevels(pH3orhigher)ingastricatrophytriggerhigher gastrin levels as the stomach tries to compensate for the loss ofacidity.Astandard20-mgdailydoseofPriloseccausesuptoathree-tofour-foldincreaseingastrinlevels.43Inpeoplewhoseheartburn/GERDfailstorespondtothe standarddose, long-term treatmentwithdoses ashigh as40or 60mghasproducedgastrinlevelsasmuchastenfoldabovenormal.44–47

Chronicallyelevatedgastrinisaconcerndueprimarilytoitsabilitytoraisethe risk of developing stomach cancer. The hormone normally promotes thegrowthandproliferationofnewhistamine-secretingECLcellsaswellasacid-producing parietal cells in the lining of the stomach.A steady supply of newECLandparietal cells is required to replace those that succumb to thehostilegastric environment, especially in the fundus, where acid levels are highest.Thus, turning up the gastrin flow not only increases stomach acid, but it alsospeeds up the ECL cell assembly lines. As long as the increase in gastrinmatches the decrease in acid, everything hums along normally. But when thegastrin supply badly exceeds the demand,ECL cell growthmaybe excessive.Known as hyperplasia, excess ECL cell growth is common in people with

atrophicgastritisandhasbeenobservedinpeopletakingPrilosecaswell.48–49Insomepeople,suchgrowthcanturncancerous.Thismaybesimilartothe

situationinwomen,wheretoomuchestrogeninthebreastoruterusstimulateshyperplasia,whichoccasionallydevelopsintocancer.Thereiscurrentlynoclearevidence that taking acid-suppressors for a long time directly causes stomachcancer. However, it is known that the risk increases in people with atrophicgastritis,whichcantakedecadestodevelopfully.FewpeoplehavebeenusingPrilosecorotherevenmorepowerfulPPIsregularlyformorethansixorsevenyears,sofar.

Ifratstudiesarealesson,though,long-termuseofacid-suppressingdrugsmay indeed be risky. In one study, twenty-four months of use caused astatistically significant dose-related increase in ECL hyperplasia and gastriccarcinoid tumors (knownasECLomas).50Whenpeople takePrilosec forup tofiveyears,examinationhasrevealedapositivecorrelationbetweenprecancerouschangesinthestomachliningandthedegreeofatrophicgastritis.51–52Nocasesof stomach cancer have been attributed outright to the use of Prilosec or anyotheracidsuppressoryet,however.

Carcinoid tumors are usually less serious than adenocarcinomas, but theycanstillbetroublesomeandextremelydangerous.Thisisbecausetheyfloodthebodywithgastrin,which respondswithavirtual floodof stomachacid. In thecondition known as Zollinger-Ellison Syndrome (ZES), carcinoid-inducedhypergastrinemia leads to extremely high gastric acid levels. All that acideventually overpowers the stomach’s natural acid protections and leads to theformationofmultiplesevereulcers,especiallyintheduodenum.53ZESisoneofthefewconditionsknowninwhichstomachacidlevelsareactuallytoohigh.

Dramatichypergastrinemiaisalsoakeysymptomofthediseaseknownaspernicious anemia, which is associated with severe atrophic gastritis andmalabsorption of vitamin B12, as well as both carcinoid tumors and gastricadenocarcinomas. In pernicious anemia, atrophic gastritis is so severe thatparietal cells lose the ability to secrete not only acid, but intrinsic factor also.SincebothHClandintrinsicfactorarerequiredforthedigestionandabsorptionofvitaminB12,malabsorptionresults.

Numerous reportshavebeenpublished relating casesofhypergastrinemiainpeoplewithachlorhydria/perniciousanemiawhoweretreatedwithhighdosesof Prilosec.54–59As one author reviewing the published scientific literature onelevated gastrin levels understated, “The evidence indicates that chronichypergastrinemiamaynotbetotallybenign.”60

Elevated gastrinmay also be a factor in some cases ofhuman colorectal

cancer, although the data are much fuzzier than they are for gastricadenocarcinoma.Nevertheless, itappears that theriskofdevelopingcarcinoidsandgastricadenocarcinomaduetochronichypergastrinemiamaybeincreasedifonepossessesaspecificgene.Whetheracid-suppressingdrugscancontributetocolorectalcancerremains“upintheair”atthistime.61

StomachAcidandCancer:TheBacterialLink

We have known about the link between low stomach acid levels and gastriccancer sinceas earlyas1879.Thatwaswhenphysicians,mainly inGermany,firstbeganreportingtheirobservationsthatpeoplewithstomachcanceralmostalwayshadlittleornoHClintheirstomachs.62Moresystematicstudiesovertheyearshaveconfirmedthatatrophicgastritis, inassociationwithachlorhydriaorserioushypochlorhydria,isamajorriskfactorforstomachcancer.Andtheriskincreaseswith the severity of thegastritis and the lengthof time a personhasit.63 In oneDanish study, peoplewith themost severe atrophic gastritis had afour-tosixfoldincreasedriskofdevelopinggastriccancer.Insomecases,ittookuptoseventeenyearsafterachlorhydriawasdiagnosedforcancertodevelop.Inthreecases,ittookmorethannineyears.64

Howdoes atrophic gastritis develop into cancer?Nooneknows for sure,butthemissinglinkmaybebacterialovergrowth.Accordingtothemostwidelyaccepted theory, some bacteria (but not H. pylori) are able to turn nitratemolecules,foundcommonlyinfood,intonitritemolecules.Notedonereviewofthescientificresearchonthisconnection,“Thisisapowerfulhypothesiswhichissupportedbymuchexperimentalevidence.”65

Nitriteswere oncewidely used to cure, or preserve,meats such as baconandham.Butinthe1970s,itwasdiscoveredthatahealthystomachcanconvertnitrites to chemicals callednitrosamines,whichareknown tobe carcinogenic.Asaresult,nitritesareusedfarlessofteninfoodpreservationtoday.

Nevertheless,nitritesproducedin thestomachbybacteriafromnitrates inordinary foodcanbe justasdangerousas theonesweget fromachar-broiledbaconburger.Studieshaveshownthattheconcentrationofnitriteingastricjuicerises along with the pH and the extent of bacterial overgrowth. People withchronic atrophic gastritis and hypochlorhydria make significantly more nitritefromdietarynitratecomparedwithhealthycontrols.66

Given these reactions, it should come as no surprise that taking acid-suppressingdrugsraisesnitriteandnitrosamineconcentrations.Inpeopletaking

Tagamet for peptic ulcers, for example, a 73 percent reduction in basal acidsecretion resulted in statistically significant increases in nitrites andnitrosamines.Evenwhenthedosewasreducedtoamaintenancelevelforthreemonths,nitriteandnitrosamineconcentrationsremainedelevated,suggestingthepresenceofaprolongedcarcinogenicstimulus.67

Directevidencethattheprolongeduseofacid-suppressingdrugsincreasestheriskofgastriccancerhasbeenlimitedanddifficulttointerpret.Useofsomeacid-suppressing drugs but not others has been reported to cause gastricmalignancy in laboratory animals, but extrapolation from rats to humans isalwaysfraughtwithdifficulties.68

AnecdotalreportsofgastriccarcinomasinpeopletakingTagametforulcersbeganappearingshortlyafterthedrugwasintroduced.69–71Inaverylargestudycomparing nearly ten thousand Tagamet users with more than nine thousandcontrols, thedeathrateandtheincidenceofGIcancerswerebothsignificantiyhigherintheTagamet-treatedgroup,althoughitappearedatthetimethatmostofthemalignanciescouldbeexplainedmoreeasilybyothercauses.72InanothersurveyofaboutseventeenthousandTagametusers,theriskofcancerwasfoundtobetentimesgreaterthanexpected.However,theseresultswerealsodifficulttointerpret,becausetheriskdeclinedoverallwithfurtheruse,whileitincreasedinwomentakingthedrugforsevenyearsorlonger.73–74

IfA=BandB=C,DoesA=C?

Absentanydirectproofthatacid-suppressingdrugsmayleadtogastriccancer,we need to fall back on the circumstantial findings. For example, there is nodoubt that acid suppression promotes bacterial overgrowth and that bacterialovergrowthpromotesproductionofcarcinogenicnitrosaminecompounds.Thereis also no doubt that acid-suppressing drugs increase the progression andseverityofatrophicgastritisinpeoplewithH.pyloriinfection,andthatatrophicgastritisisamajorriskfactorforgastriccarcinoma.Commentingontheserisksin 1989, before Prilosec use had become as widespread as it is now, oneresearcherwrote: “Until information is available about the effects of powerfulgastricsecretoryinhibitorsontheproliferativeindicesandpatternsofthehumanmucosa,thedrugsmustbecategorizedastoodangeroustousetherapeutically,especially since the proposed therapeutic benefits are minimal”75 (emphasisadded).

APrediction

Wewanttobeclear:Atthistime,thereisnooutrightproofthatprolongeduseof acid-suppressing drugs causes cancer. Given all the presently known facts,however,wefinditquitereasonabletopredictthat(ifthepossibilityisseriouslystudied) at least some acid-suppressing drugs will be found to significantlyincreasetheriskofcancer,especiallyiftheyareusedforalongtime.

*Bycontrast,vitaminAhelpspreventpneumoniaandotherinfections.

*OneresearchteamhasdemonstratedthatintravenouslyadministeredvitaminAreducedtheoccurrenceof“stressulceration”inseverelystressed,hospitalizedindividualsfrom63percentto18percent(MSChernovetal.,“StressUlcer:APreventableDisease.”JTrauma1972;12:831–846).AsvitaminAisnotpatentable,itsuseforthisandotherpurposeshasbeenlessthanemphasizedbypatentmedicinecompanies.

*Gastriculcersoccurinthestomach,whileduodenaluclersoccurintheduodenum.Bothtypesofulcerareknowncollectivelyaspepticulcers.

CHAPTER6

HowLowStomachAcidCanMakeYouSick:

Asthma,RheumatoidArthritis,andOtherDiseases

“Itappearstomenotunreasonablethatthepoison,asitmaybecalled,whichisgeneratedbyfoodillassimilated,findsitswayintothecirculation;andhencearisesthemiseryofhereditaryasthma.”

—H.L.Pridham,“ObservationsontheTreatmentofAsthma,”BrMedJ.1860;1:434–435

“We’re here to finish offBobby’s asthma,”RebeccaCutler declared. “He’slotsbetteralready,butwecan’tdoitallourselves.We’vedoneeverythingyoutold the Pizzolis to do for their son, Vincent, and it’s working! We’re allmembers of the same church, Bobby and Vincent are classmates, and whenVincent’s asthma disappeared in three months, we couldn’t believe it. So wedecidedtotry.”

“And Bobby’s asthma is more than halfway gone,” his father, David,added.“IthinkwejustneedthatinjectablevitaminB12,someallergywork,thattestforhisstomach,andmaybewecangetitgonecompletely.Atleastwehopeso.Bobby’shadatoughtime…we’vehadtorushhimtotheemergencyroomfive times in just the last two years. Since we started as much of Vincent’sprogramaswecould,he’soffthetheophylline.Thatstuffmadehim‘hyper’allthetimeandmadehisheartrace.Hestillneedstousehisinhalerfairlyoften,buthiswheezing is a lot lesswhen it happens, and it goes away easier.Andhe’ssleepingbetteratnight,notwakingupnearasmuch.”

I turned toBobby. “What haveMomandDadhadyoudoing about yourasthmalately,Bobby?”

“I can’t have any more milk or cheese or ice cream, and I hafta take abunchofvitaminsandstuff.”He lookedworried.“DoIhafta takeshotsevery

daylikeVincent?”“Isyourasthmabetter sinceyoustoppeddrinkingmilkandstarted taking

yourvitaminslikeVincent?”“Yeah.”“Thenit’spossiblethatshotsmighthelpyoulikeVincent,too,isn’tit?”Bobbylookeddubious.“Iguess.”“Ican’ttellyouforsurethey’llwork,Bobby,butitsoundslikely.”Iturned

backtohisparents.Hismotherhandedmealist.“Here’sasummaryofwhatwe’redoingsofar,”shesaid.“Bobby’sseven,

thesameasVincent,sowejustgavehimthesame,asmuchaswecould.”Ireadfromthelist.“Let’ssee:nomilkordairyproductsofanykind.All

otherfoods,eachoneeatenonlyeveryfourdaysorless…”“Wedid it thatway ’causewe have no idea exactlywhat foodsBobby’s

allergictoyet,”Rebeccasaid.“ButMonica,Vincent’smother,toldmeyousaidnocow’smilkordairyunderanycircumstances.Andyouaskedherto‘rotate’Vincent’sless-allergicfoodseveryfourdays.Sowemadeeverythingeveryfourdaysuntilwehadhimtested.”

“Makessense.”Iresumedreadingthelist.“VitaminB12,1000microgramsthreetimesaday,magnesium,125milligramsthreetimesdaily;vitaminB6,50milligramsthreetimesdaily.…”

“ThePizzolissaidvitaminB12 shouldbe injected,butsince it’sharmless,we thoughtwe’d tryhavingBobbyswallowitanywayuntilwecouldseeyou.Theyalsosaidthatbuildinguptissuemagnesiumlevelsreducesthetendencytomusclespasm,includingbronchialmuscle,”Davidremarked.

“Exactly. Let’s see: vitamin C, 1000 milligrams three times daily; onetablespoonofcod liveroildaily,andahigh-potencymultiplevitamin-mineral,one-third the adult quantity, three times daily. Everything in capsules, nottablets.”

“That’sbecausemostasthmaticchildrenhavepoordigestion,andcapsulesusuallydigestbetterthansometablets,right?”Rebeccaasked.

“Rightonboth,thoughit’snot100percentoneither.”“Also, we threw every bit of sugar, refined carbohydrate, hydrogenated

vegetableoil,andfoodchemicalsoutofthehouse,”Rebeccasaid.“Monicatoldmeyourecommenddoingthatnomatterwhattheproblemis,andalsojustforstayingashealthyaspossible.”

“Absolutely!” I replied. “Noneof those itemshaveanyplace inhealthfuldiets.”

“Takessomegettingused to,butsincewedid, I’vefelt less tired,”David

observed.“Let’s check Bobby over, and then have lab tests done, with your

permission,ofcourse,”Isaid.“That’swhatwebroughtBobbyhere for,”David said. “Monica said that

food allergies aremore important than inhalant allergies in childhood asthma,andyou’dcheckboth.ButIdidn’tunderstandwhattestinghisstomachhastodowithasthma.Couldyouexplain?”

“Sure.Ina1931publication,Dr.GeorgeBray,anasthmaspecialist,notedthat80percentof twohundredasthmaticchildrenhadunderproductionofacidandpepsininthestomach.This,ofcourse,impairsdigestion,loweringnutrientabsorption, and gradually increasing allergies to foods. In 1979, otherresearcherspublishedproofthatfoodallergy,particularlycow’smilk,cancausethestomachprobleminthefirstplace.”

“Soit’ssortofcircular…foodallergycausesthestomachtomalfunction,whichleadstomorefoodallergyandasthma.”

“Forapproximately80percentofasthmaticchildren.”“AndinjectingvitaminB12insteadofjustswallowingit?”“StomachmalfunctionimpairsvitaminB12nutrition.Also,inthelate1940s

andearly1950s,extravitaminB12byinjectionwasfoundtobeveryhelpfulinmostcasesofchildhoodasthma.”

“Howoftendoesallofthiswork?”“I can only give you approximations, but about 50 percent completely

eliminate theirwheezing, about30percenthavemajor improvement, about10percentonlyminorimprovement,andonlyabout10percentnochange.”

“AndI’vereadthedeathratefromasthmahasbeenclimbingthe last fewyears,”Rebeccaremarked.

Sixmonths later,Bobby’swheezingwas gone.Although I recommendedlifetime exclusion of cow’smilk and dairy products, the largemajority of hisfoodandinhalantallergieshadbeendesensitized,andhismotherhadliberalizedhis diet, while keeping all the “junk” out. His was taking capsules ofhydrochloric acid and pepsin to aid his digestion, and vitamin B12 injectionswere down to a maintenance level. He continued his other oral supplements.Severalyearslater,heremainsfreeofasthmaticwheezing.*

In thepreviouschapter,wediscussedavarietyof illnesses thatcan resultfromchronicallylowstomachacidsecretion.Mostof these, likegastriccancerand bacterial infections, are diseases of the GI system itself. But theconsequences of low stomach acid can extend far beyond theGI tract. In this

chapter,wedescribehowalargenumberofseriousdiseasesthatappear—onthesurface,at least—tobe totallydivorced from theworkingsof the stomachandintestines,maysometimeshavetheirroots inashortageofstomachacid.And,yes, restoring normal GI function can often yield remarkable degrees ofimprovement.

As we can see in the box on page 103, these are all dangerous anddebilitating diseases, conditions that are notoriously difficult or impossible totreat effectively by conventionalmeans.Most practitioners using conventionalpatentmedicineswouldneverconnectthesewithlowstomachacid.

Conventionalmedicine is anchored to the belief that synthetic symptom-suppressingdrugsarenearlyalwaysthebesttherapyformostdiseases.Thus,thestandard treatment for inflammatory diseases, including allergies, asthma,rheumatoid arthritis, ulcerative colitis, and many others, consists primarily ofpowerful “anti-inflammatory” drugs that bring about temporary relief bysuppressing the inflammation.Whatever it is that’s causing the inflammatoryreactioninthefirstplaceisusuallycompletelyignored.

Yet,ifwelookbeneaththesurfacesymptoms,wefindacommonthread,athread based in a majority of cases on fundamental molecular and geneticresearch. Investigators of human DNA have identified a complex of genestermed“histocompatibilitylocusantigens”(HLA)thatappeartoregulatemanyfeaturesof immunity.Furthermore, theyhavefound thatmanydiseasesappearto“cluster”morefrequentlyaccordingto“HLAtype.”

DiseasesThatMayBeRelatedtoDeficientStomachAcid

AcnerosaceaAddison’sdiseaseAllergicreactionsCeliacdiseaseChildhoodasthmaChronicautoimmunehepatitisDiabetes(typeI-Juvenile)Eczema(severe)GallbladderdiseaseGraves’disease(hyperthyroid)Lupuserythematosus

MaculardegenerationMultiplesclerosisMyastheniagravisOsteoporosisPerniciousanemiaPolymyalgiarheumaticaReynaud’ssyndromeRheumatoidarthritisSclerodermaSjögren’ssyndromeUlcerativecolitisVitiligo

All of the diseases listed in the box in bold type have been found byvarious investigators to clustermore frequently in theHLA typesDR3,DR4,andB8. Thismeans that even though these diseases and their symptomsmayappear very different on the surface, on the genetic and molecular level theyshare at least one (and probably many more) common features. A major“common thread” in all these diseases is a dysfunction of the upperGI tract.Although not found in 100 percent of cases of the diseases listed above, it isusually found (if looked for) in over 50 percent of those diagnosedwith eachdisease.*

More importantly, we find that by simply (and safely) restoring normalgastric function, many people with these diseases experience “amazing”improvement. These treatments do not suppress any symptoms. Instead, theyhelpalleviatethecauseoftheinflammationorothersymptoms.Thisdistinctionisextremelyimportant.Asananalogy,imagineasplinterinyourfootiscausingyou pain and discomfort. You could take a pain-killing drug (temporarysymptomsuppression)oryoucould take the splinterout (remove thecauseoftheproblem).Whichsolutionmakesmoresense?

Asthma

Asthma (especially childhood asthma) and stomach acid? People are oftensurprisedtohearthatthisseriousandincreasinglycommonrespiratorydisorder,in which the airways become inflamed and constricted, making breathing

difficult,mayoftenbegininthestomach.

Figure6-1.The1698ATreatiseoftheAsthmacontainsthefirstmentionthatimpairedgastricfunction,latershowntobelowstomachacid,mightbeacauseofasthma.FromtheNationalLibraryofMedicine.

Mostphysiciansroutinelyignoretheconnection,remainingtotallyunawareofamedicalliteraturelinkingasthmaandstomachtroublethatgoesbackmorethan300 years. In fact, the earliestmention of a gastric deficiency in asthmaappearedintheveryfirstmedicaltexteverpublishedinEnglishonthesubjectofasthma.SirJohnFloyer’sATreatiseoftheAsthma(seeFigure6-1),whichfirstappeared in London in 1698, reported a “defect” in stomach juices. WroteFloyer,“Thisdefectofdigestionandmucilaginousslimeinthestomachareveryobviousandobservedbywriters,andweresupposedtheimmediatecauseoftheasthma.”(emphasisadded).

Althoughwe know today that asthma is a complex diseasewithmultiplepotentialcausesandtriggers,thereshouldbelittledoubtthatlowstomachacidcan often play an important role. One of the most important scientificcontributionsinthemodernagewasaresearchreportpublishedin1931bytheEnglishphysicianDr.GeorgeWBray, fromtheAsthmaClinicat theHospitalfor Sick Children in London. In an era before the patent medicine industrybecamethedrivingforcebehindmostmedicalresearch,Dr.Brayexaminedthestomachcontentsofmorethantwohundredchildren,agedsixmonthstotwelveyears, who came to his hospital wheezing from asthma. He recovered gastricjuiceatregularintervalsafteramealviaasmalltubepassedintothechildren’sstomachs. As his cases accumulated, he soon saw a pattern developing: (seeFigure6-2).1

• Overall, 80 percent of the asthmatic children had below normal acidsecretionintheirstomachs

•23percenthadmildhypochlorhydria

•48percenthadpronouncedhypochlorhydria•9percenthadachlorhydria

AsDr. Bray followed these children formany years, he noticed that theaciddeficiencywasmostpronouncedinchildrenundertheageofsevenyears.As they grew older, though,many of the children’s acid secretion returned tonormal, which often coincided with the remission, or “spontaneous cure,” oftheirasthma.

Figure6-2.Repeatedsamplingofthestomachcontentsofmorethantwohundredchildrenwithasthmarevealedvaryingdegreesofaciddeficiencyinthevastmajorityofcases.AdaptedfromBray,1931.

Eventoday,physicianswhotreatchildrenwithasthmaarewellawarehowcommonit is for themto“outgrow”theirasthmaas theypass throughpubertyand beyond. About half of all asthmatic children experience spontaneousremissionsas theyenter their teens.2Oneof the few investigations sinceBraythat has tried to understand why this happens reported that “spontaneousremission” occurred only in children when there was “no obvious cause” fortheir asthma.Could thesechildrenhavehad lowstomachacid that returned tonormal? We wouldn’t be surprised, but we’ll never know, because theresearchersneverlooked.3

When George Bray found that so many of his asthma patients had lowstomachacid,hedidthelogicalthing:hehadthemreplacethemissingacidbytakingadilutesolutionofHClandpepsinbeforeorduringtheirmeals.Whathefoundwouldbeconsideredimpossiblebythestandardsofconventionalasthmatreatment.Overthecourseofthreemonths,theacidtherapyaloneresultedinthechildren’s eating better, gaining weight, and wheezing less. Eventually, theirasthmaattacksceasedaltogether.“Thechild thenappearsperfectlywellwhilsttakingthemedicine,”wroteBray.But,henoted,iftheystoppedtheacidtherapyorcaughtacold,theymightsuffersomemildattacks.

EvenmoreimpressivewaswhathappenedwhenBraynotonlyreplacedtheacid,butalsolimitedthechildren’sexposuretotheallergensthatweretriggeringtheir attacks. Their improvement was immediate. If the children continued totaketheirmedicinethroughoutthewinter,theyremainedasthma-freeandcouldthen safelydiscontinue the treatment.4This sounds suspiciously like a cure. Ifthese children had been put on conventional anti-inflammatory corticosteroidsand bronchodilators, they would not have been cured, but would likely havebecomedependentonthesedrugsfortherestoftheirlives.

It is an unhappy fact of life that conventional medicine, with its single-minded focus on drug-induced symptom suppression, doesn’t know what tomake of children who get over their asthmawithout the help of drugs. Suchpeople may be regarded, often with a considerable degree of skepticism, as“curiosities.” As their asthma wanes, they stop going to the doctor, who isusually toobusywith“sick”children to followupon thosewhosomehowgetbetterontheirown.

Norcanwecountonthepatentmedicineindustrytofindoutwhyasthmagoesawaybyitselfsooften.They’vegottoomuchinvestedinlifelongsymptomsuppression to spend much of their considerable resources on investigatingsomething that might lead to a real cure and would make their symptomsuppressorsobsolete.They’reespeciallyuninterestedifthepotential“cure”isanatural—and therefore unpatentable—substance like HCl, pepsin, or vitaminB12,whichwouldnotearnthemenormousprofits.(Neverlosesightofthefactthatpharmaceuticalcompaniesarenotinbusinesstocurediseases,butrathertomakemoneyfortheirstockholders.Onceapatientiscured,thatpatientdoesn’tneed to buy anymore drugs.But if his or her symptoms are suppressed, theymaybe“hooked”onthedrugsforlife.)

Most physicians never suspect that many of the children they see who“outgrew” their asthma might have done so because their gastric secretionsgradually normalized with age. As a result, they don’t have a clue that theymightbeabletohastenthedisappearanceofasthmabyprovidingthechildren’sstomachswhatthey’remissing.Theydon’thaveaclue,becausetheydon’tknowenough to look in the children’s stomachs. Hardly any physicians measureintragastric pH on a routine basis, especially in cases of asthma. If they did,they’dbeastounded!Childrenover age six (usually theyoungest able tohavetheir stomach acid accurately tested) with asthma have an approximate 50percent to 60 percent incidence of mildly to severely low stomach acid.“Indirect” indicators of low stomach acid (the best easily available for veryyoung children) suggest an even higher incidence of low stomach acid,

approachingthe80percentfigurepreviouslyreportedbyDr.GeorgeBray.Adults with asthma commonly have reflux esophagitis and GERD (see

below).However,theirdiagnosesareoftenmadebymeasuringesophagealpH,notgastric pH.Remember, excess acid in the esophagusdoes not necessarilysignalexcessacidinthestomach.Infact,alltoooften,excessesophagealacidityisassociatedwithtoolittlestomachacid.

Measuringstomachacidityisquitesimple,andtheinformationitprovidesis extremely valuable. The test we use to measure stomach acid secretion isdescribed in chapter 7. It should be an essential part of any thoroughmedicalexamination.Unfortunately,ithardlyeveris.

PermanentNaturalAsthmaRelief…WithoutDrugs

Inmythirtyyearsofclinicalpractice,Ihavefoundthatabout50percentofallchildrenwhocome to theTahomaClinicwithasthmafindpermanent reliefoftheir wheezing within thirty to sixty days, without taking corticosteroid andbronchodilatordrugs.Here’swhatwedo:

• Inject vitamin B12, which is poorly absorbedwhen stomach acid,pepsin,and intrinsic factoraredeficient (seechapter4).Frequently,theamountsofvitaminB12neededtoeliminatewheezingare(relatively)large,but,fortunately,vitaminB12isquitesafe.

• Restore the stomach to normal function by replacing HCl andpepsin. Although acid and pepsin are required to free up vitamin B12from itsproteincarriersand thusallow forbetter absorption, it’s likelythat improving the digestion is just as important for reducing theoccurrence of food allergies,which are the principal offenders inmostcaseofchildhoodasthma.

• Paycloseattentionto foodallergies,especially tocow’smilk.Suchallergies may result in varying degrees of allergic gastritis, leading tohypochlorhydria, low pepsin secretion, and possible failure to produceintrinsicfactor.

• Supplement magnesium and vitamin B6, both of which have beenshowntolessentheseverityandfrequencyofasthmaticattacks.

TheCrucialRoleofVitaminB12inChildhood(andOther)FormsofAsthma

The first hint that vitamin B12 might be useful against wheezing cameserendipitouslyin1949.5Again,itwasalonephysicianinvestigatingtheeffectof vitaminB12 on “growth failure” in children in anOhio camp.He gave thechildrencapsulescontaining10microgramsofcrystallinevitaminB12eachdayto testwhether itwouldpromotegrowth.Oneof thechildrenat thecamphadwhat was described as “intractable” asthma with constant wheezing day andnight. Within a week after the child started taking vitamin B12, though, hisasthmaticwheezinghadvanished.

Figure6-3.EffectofvitaminB12onpeoplewithasthma.ThepercentageofpeoplewithasthmawhosesymptomsimprovedwithvitaminB12treatmentisextremelyhighinyouthbutdeclineswithadvancing

age.AdaptedfromCrockett,1957.

Two years later in another small trial, twenty adults with “intractable”asthmaweregiveninjectionsof1000microgramsofvitaminB12onceaweek.Afterfourweeks,eighteenofthemreportedimprovementinbreathing(althoughsomewheezingremained),sleep,andintheirgeneralcondition.6

An Italian study thatwas later abstracted in the Journal of theAmericanMedicalAssociationin1952reportedtheeffectsofdailyintravenousinjectionsofveryhighdosesofvitaminB12(30milligrams,equalto30,000micrograms;fortunatelyit’snearlyimpossibletooverdosewithvitaminB12)intwelveadults

with asthma. After fifteen to twenty days, wheezing completely ceased in 83percent(tenoftwelve)ofthestudyparticipants.Ofthetenwhowerecompletelyrelieved,twolaterhadarelapse,whichrespondedtoarepeatofthevitaminB12treatment.7

In 1957, the English physician JA Crockett reported on a study he raninvolving eighty-five people of all ages who had asthma.8 All were givenintramuscularinjectionsof1000micrograms(1milligram)ofvitaminB12,firstatweeklyintervals,andlateratunspecifiedintervalsuptofourweeks.Usingafour-level scoring system (“no change,” “slight improvement,” “moderateimprovement,”and“markedimprovement”)Dr.Crockettobservedimprovementin56percent(forty-eightoutofeighty-five)ofhistestsubjects.Healsofoundthat the ability to improve varied with age. It was extremely high in youngchildren(83percent)butdeclinedwithage.Eveninthefifthandsixthdecadesof life, though, B12 injections resulted in nearly 40 percent improvement (seeFigure6-3).9

BasedontheseandothermedicalreportsconcerningvitaminB12 therapy,in1976westartedadvisingparentstogivetheirasthmaticchildrendailyvitaminB12injections,500to3000microgramsdaily(dependingonthechild’sageandweight).We have found that within thirty days of treatment, 50 percent stopwheezing entirely, and another 30 percent improve from a little to a lot. Theinjectionsarethentaperedaccordingtoresponse,resumingorincreasingagainifthewheezingreturnsorbecomesmoresevereagain.

ParentsunderstandablyinquireaboutoralinsteadofinjectablevitaminB12treatment.Ifwheezingisn’tsevere,there’snoreasonnottotrythe“oralroute”first.Ifitdoesn’twork(whichisfrequent)wecanthenproceedtoinjection.

Vitamin B12 does not work immediately to clear a particular wheezingepisode.(ArelativelyrapidintravenousinjectionofmagnesiumaccompaniedbyvitaminB6ismuchmoreeffectiveinclearingacutewheezing.)Parentsusuallyreport improvement in chronicwheezingbeginningafter five to sevendaysofdaily B12 shots. “Full results” and a “maintenance level” are usually reachedafterapproximatelythirtydays.

AlthoughvitaminB12caneliminateordramaticallylessenthewheezingofchildhoodasthma,itdoesnoteliminatetheallergiesthattriggerattacks,nordoesit repair the frequently underlying stomach problem, or restore the rest of thenutrients not getting absorbed due to poor gastric function.All these possibleproblems present in childhood asthma must be vigorously pursued or theafflictedchildwon’tbeashealthyaspossible.

AsthmaandGastricReflux:What’stheConnection?

ThesuccessofHCl,pepsin,andvitaminB12 therapysuggests that therootsofasthma lie not in the lungs, where the symptoms appear, but in the stomach,where acid secretion and vitaminB12 digestionmaybe compromised.True toform, though, the patent medicine industry has largely ignored this lead and,instead, focused its considerable resourcesdirectlyon symptomsuppression inthelungs.

Theresulthasbeenthedevelopmentandwidespreaduseofpowerful—anddangerous—corticosteroids (e.g., prednisone, beclomethasone, triamcinolone),bronchodilators (e.g., albuterol, ephedrine, theophylline), and other drugs thataredesignedtosuppressinflammationanddilateconstrictedairways.Thankstothousands of pharmaceutical industry-sponsored research studies and hundredsofmillionsofdollarsinadvertising,promotion,and“education,”abouttheonlythingmostphysicianstodayknowaboutasthmatherapyisthiskindofsymptomsuppression.Theyaretaughttoviewasthmaasasometimes-“incurable”illnessthat can be “controlled” only by using anti-inflammatory and bronchodilatordrugs (as well as inhalant allergy control). The cause(s) of asthma are notaddressedby thisapproach.Althoughfactorssuchasallergicreactions,airway“hyperreactivity,”andageneticpredispositionarecertainlyimportant,therolesof lowstomachacidityanddeficientvitaminB12arecompletely“off theradarscreen”today.

Nevertheless, there is a growing awareness in conventionalmedicine thatwhatgoesonin thestomachdoeshavesomethingtodowith thesymptomsofasthma. In just the last ten years, more than four hundred scientific articlesconcerned with the connection between asthma and gastric acidity have beenpublished. It turns out that one of the most common features of asthma, inaddition towheezing, is gastroesophageal reflux, often a sign of low stomachacid. It is estimated that between 30 percent and 89 percent of people withasthmaalsohaveGERD.Comparedwithhealthypeople,thosewithasthmaalsohavesignificantlymorerefluxepisodesandmoreacid-inducedirritationoftheiresophageallining.10

Whatistheconnectionbetweenrefluxandasthma?Nooneknowsforsure,butitiscertainlycomplex.Itisunclear,forexample,whetheracidrefluxcausesasthma,whether asthma causes reflux, orwhether both result from a commoncause, such as lowgastric acidity or activity in the vagus nerve,which serves

boththegutandtheairways.Itisknownthatdrugsthatarecommonlyusedtotreatasthma,suchasthe

bronchodilators theophylline, albuterol, ephedrine, and pseudoephedrine, canweakentheLESvalve,andthuspromoteacidreflux.Ithasalsobeensuggestedthat the act ofwheezing places added pressure on the LES during expiration,causingittoleakacidicgastricjuicebackintotheesophagus.”11–13

Do any of these mechanisms suggest that people with asthma have toomuchHClintheirstomachs?Ofcoursenot.Aswehavepointedoutadnauseum(no pun intended), excess acidity is relatively uncommon and is usuallyassociated with conditions such as duodenal ulcer and Zollinger-Ellisonsyndrome.Itisfarmorelikelythatpeoplewithasthma,especiallychildren,havetoo little gastric acid. Unfortunately, although low stomach acid is oftenassociatedwith reflux, stomach pH is virtuallynevermeasured inpeoplewithGERDletalonethosewithasthma.Mostresearchersaresatisfiedtoreportthatesophageal acidity is elevated, but this hardly qualifies as news, nor is itparticularlymeaningful.Certainly,thepHintheesophaguswillbemoreacidicthan it should be. That is the definition of acid reflux. However, it tells usnothing about the amount of acid the stomach is secreting, just that the LESvalveismalfunctioning.

Evenso,toconventionalmedicine,theco-occurrenceofrefluxandasthmais becoming yet another reason to prescribe powerful acid suppressing drugs.Here’s the rationale: It is not unusual for refluxed gastric juice to be inhaled(aspirated) into the lungs, especially when reflux occurs during sleep. Insusceptible individuals, theacidicmaterialmight triggeranasthmatic reaction.Studiesshowthatwhenacidgetsintothewindpipe,thereisatenfolddropintheabilityoflungstotakeinandbreatheoutair.14–15Theoperativetheoryisthat,ifacidrefluxistriggeringasthmaticattacks,thenremovingtheacidshouldrelievetheasthma.

Doesthistheoryholdup?Notreally.Severalstudieshaveinvestigatedtheuse of Prilosec in people with asthma and GERD, and the results have beenequivocal,atbest.Ingeneral,improvementinpulmonaryfunction,ifandwhenitoccurs, tends tobemodestand is seenonlyatveryhighdoses thatvirtuallyeliminate all stomachacid secretion.The standard therapeuticdoseofPrilosecforGERD,20mgonceaday,producesno improvement in asthma symptoms(e.g.,wheezingand“airwayconstriction”)orpulmonary lungfunction.16Aftersixweeksoftreatment,adoseof40mg,twicethedailydose,resultedinjusta20 percent improvement in the amount of forcefully exhaled air (a standardmeasureofpulmonaryfunction)in27percent(fifteenoutoffifty-six)ofpeople

with asthma andGERD.17 In a third trial, a dose of 40mg twice daily (fourtimesthestandardGERDdose)yieldedonlyasmall,butstatisticallysignificant,improvement in lung functionafter threemonths,but thepatientscontinued towheezeandtoneedbronchodilatorsandothermedicationsasmuchasever.18AEuropean studyusing the sameveryhighdose ofPrilosec in thirty-six peoplewith GERD and asthma found “no beneficial effect” on any measure ofpulmonaryfunction,despiteproducingwhatwasdescribedasa“profoundeffecton acid reflux.” The researchers, from The Netherlands, concluded that theirresults “… do not support a role for intensive anti-reflux therapy to improvepulmonarysymptomsandfunctioninpatientswithasthma…whohaveairwayhyperresponsiveness despite maintenance treatment with inhaledcorticosteroids”19(emphasisadded.)

Areviewof studiesonacid-suppressingdrugspublishedover thirtyyears(1966–1996) in major medical journals found that overall, asthma symptomsimprovedin69percentofpeoplewithGERD,asthmamedicationusedroppedin62percent,andeveningexpiratoryabilityimprovedin26percent.Andyet,notone person showed significant improvement in lung function. The authorsconcluded that acid-suppressing drug treatment “improves asthma symptoms,may reduce asthma medication use, but has minimal or no effect on lungfunction”20(emphasisadded.)

Hardly a ringing endorsement! Yet, physicians who hear about patentmedicine company-sponsored research by reading patent medicine-sponsoredjournals or Web sites, by going to patent medicine company-sponsoredconventions,bytakingrequiredpatentmedicinecompany-sponsoredContinuingMedical Education (CME) courses,* or by accepting “free” drug samples arebeginningtogetthemessagethatsomeimprovementmightbepossibleinsomepatientswhoseasthmamayberesistanttocorticosteroidtreatment.Asaresult,some physicians, such as allergists and family physicians, who may have nospecificexpertiseinGImedicine,arebeginningtoprescribePrilosecandotheracid-suppressors “off-label” to their asthma patients. Sometimes they mayprescribe the drug even if the patient doesn’t complain of “acid indigestion,”underthepresumptionthattherefluxmaybe“silent”insomecases.21–22

It’sasafebet that thesedoctorsgivenarya thought towhat the resultingacidsuppressionmaybedoingtotheirpatients’stomachs,nottomentiontheirgeneral health. Do they actually measure stomach acid levels? Do they evenmeasure esophageal pH?Do they ever test for atrophic gastritis, forH. pyloriinfection,orforvitamin/mineralmalabsorption?

Ofcoursenot.Inthevastmajorityofcases,theapproachisempiric:Trythe

drug. If it works, fine, prescribe it forever. As one researcher has noted,“Because[GERD]isachronicandunrelentingdisease,aggressivetherapymaybealifetimecommitment.”23Ifallthesedrugsdoiseliminatethestomachacid“nuisance,”whatcouldbetheharminthat?

Such high doses of acid suppressors wipe out nearly all stomach acidsecretion,creatingastateofchronicachlorhydria.Despitethis,onlymodest,atbest, improvement in asthma symptoms is achieved. The implications of thistype of treatment are truly frightening. If chronically low acid secretion cancauseasthma,asDr.Brayandothershavesuggested,isn’titpossiblethattakingthese drugs over the course of many years will actually increase the risks ofasthma in some sensitive people and make them even more dependent onconventional corticosteroid and bronchiodilating drugs? Can such a smallimprovement in symptoms, if andwhen itoccurs,beworth thepotential cost?It’shardtoseehowthiskindoftreatmentcouldbejustified.

Aswewillseeinchapter7, therearefarbetter,naturalwaysofreducingacidrefluxandrelievingasthmathatgodirectlytothecausesofthesedisorders,producingsignificant improvementwithout suppressingsymptomsandwithoutendangeringourhealthintheprocess.

Allergies,FoodSensitivities,andLeakyGuts

Over the years, reports have consistently appeared in themedical literature—especially in Europe—linking hypochlorhydria and achlorhydria not just withasthmabutwithawiderangeofallergicreactionsandskindisorders.FromhisvantagepointattheAsthmaClinicattheHospitalforSickChildreninLondon,Dr.GeorgeBray found thatasthmawasnot theonlyproblem inchildrenwithlow stomach acid. Compared to childrenwith normal stomach acid, they alsoseemed to have a disproportionate risk of conditions like hay fever, hives,eczema, andmigraines.24 (Dr.Bray also reported that 50 percent of asthmaticparentsofasthmaticchildrenhad“adefinitedeficiencyoffreeacidsecretion,”while theother50percentwerenormal.)Since then,othershavealso reportedassociations between low stomach acid and severe acne,25 chronic hives,26

dermatitisherpetiformis(atypeofskinrash),27–29gallbladderdisease,30–31andhayfever(allergicrhinitis).32

Howcanadeficiencyinstomachacidcauseustosneeze,wheeze,oritch?No one knows for sure, but ever since Dr. Bray’s day, the answer has beenthoughttolieinfoodallergiesandsensitivities.

Whether hypochlorhydria causes food allergies or food allergies causehypochlorhydria is a chicken-and-egg issue.Nomatterwhich one sets off theprocess, a vicious circle soon ensues in which an allergic reaction to foodinflames the gastric and intestinal linings, inhibiting HCl secretion andpromotingallergicreactionsalloverthebody,notjusttofoods,buttoinhalantsandmicroorganisms,aswell.

It is well known that for some sensitive people, inhaling certain allergy-causing substances (allergens) like dust, molds, or chemicals can trigger anallergic inflammatory reaction in the airways—an asthmatic attack where theairwaysbecomeinflamed,swollen,andconstricted.Lesswellrecognizedisthefactthat,forsomechildren,wheezingcanoftenbeginwithaglassof“Nature’smostperfectfood,”thesourceofcountlesscelebritymustaches,goodoldcow’smilk.Thankstomyth,custom,advertising,andpoliticalinfluence,cow’smilkisright up therewithmotherhood and apple pie as an untouchable icon inU.S.society.Butthefactis,forquitealargepercentageofthepopulation,cow’smilkisapoisonthatcanmakethemverysick.Ininfants,anallergytocow’smilkisawell-knowncauseofgastroesophagealreflux.33–40Thereseemstobelittledoubtthatdrinkingcow’smilkcanalsocausesomeinfantstodeveloptypeIdiabetes,which can leave them dependent on insulin injections for the rest of theirlives.41–42When people cannot tolerate cow’smilk* (or any other substance),consuming a glassful can cause an inflammatory reaction in the stomach,intestines,orboth.

InflamingtheStomach

Whenthestomachlininggetsinflamed,parietalcellsdie,andHClsecretionfallsoff.Finnishinvestigatorsfoundseverelyimpairedgastricacidsecretionineightoutofeightcow’smilk-intolerantinfants, includingthreewhohadvirtuallynoHCl in their stomachs. An inflammatory reaction had seriously damaged theinfants’ gastric mucosal lining, leading to atrophic gastritis (proven withstomachbiopsies).After the infantswereswitchedtohumanorsoymilk, theirgastricfunctioneventuallyreturnedtonormal.43

AstheFinnishstudyshowed,whenchildrencontinuetodrinkmilkdespitethefactthattheymaybeallergictoit,thedamagetotheirstomachliningmaybesufficient tocausehypochlorhydriaorworse,which impedes theproductionofpepsin and intrinsic factor.The combinationof lowacid, lowpepsin, and lowintrinsic factor impairs the digestion of proteins and the absorption andutilizationofvitaminB12(seechapter4).

BreachingtheIntestinalBarrier

Milk or other allergenic proteins that reach the bowels undigested or partiallydigested due to hypochlorhydria or achlorhydria can trigger an inflammatoryreactionhereaswell.Theresultingdamagetotheintestinalliningpunchesholesin one of the body’smost important protective barriers, resulting in intestinalhyperpermeability,sometimesknownas“leakygut”syndrome.44–47

SincetheGItractisessentiallyanextensionoftheoutsideworld,oneofitschieffunctionsistokeepundigestedforeignproteinswheretheybelong,inthebowels, but “outside” the body. A healthy intestinal lining allows vitamins,minerals,aminoacids,andotherproductsofdigestion topass through itscellsand into the general circulation. But it keeps out “foreign” food proteins,bacteria,viruses,fungi,andanythingelsethatmightcomedowntheesophagus.

In sensitive people, “foreign” proteins thatmanage to cross the intestinalbarrierandleakintothegeneralcirculationcanbecometheobjectofavigorousallergic “rejection” reaction by the immune system. We may experience thisreactioninrangeofdifferentways,fromGIdiscomfortandhivestoapotentiallyfatalgeneralized“anaphylactic” reaction, inwhichmajor systemsof thebody,includingtherespiratorytract,begintobreakdown.Ordinarily,onceanallergenisremoved,thereactiondissipates.Avoidtheallergenandweavoidthereaction.

Insomepeople,though,thepicturebecomesmorecomplicated,becausetheinitialallergicreactioncansomehowtriggertheimmunesystemtoturnitsattackon the body itself. Depending on which part of the body suffers the immunesystem’smisguidedattack,avarietyofdifferentautoimmunediseasescanresult.These include rheumatoid arthritis, lupus erythematosus, multiple sclerosis,ulcerative colitis, and many others. (See below for more about autoimmunediseases.)

Among the most important factors that influence whether or not theintestinalbarrierspringsaleakisnoneotherthanthegastricpH.(Thisisgettingmonotonous, isn’t it?GastricpHseems toplay important rolesallover theGItract.)Inthiscase,anelevatedpHinterfereswithproteindigestionandpermitsbacterialovergrowth,whichcombinetopromotegutleakage:

• Impeding protein digestion. The digestion of protein by pepsin intoaminoacidsoccursmostefficientlywhen thepHin thestomach is lessthan3.IntheabsenceofsufficientHClinthestomach,thepHrisesandlargeamountsofproteingoundigested.Insteadofthecomponentaminoacidspassingintothesmallintestine,wholeproteinsmayslipthrough.

• Making the gut leak. In earlier chapterswe described how bacterialovergrowth(duetoatrophicgastritisand/oracid-suppressingdrugs)caninhibit nutrient absorption and lay the groundwork for stomach cancer.Bacteriamay also be themissing link between low gastric acidity andsomecasesofjointandconnectivetissueinflammationandotherformsof autoimmune disease. For example, people with rheumatoid arthritisoften have considerable bacterial overgrowth in their stomachs. It isthought that products of these bacteriamay directly damage joints andothertissues,buttheymaywreakevenmorehavocwhenbacterialtoxinsdamagetheliningofthesmallintestine.48Suchdamagecanweakenthelining, making it more permeable—or leaky—to proteins and othernutritional molecules that would not normally be permitted to passthrough.

RheumatoidArthritisandOtherAutoimmuneDiseases

Rheumatoid arthritis (RA) is a crippling systemic inflammatory disease thataffects many different organs, especially the joints. Over time, chronicinflammation can destroy the knee, hip, wrist, and other joints, makingmovementpainfulandultimatelyimpossible.RAisanautoimmunedisease.TherelationshipbetweenRAanddigestivefunctioningmayserveasamodelforallautoimmunedisorders.

Inmanypeople,RAbeginswithaleakygut.Whenthegutbecomesleaky,nomatterwhatcaused it, foreignproteinscanslip through the intestinal liningandenterthecirculation,wheretheydon’tbelong.It’snotlongbeforetheylightup the immune system’s radar, which responds by scrambling a battalion ofproteinscalledantibodies,whichareprogrammedtosearchoutanddestroytheinvading proteins (allergens). The subsequentmeeting of the two forces oftentakes the form of an inflammatory sensitivity or allergic reaction. For someallergens, the battlefield may be the skin (e.g., hives, rashes); for others, theairways(e.g.,asthma). It isquitecommonfor thebattle tobefought in theGItract itself, resulting in such diseases as atrophic gastritis, celiac disease,inflammatoryboweldisease,ulcerativecolitis,andothers.49–53

Ifalltheseantibodieseverdidwasdestroytheinvadingantigen,wemightexperiencetransientdiscomfort(possiblysevere)fromanallergicreactionuntilalltheantigensweredestroyedorneutralized.Thentheantibodieswouldretreat

to a neutral corner of the body and wait for the next invasion. However, incertain vulnerable people, under circumstances that are not well understood,antibodies created to attack a specific foreign protein (e.g., cow’s milk)sometimes start attacking cells in the body that merely resemble the milkprotein,inotherwords,anautoimmunereaction.

Autoimmune diseases can take many different forms, depending on thetissue involved. These diseases include Goodpasture’s syndrome (lung andkidney),Hashimoto’s thyroiditis andGraves’disease (thyroidgland), systemiclupus erythematosus (connective tissue), rheumatoid arthritis (joints),scleroderma (skin and connective tissue), glomerulonephritis (kidneys), type 1diabetes mellitus (pancreas), Sjögren’s syndrome (eyes, tear glands, salivaryglands, connective tissue, joints), inflammatory bowel disease (the GI tract),multiplesclerosis(nervetissue),andmanyothers.Itisfairlycommonforpeoplewithonetypeofautoimmunediseasetoalsohavesymptomsofothers,aswell.54

Whatever form they take, though, autoimmune diseases are usually veryserious and notoriously difficult to treat by conventional medicine. Once thebodystartsmistakenlychurningoutantibodiesagainstitsowntissues,ofwhichthere’savirtuallyendlesssupply,there’smaybenostoppingit—atleastuntilallthetissuesaregone.That’swhyautoimmunediseasesaresuchseriousbusiness.

ZeroinginontheWrongTarget

Since conventionalmedicine has nevermet an inflammatory reaction it didn’ttry to suppress, the standard treatment for RA (and most other autoimmunediseases)haslongbeensomekindofanti-inflammatorydrug.Bysquelchingtheinflammatoryresponse(inotherwords,suppressingpartoftheimmunesystem),thesedrugsmayachieveadegreeoftemporarysymptomaticrelief.Ultimately,though,theyalwaysfail,becausesymptomsuppressiondoesnothingtoremovethe cause or to arrest the progress of the inflammation. If we stop taking thedrug,theinflammationcomesrightback.(Anotherrecurringtheme:Recallwhathappens when you stop taking acid-suppressing drugs—the heartburn comesback,sometimeswithavengeance.)

Anti-inflammatorydrugsofallclasseshavealwaysbeendangerousagentswith long lists of potential adverse effects, including death. The major anti-inflammatoriesusedtotreatRA(andotherinflammatorydiseases)include:

• Steroids. These are among the most powerful anti-inflammatoriesavailable. Most steroids are patented or formerly patented synthetic

chemicalcousinsofthenaturaladrenalsteroidhormone,hydrocortisone(e.g., Prednisone). They are very dangerous immune suppressors, evenwhenused“asdirected.”

• Nonsteroidal anti-inflammatory drugs, or NSAIDs (e.g., aspirin,Motrin,Advil,andotherformsofthedrugibuprofen).Lesspowerfulthatthe steroids, many of these drugs are available without prescriptiondespitethefactthattheycanbeextremelydangerous,particularlyifusedfora long time,as theyarebypeoplewitharthritis.AlthoughNSAIDsare generally considered to be safer than steroids, their use is stillassociated with seventy-six thousand hospitalizations and seventy-sixhundreddeathsperyearintheUnitedStatesalone,mostlyduetodamagetotheGItract(e.g.,ulcers).55

• COX-2 inhibitors (e.g., Celebrex, Vioxx). These second-generationNSAIDsarethoughttobekindertotheGItractthantraditionalNSAIDs,but the jury is still out due to the lack of large-scale, longtermexperience.COX-2inhibitorsareknowntoinhibittheformationofnewbloodvessels,suggestingthat theymight interferewithulcerhealinginthestomach.56

GastricHypoacidity:ARootofRA?

Byzeroinginonsymptomsuppression,conventionalmedicinehaslongignoredanintriguingcentury-oldareaofresearchpointinginatotallydifferentdirection.According to these studies, the roots of RA (and other autoimmune diseases)maysometimeslieinadeficiencyofstomachacid.Asfarbackas1912,agroupofBritishphysiciansreportedontenpatientswithchronicRA,allofwhomhadbelow-normal gastric acid levels. In some cases, acid was completely absent.TheyfoundthatiftheycouldrestorethestomachtoamorenormalconditionbyessentiallyputtingbackwhatwasmissingHCl,pepsin,andother factors—theirpatientsachievedadegreeofimprovementintheirarthriticsymptoms.57

Resultssimilartothesehavepersistedacrossthedecades,withmoststudiesemanating from laboratories and clinics outside the United States, especiallyfrom Europe, Asia, and South America.58–63 A 1939 investigation fromGermany, for example, found that those RA patients with the worst diseasetended to have little or no acid in their stomachs. For some unknown reason,

though,stomachacidsecretioneventuallyreturnedtonormalinseveraloftheseindividuals,andasitdid,theirswollenjointsbegantoheal.64AnItalianreviewin 1945 cited ten other studies, each demonstrating a high rate ofhypochlorhydria and achlorhydria in peoplewith RA. In one of these, peoplewith RA were five times more likely to have achlorhydria than normalcontrols.65 Experience at Tahoma Clinic confirms the high likelihood ofhypochlorhydriaandachlorhydriainindividualswithRA.

Duringthe1920s,1930s,and1940s,whenhigh-doseaspirinwasvirtuallythe only pharmaceutical anti-inflammatory drug available, the connectionbetweengastricacidityandRAwasoneofthefewrealleadsmedicinehadintothecause,safetreatment,andpossiblecureofRA.Beginninginthelate1940s,though,patentmedicinecompaniesstartedbringingout—andheavilypromoting—their powerful anti-inflammatory drugs. The quick fix of symptom(inflammation)suppressionquicklybecameestablishedasthetreatmentforRA.

The promising research suggesting the value of investigating and dealingwith problems of gastric acidity was unsupported by any patent medicinecompanymoney,becausenopatentableproductsappeared tobe involved, justinexpensive,unpatentablenaturalproducts,likeHClandpepsin.*

A lackofpatentmedicinecompanysupportusually represents thekissofdeathformedicalresearchinthiscountry.Thelarge,well-controlledstudiestheFDAandmedicalestablishmentdemandtovalidateanytherapeuticentityaresocostly to conduct that only the patent medicine companies themselves (andsometimesthefederalgovernment)havedeepenoughpocketstopayforthem.Moreover, small, independent studies of “alternative” treatments, which areusuallytheonlykindspossible,rarelygetpublishedinmajormedicaljournalsorpresentedatmedicalconventions,whichare sponsoredprimarilyby thepatentmedicine industry.With thecredentials theseoutletsprovide lacking, it iseasyformedical authorities—in a perfect example of “catch-22” logic—to dismissnonpatentmedicineresearchas“unproven”atbestor“quackery”atworst.

Thus, it is not surprising that once the anti-inflammatory train left thestation, the“gastricacidityconnection” toRAwas soon forgottenbyallbut afewphysiciansandresearcherswhounderstoodthedeadendthatcortosteroids,NSAIDsandtheotheranti-inflammatoriesrepresented.Yettheflamecontinuesto burn. As recently as 1986, a group of researchers—from the prestigiousKarolinska Institute in Sweden—confirmed the findings of their earliercolleagues.66 Examining the stomach contents of forty-five RA patients, theyfoundthatsixteen(36percent)hadvirtuallynoacid,suggestingtheyhadsevereatrophicgastritis.ThosepeoplewhohadsufferedfromRAthe longesthad the

least acid.Also confirming numerous older studies, the Swedes found that 20percent of the RA patients they saw had elevated gastrin levels(hypergastrinemia), usually a sign of low stomach acid. Figure 6–4 shows thehigh rateof atrophicgastritis (65percent) found inRApatientsbyagroupofItalianresearchers.67Figure6–5showstheresultsofaBritishstudyinwhichthemeanvolumeofstomachacidsecretionwas found tobesignificantly lower inpeoplewithRA(andarelatedformofthedisease).68

Figure6-4.Peoplewithrheumatoidarthritishaveanextremelyhighrateofatrophicgastritisassociatedwithlowstomachacidcomparedwithnormalindividuals.AdaptedfromRMarcolongoetal.,1978.

Figure6-5.DrasticallyreducedsecretionofHCIbythestomachsofpeoplewithrheumatoidarthritis.AdaptedfromOlhagenetal,1974.

OpeningtheDoortoAutoimmuneDiseases

AlthoughNSAIDs(andotheranti-inflammatorydrugs)aresupposedtoimprovelife for RA patients, they are particularly dangerous in the long run, first,becausetheyaresolikelytocauseGIdistress,andsecond,becausetheyareso

widelypromotedandsoeasytoget.Likefoodallergens,NSAIDscaninjuretheintestinal lining, causing it to leak.69–71 And a leaky gut, whether caused byachlorhydria,bacterial infection, foodallergy,excessivealcohol,drugreaction,or other causes, may open the door to all kinds of allergic and autoimmunediseases.

Gallstones,GastricSecretion,andFoodAllergies

Thegallbladderstoresbile,whichisproducedintheliver,andreleasesittoaidinthedigestionandabsorptionoffatsandothernutrients.Manypeopledevelop“stones” in the gallbladder, which can block the flow of bile, causing thegallbladder to become inflamed or infected, oftennecessitating surgery. Inaddition to recurring abdominal pain, gallstones are also associated withbloating,belching,heartburn,andgas.

Numerous studies dating back to the early 1900s have linked gallbladderdiseasewith low stomach acid secretion.72 For example, in one study of fiftypatients with gallstones, twenty-six had below-normal stomach acid output.73Does low stomach acid cause gallbladder disease?Or are both the result of acommoncause?

There is verygood reason tobelieve that inmost casesofgallstones, thesymptomsaretheresultoffoodallergy.Whensixty-ninepeoplewithgallstoneswereplacedonaneliminationdiet*foraweek,everyoneofthemexperiencedsymptomrelief.Asthefoodswereaddedbackonebyone,thesymptomsoftenreturned. It has been hypothesized that food allergy causes the bile ducts toswell, restricting the flow of bile from the gallbladder and promoting theformationofstones.74

CanAvoidingFoodAllergensLeadtoImprovementinPeoplewithAutoimmuneandOtherRelated

Diseases?

Absolutelyso!AtTahomaClinicandthroughoutthe“naturalmedicine”world,amainstay of any autoimmune disease treatment program is the identification,elimination, and desensitization of food (and other) allergies and sensitivities.Although this step alone rarely cures autoimmune diseases outright, the

improvements achieved are frequently major. No matter what the specificautoimmune problem (please review the list at the beginning of this chapter),workingwithfoodallergyisalwaysamajortool.

Similarly,anothermainstayoftreatmentforanyautoimmunediseaseistheexamination for and (when found) treatment of low stomach acid and otherdigestive malfunction. Low stomach acid is so common in any autoimmuneconditionthatwe’resurprisedwhenwedon’tfindit.Correctingthelowstomachacidorotherdigestivemalfunctioncanalsoresultinmajorimprovementintheautoimmune disease. Although “natural medicine” doctors see improvementachieved repeatedly by following this lead, practitioners of conventionalmedicine rarely if ever look for low stomach acid andpoor digestion in thosewithautoimmunedisease.

Unfortunately, only a handful of small studies have systematicallyexamined the food allergy and autoimmunedisease connection, but the resultsindicate that some people can benefit. For example, in one study, twenty-twopeople with RA followed an allergy-elimination diet. Arthritis improved fortwenty(91percent)ofthesepeople,andnineteenwereabletoidentifyspecificfoodsthatmadethemworse.75SeveralothersmallstudiesalsoreportfavorableresponsesassociatedwithchangesindietinsomepeoplewithRA.76–79InRA,AlanGaby,M.D.,reports thatavoidingallergenicfoodsworksbest inyoungerwomen(aged twenty-five to fortyyears)whohave lessseverecases.Henotesthathehasseenaboutfifteenpatientswhofitthatdescription,andeveryoneofthemimproveddramaticallywithonlydietarychanges.80

With lupus, the support is similarly sketchy, but still suggestive. In onereport, physicians examining a child diagnosedwith lupus found him to haveantibodies to milk in his blood. This suggested that his immune system wasreactingagainstmilkprotein.Whenmilkwasremovedfromthechild’sdiet,hislupus symptoms resolved. On two subsequent occasionswhen he drankmilk,they returned.81 An Australian study of four people with lupus also foundmarkedimprovementinsymptomswhentheyavoidedallergenicfoodsandtookcertain nutritional supplements. Standard tests used to diagnose and monitorlupusshowedtheseindividualstobenormal.82

Muchmoreworkneedstobedonetoidentifywhichpeoplearemostlikelytobenefitandtodevelopevermoreeffectivetreatmentstrategies.Clearly,suchresearch will not come from the pharmaceutical industry, which has longdemonstrated its interest only in patentable therapies that do little more thansuppresssymptoms.

Wouldn’t it make much more sense, therapeutically speaking, to try to

repairaleakygutor,betteryet,keepitfromspringingaleakinthefirstplace?ToremovethedrugsandallergenicfoodsthatmaybeirritatingtheGItract,andpossibly triggering dangerous autoimmune reactions? To restore missingstomachacidthatwouldquicklydestroycolonizingbacteriaandalso(alongwithpepsin) break down proteins before they can leak out into the generalcirculation?

RestoringtheGItracttoanormal,healthystatesothatbacteriadon’tgrowin the stomach and foreignproteins don’t leakout across the intestinal barrierrequiresnoexpensive,dangerousdrugs.Itcanoftenbeaccomplishedsafelyandeffectivelywithavarietyofnatural—unpatentable—substances.

Because there are no profits to be made from selling these naturaltreatments, the pharmaceutical industry, which controls the vast majority ofmedical research in the United States, will never investigate them ormanufacture them. In fact, theywilldoeverythingpossible todisparage them,because, should the word get out that they exist, natural treatments couldthreatentheirstrangleholdonthepracticeofmedicine.

Onemightask, if thepossibilitiesof thesenatural treatmentsaresogood,why isn’t the FDA sponsoring or promoting research? Again, the answer issimple. The FDA and the patentmedicine industry are two sides of the samecoin.TheFDA’srolehasneverbeentoadvancethescienceofmedicine.Ithasno interest in finding a cure for lupus or any other disease. Instead, its roleassignedbyCongressis tomakesurethedrugsandfoodsthatgetmarketedintheUnitedStatesaresafeandeffective.

Tothisend,theFDAhassetupadrugapprovalprocessthatissoexpensiveand so onerous that it virtually guarantees that only the patent medicinecompanies can afford to develop new treatments and get them “approved.”Thanks to thissystem,natural treatments,nomatterhoweffectiveorhowsafetheymay be, are forever destined to carry the label “unproven,” as far as theFDA and the medical establishment are concerned. At best an “unproven”treatmentmaybeviewedasharmlessandawasteofmoney.Atworst,itmaybedeemed “dangerous” and the stuff of “quacks.” The fact is,without sufficientresearch, they’ll never knowwhat it is really, and that seems to be fine withthem.

Tothoseofuswhousethesetreatmentseverydayandwhoknowhowsafeandeffectivetheycanbe,usingthemis,astheysay,a“no-brainer.”Everyday,our patients with “incurable” chronic diseases achieve remarkable relief, andoftencures,usingnothingmore thanacarefullyselectedandcarefullyappliedarsenalofnaturaltherapies.Inthenextchapter,wewilldiscussthepossibilitiesofnaturaltreatmentsforGIandGl-relateddisorders.

*ReprintedfromDr.JonathanVWright’sNutrition&Healingnewsletter,AgoraSouthLLC,Baltimore,Maryland21201,(410)223–2611.

*ThismolecularandgeneticcommonalitygoeswellbeyondaffectingjusttheupperGItract.Forexample,appropriateuseoftheandrogensDHEAandtestosteroneisveryoftenbeneficialinalloftheHLA-linkeddiseases.

*MostphysiciansarerequiredtoearnacertainnumberofCMEcreditseachyeartomaintaintheirlicenseorcertification.Typically,CMEcreditsarcearnedbytaking“courses”thatareofferedbymail,online,orlive at meetings held at conventions and other locations. It is very common for such courses to beunderwritten by pharmaceutical (patent medicine) companies. Although the courses are supposed to beneutralwithregardtothepromotionofanyspecificproduct,andthecompanvissupposedtohavenovoiceintheircontent,thisisaveryfuzzvlinethatisoftencrossed.Forexample,thefacultyisalmostalwaysonthecompanypayroll,andthetopicareaandapproachtothesubjectareinvariablydrivenbythecorporatesponsor’s desire to promote its drugs. Inmany cases, the company influence is evenmore blatant.As aresult,such“educational”programsoftenturnouttobelittlemorethanbarelydisguiseddrugpromotionsthatphysiciansarerequiredtositthroug.

* It is important to distinguish a true milk sensitivity reaction from “lactose intolerance.” In lactoseintolerance,theimmunesystemisnotinvolved.Instead,theindividualcannottoleratemilkbecauseheorshelacksanenzymerequiredtodigestlactose,aprimaryformofsugarfoundinmilk.Whentheundigestedmilksugarreachestheintestines,itcausesnausea,cramps,bloating,gas,anddiarrhea.

*Another promising but neglected area ofRA research originatedwithDr.RogerWyburn-Mason,whoreportedfindingaspecificamoebainthejointsofallindividualswithRAwhomheexamined.Hereportedsuccessful treatmentof thesecaseswithanti-amoebic therapy.Nodirect linkhasbeenobservedbetweenDr. Wyburn-Mason’s amoebae and low stomach acid, but in general it’s well known that a principalfunction of normal stomach acid is killing food and water-borne microorganisms, often the source ofamoebicinfection.Forfurtherinformation,contacttheRheumatoidDiseaseFoundationat(615)799–1002.

*Inanallergy-eliminationdiet,likelyoffendingfoodsareremovedfromthedietforaperiodoftimeandgraduallyaddedbackintoseewhichstimulateareaction.

CHAPTER7

TreatingHeartburnand“AcidIndigestion”theNaturalWay

“I still can’tbelieve it!” JonHitchcockexclaimed.“Takinghydrochloricacidcapsulesmakesmyheartburnand‘acidindigestion’goaway!Wouldyoutellmehowthatworks,again?”

BeforeIcouldanswer,hiswife,Sara,said:“Don’tyouremember,Jon?Thedoctortoldyoulasttime…afteryouhadyourstomachacidmeasured.Nooneknowshowitworks,butforoveronehundredyears,doctorshaveobservedthatbringing low stomach acid towards normal frequently eliminates heartburn,stomachbloating,indigestion?Maybeweshouldtalkaboutsomethingforyourmemory.”

“But it’s just so hard to believe,” Jon answered. “For the last ten years,doctorshavebeen tellingme Ihave toomuch stomachacid,whichcausesme‘acidindigestion’and‘acidreflux.’They’vebeenprescribingantacidsandacidblockersandtellingmeI’dbetterstayonthemevenwhenmysymptomsaren’tparticularly bad, because ‘all that acid’ might permanently damage myesophagus.Areyousuretakingthosehydrochloricacidcapsuleswon’tburnmyesophagus?”

“Doyoufeelanyburning?”Iasked.“Jontoldmehehasn’thadanyheartburnaftermealssincethesecondweek

hestartedtakingthem,”Saraobserved.“That’s true,” Jon said. “But I’d still like to understand. Not just the

doctors,butallthoseTVcommercials,allofthemtellingusabout‘hyperacidity’andevenshowingcartoonsof‘acidattacks’ontheesophagus.Iwouldn’thavebelieveditifIactuallyhadn’thadmyownstomachacidmeasured.”

“I’m glad you did,” I said. “After looking at literally thousands of verypreciselymeasuredstomachacidtests,I’veobservedthatmorethannineoutoftenofuswhosufferfromso-called‘acidindigestion’actuallyhavelack-of-acidindigestion.Replacingsomeorallofthemissingacid…alongwiththestomach

enzyme pepsin… eliminates heartburn, gas, bloating and indigestion inmostcases.”

“ButI’dstillliketounderstandhowitworks,”Jonsaid.“I’manengineer.Itbugsmenotknowing.IfIhadn’tseenthemeasurementonmyownstomach,Iwouldn’tevenhavetriedthatbetainehydrochloride-pepsinstuff.”

“I’m sorry I don’t have an explanation for how it works,” I said. “Withenoughresearchmoney,I’msureitcouldbefiguredout,butthere’snomoneyinresearching natural, unpatentable remedies. So for now, we just go withobservedresults.”

Jon smiled. “I have to admit that engineering isn’t a 100 percent exactscience at all times, either.We engineers like tomaintain the public illusion,though. Butwe are a lotmore exact thanmedicine appears to be.Nearly tenyears of diagnosing ‘overacidity,’ and no one actually measured my stomachacid.”

“I’m glad Sara persuaded you.” I paused for a moment. “You’re anengineer.Howaboutanengineeringtheory?Unproven,ofcourse.”

“Whynot?Atheory’sbetterthannoansweratall.”“Howaboutafeedbacklooptheory?”“That’sbasicengineering.Tellmeaboutit.”“Hopeyouhaveafewminutes.”“Longasyoudon’tchargeextra.”Jonsmiled.“I won’t, I promise. OK … What you’ve seen on TV and heard from

doctors ispartly true.Heartburnpainiscausedbyacid,butnot toomuchacid.Even though there’sactually too littleacid, evena small amount in thewrongplace, the esophagus, can really hurt. Remember, acid doesn’t burn a normalstomach.Ourstomachsarebuilttowithstandacid,toproduceacid,acidasmuchasone-hundred-thousandtimesstrongerthannormaltissueacidity.Acidofthatstrengthisabsolutelynecessaryforoptimaldigestion.

“Bycontrast,ouresophaguses…esophagi?…whatever…aren’tbuilt tohandleanyacidatall,notevenweakacid.Soundernormalcircumstances,theesophagusisprotectedagainstacidrefluxbyacircularmusclecalledtheloweresophagealsphincter.Whenfunctioningnormally, thesphincteropenstoallowfood and liquids to drop through, and closes to prevent stomach acid fromrefluxingbackupintotheesophagus.

“Anumberof thingscause the loweresophageal sphincter tomalfunctionand lose itsability toclosewhen it should.Nicotineandcaffeinearecommonoffenders. Alcohol does it for some. Unrecognized food allergies andsensitivities are a much more common cause of lower esophageal sphinctermalfunctionthanisusuallyrecognized.Butinmyexperience,lowstomachacid

isthemostcommoncause.“NowI’llgettothat‘feedbackloop’theory.Let’ssee…Iknow,you’rean

engineer,butIdon’tthinkSarais,so…Iknow.”IturnedtoSara.“Evertakenthetopoffthebackofthetoilet?”

Saralookedsurprised.“Yes.”“I’msureyounoticedwaterrushinginwhenthetank’sempty.Asthewater

levelrises,itliftsafloat,whichactivatesavalve,whichslowlyturnsdownthewater inflow until it shuts off.” I turned back to Jon. “I realize that’s animperfectanalogyfromamechanicalsystem,but it’sclose. It’squitepossible,although not proven, that as the acid level rises… technically, the pH leveldrops… that a normally functioning lower esophageal sphincter (or a tissueclosetoit)‘senses’theincreasingacidity,andshutsitself.Brieflyput,an‘acid-sensitive feedback loop’ leading to sphincter muscle closure. But it’s just atheory,noproof,andrealitymaybesomethingelse.”

Jonthoughtforamoment.“Soundsreasonable.Butnoone’scheckedthisout?”

“Not that I…we… can find.What Imean by that is, I’ve looked, andsomeveryableyoungdoctorshavespenthoursinmedicallibrarieslooking,butwecan’tfindanyresearchonthepoint.”

“Well, I’ll just take thepracticalengineeringpointofviewandagree thatmyexperience…likeyours…showsthattakinghydrochloricacidincapsulesshutsoff acid reflux intomyesophagus,” Jon said. “Thenextquestion is: I’mforty-nine.WillIneedtotakehydrochloricacid-pepsincapsuleswithmealsforthenextforty-nineyears,shouldIlivesolong?”

“You’remore likely to have those next forty-nine years if you do,” Sarasaid.“That’swhyInaggedyoutocomeinheretogettestedinthefirstplace!Don’tyouremember…wereallydoneedsomethingforhismemory,Doctor,”shesmiled.“Don’tyouremember I toldyou that ifyoukept taking thoseacidblockers, you wouldn’t be digesting your protein properly, you wouldn’t begettingall theaminoacidsfromit thatyoushould?Youwouldn’tbedigestingand absorbing minerals as well as possible. I’ve noticed you have a little bitmore energy, a bit more ‘get up and go’ in just the short time since you’vestartednormalizingyourdigestion.You just can’t live as longor ashealthy ifyou’renotgettingyournutrition!”

“Sara’sright,”Iagreed.“Andallthatenthusiasmshowsshecares,too.Buttoansweryourquestion…althoughit’shardertodoaswegetolder,afewofusdo get our stomachs back to fully normal, acid-producing function. It doesn’t‘justhappen’though.Itusuallytakesworkingonit,onpurpose.”

“How?”

“There are two basic aspects: Removing ‘bad stuff’ that interferes withnormal function, and using ‘good stuff’ and other techniques to encouragenormal function. Included on the ‘bad stuff’ side is checking for the stomachbacteriaHelicobacter pylori—we checked you for that, it was negative—andgettingridofitwhenit’sfound.Other‘badstuff’fornormalstomachfunctionincludesfoodallergiesformanyofus,especiallytomilkanddairyproducts.It’sbeenproventhatinsomecases,foodallergyorsensitivitycanseriouslyinterferewith normal function. For infants, it’s absolutely nailed down that cow’smilkcauses gastroesophageal reflux, and removing cow’s milk eliminates theproblem.”

“Howaboutrefluxinadults?”“I’ve found foodallergy, especiallycow’smilkanddairyallergy, tobea

frequentcauseof,orcontributorto,gastroesophagealrefluxinmanyadults,butunfortunately no one’s published ‘controlled’ research.Now,wherewerewe?Ohyes…it’salsobesttoeliminaterefinedsugar,becauseit’sadirectstomachirritant.Iknowyoudon’tsmoke,butifyoudid,I’drecommendyoustop.”

“Whataboutalcohol?”“Beerandwinedon’tappeartobeaproblem,especiallywine.Theremay

even be something to the adage that a little wine with meals improves thedigestion,thoughit’snotproven.Butdistilled,higher-proofalcoholisdefinitelya no-no.High-proof alcohol is actually a goodway to ‘pickle’ or abnormallypreservetissue.

“But that’s not all. Fluoride and chlorine in thewater can inhibit one ormoreoftheenzymesthatourstomachsusetomakeacid,soeventhoughthereareonlyverysmallquantitiesofeitheroneinmostmunicipalwater,it’sbesttodrinkwaterwithnochlorineorfluoridecontent.

“Now, the ‘good stuff’ side. For literally centuries, in many Europeancountries, older folks have drunk ‘bitters’ before meals to improve digestivefunction. Bitter drinks taken before meals are called ‘aperitifs.’ In the early1900s,oneresearcherclaimedthatbittersdidn’thelpdigestion,butothersfoundthatbittersactuallyincreasestomachsecretionofhydrochloricacidandpepsinifdigestive secretion is below optimum to beginwith, if the bitters are actuallytasted—they don’twork if they’re swallowedwithout being tasted—and theremustbefoodinthestomachforthemtowork.”

“That allmakes engineering sense.Nopoint having themwork if there’snothinginthestomachtoworkon,orifthestomachisworkingOKanyway.”

“Moremodernresearchhassupportedtheearlierwork.Liquidpreparationsof both gentian and artemisia—two of the most commonly used bitterspreparations—takenfiveminutesbeforemeals, stimulatesecretionofdigestive

juices.Bothliquidherbalsalsoimprovebileflowfromtheliver,andthathelpsdigestion,too,althoughatalaterstage.”

“SoifIdecidetousethem,whatdoIdo?”“Find a liquid preparation of gentian or artemisia … it’s also called

wormwood.Ausualdoseisfivetotendropsofaone-to-fivedilutioninabouttwenty milliliters—that’s about one and one-half tablespoonsful—of water,taken about fifteen minutes before meals. Most herbalists recommend thatbitters-in-waterbesippedslowly.”

“I’mgladyou’rewritingthatdown.”“Sorry,Iknowit’sabittechnical.Yournaturalfoodstoreorcompounding

pharmacycanhelpyouwiththis,too.”“AnythingelseIcandototrytogetmystomachfunctionbacktonormal

onitsown?”“Nothing else is specifically known at the present time. As Imentioned,

there’sno financial incentive for researchon thepoint. Justdoeverythingyoucantoimproveyourhealthingeneral:gooddiet,supplements,exercise…”

“Youforgottwothings,doctor,”Sarasaid.“Tellus.”“Well,youdidn’treallyforgetoneofthem,butIknowJon,itreallyneeds

tobereemphasized.He’snotbeenaverygoodsupplementtaker,buthe’sgottoremember to take his betaine hydrochloride-pepsin capsules with every meal!Notonlywilltheyhelphimdigestandabsorballhisnutrientsbetter,butthey’realso essential to his chances of digesting and absorbing all the nutrients hisstomachneedstorepairitself!”ShelookedatJon.

Jonthrewuphishands.“OK,OK,Igotit,Sara.I’llbegood.”“I’mnotjustpickingonyou,Jon.I’vereadinanynumberofplacesthatifwelivelongenough,we’reverylikelytohaveourdigestiongetweak.SoIexpecttoneedtotakedigestiveaidssomeday,too.”“Andwhat’sthesecondthing?”JonaskedSara.

“Prayer, visualization, meditation—techniques to focus your intention toimproveyourhealth,inthiscaseyourstomach.”

“Whataboutthose,Doctor?”Jonasked.“Youpickedaverywisewomantomarry,”Ireplied.

…

Acidneutralizationand/orsuppressionseemliketheyoughttobegoodwaystotreat heartburn/GERD/ “acid indigestion”… as long aswe pretend that theseconditions are caused by toomuch stomach acid and that, although the bodygoes togreat lengths to concentrateHClonly in the stomach, it doesn’t really

needit.ThevastmajorityofAmericans—physiciansandnonphysiciansalike—urgedonbyapharmaceutical industryrakinginmorethan$7billionayearinanti-acid product sales, understandably chooses to believe these myths. Theyminimizetherisksassociatedwithbacterialovergrowth,andtheydenythevalueofHClforproteindigestion.Asoneprominentintroductorymedicaltextbook,ADigestofDigestion, statesquiteclearly:“Acidandpepsinarenotessential forproteindigestion.”Theauthorpositsthatpancreaticenzymesaresufficienttodothejob.

Heiswrong,ofcourse.Hecompletelyignorestheeffectofacidonmineraldigestionandabsorption.Heoffersnoprooffromcontrolledstudiesthatproteindigestionandsubsequentaminoacidandpeptideabsorptionisthesamewithorwithoutstomachacid.Heneglects tomentionthatpancreaticenzymesecretionmaybe impaired in states of hypochlorhydria and achlorhydria (remember the“digestivecascade”?).Butbecausethisviewistaughtinmostmedicalschools,young doctors soon learn to ignore the value of HCl and pepsin for properdigestion. They forget about the bacterial barrier stomach acid provides. Theonlytimeacidseemstocomeupontheirradariswhenit’s“causing”anulcer,heartburn,GERD,oresophagealcancer.Asaresult,acidhascometobevilifiedassomethingtobefearedandsuppressedtheminuteitappearstostartcausingtrouble,andsometimesbefore.

Ifstomachacid iscausingpainordiscomfort, then it followsthat the lesswe’vegotofit,thebetter.IfTurnsorRolaidsisn’tdoingthejob,thenwhynotroll out one of the big guns, like Pepcid or Zantac, or better yet, Prilosec orPrevacid,anddriveastake through theacidmonster’sheart? Infact, the trendtoday, as evidenced by the widespread promotion and skyrocketing sales ofpowerfulacid-blockingdrugs,istogoaftereventhemildestcasesofheartburnwith these gastrointestinal “nuclear weapons.” Hard as it is to believe, themanufacturers of Prilosec recently asked the FDA to allow them to sell theirdrug over the counter.* Fortunately, in a rare moment of sanity, an FDAadvisorypanelturnedthemdown,atleastfornow.

Aswehavebeensuggestingthroughoutthisbook,thereisabetterwaytodealwith “acid indigestion,” a naturalway, away thatworkswith the body’sphysiology,notagainstit.Webelieve,andmuchofthescientificevidence—nottomentioncommonsense—supportsus,thatstomachacidisthereforareason(several reasons, really)and thatwhen the flamesof so-calledacid indigestionstarttoerupt,it’smorelikelyareflectionoftoolittleacid,nottoomuch.

Thus, the only treatment strategy thatmakes any sense is to give theGItractbackwhatit’smissing,notdepleteitfurther.IfHClislow,replaceitwithHCl; likewise for pepsin and other digestive enzymes. Not only does this

strategyworktoeliminateheartburnandGERD,itoftengoesalongwaytowardrestoringanynutrientdeficienciesandrepairingthegastricbacterialbarrier,nottomentiontheintestinalbarrier.

SincetheGIsystemneverhasadrugdeficiency,nodrugsarenecessarytorestoreittoitsnormalstate.Everythingwerecommendinthefollowingpagesiseither a natural constituent of the GI system, like HCl and pepsin, or else anaturallyoccurringsubstance,likelicoriceormastic,thathelpshealbyrestoringthenormal statebuthas littleornopropensity forcausingharmwhenusedasdirected.

In cases ofmild tomoderate heartburn, “acid indigestion,” bloating, andgas,actualtestingforstomachacidproductionatTahomaClinic(seepage133)showsthathypochlorhydria(toolittleacidproduction)occursinover90percentof thousands tested since 1976. In these cases, a “natural strategy” is almostalwayssuccessful.

Even in severe cases diagnosed as GERD, actual testing also showshypochlorhydriainover90percentofcases.Unfortunately,whentheproblemissevere,particularlywhenthere’stissuedamageintheesophagus,itmaybetoolateforanentirelynaturalstrategy.Underthesecircumstances,werecommendthe relatively new surgical procedures such as “gastroplication,”which repairsthe LES valve. These procedures do not have the potential to create nutrientdeficienciesanddiseasethewayacidblockersdo.However,evensomeseverecasesofGERDcanbegraduallybroughtbackundercontrolwithnaturalmeans.

Inmoreseverecases, it’svery important toworkwithaphysicianwhoisskilled and knowledgeable in nutritionalmedicine.Also, since there are (veryrare)possibleadverseeffectsfromtheuseofhydrochloricacid-pepsincapsules,it’sbesttoworkwithsuchaphysicianwheneverusingthismaterial.

Understandably, conventional medicine looks askance at such a naturalapproach, scoffing at the strange “drugs” it endorses and the apparent lack ofresearch support. From this point of view, its basic premise, treating so-called“acid indigestion” with acid (and other natural techniques), seems patentlyabsurd.

Andwhilewe’reon the subject of patents, let’s not lose sight of the factthat all these natural treatments are unpatentable. As we’ve pointed outnumeroustimesinthisbook,patentmedicinecompanies,whichcontrolmostofthemedicalresearchinthiscountry,areinterestedonlyinpatented“proprietary”products, which only they can sell. By definition, that excludes all naturalproducts, which cannot be patented. Not only do they have no interest indeveloping them, they have every reason to disparage them, because theyrepresentsafe,effective,inexpensivecompetition.

Many journal articles and textbooks purporting to systematically examineHClreplacementhavereacheddecidedlynegativeconclusionsregardingnaturaltreatments. In one typical “legitimate” study, published in the New EnglandJournal ofMedicine, the author concluded that, in caseswhere people had nomeasurable stomach acid, “… treatment with a bland diet, sedation, andadequate attention to colonic evacuation appears to be more efficacious thansubstitution[HCl]therapy.”1

Yet, a close reading of this study reveals serious flaws.For example, theauthor noted that, in people treated with HCl, heartburn symptoms actuallydiminishedearlyinthetreatment,onlytoreturnlater,eventhoughthetreatmentwasunchanged.Insteadofseeingtheglasshalffullhere,theauthorchosetoseeithalfempty,usingthisfindingtoarguethatreplacingacidmakesnodifference.However,hereplacedonlyasmallquantityofHCl,despitethefactthathistestsubjectshadseriousachlorhydriaandcouldalsobeassumed tobedeficient inpepsin activity and vitamin B12 absorption. Those of us who treat “acidindigestion” successfully every day using natural remedies know that acidreplacement usually works best when adequate acid replacement is used andpepsinandvitaminB12arealsorestored.Nordidtheresearcheraddcalciumorirontohis testsubjects’diets,despite thefact that thesemineralsarenotwell-absorbed by peoplewith low stomach acid.And despite the fact that in somecasessymptomswereadmittedly“provokedbyspecificfoodgroups,”hedidnotrecommendeliminationofthosefoodsforthedurationoftheHCltreatment.

Isitanysurprisetheconclusionsweresonegative?Aswehavedescribedthroughoutthisbook,theuseofHClfortreatingvariousdisordersrelatedtoGIdysfunctionhasalonghistorythatpredatesthemodernpharmaceuticalindustry.Whilemanyoftheearlystudiesmaynotstanduptosomeoftherigorousdesigncriteria demanded by today’s prospective, double-blind, placebo-controlledstandards,somedoholdupquitewell.Moreover,weshouldrememberthattheearlyresearcherswerenotdrivenprimarilybythedesiretosellproducts.Largeinvestigationalgrants—suchasthoseofferedbythepatentmedicineindustry—wereunknown in thosedays.Medical research tended tobe less formal,morepersonal, andoften lessbiased.For themostpart, the early investigatorswerededicated, careful observers who conducted small-scale studies on patients intheir ownclinicsorhospitals.Withnobuilt-in commercial bias, their findingshave shown consistent benefits of HCl/pepsin/vitamin B12 replacement withhardly any serious adverse effects. There are simply too many examples todismissallthefindingsbecausetheyare“anecdotal”orfrom“poorlycontrolled”studies.

While large,well-controlled trials are certainlydesirable, theyarenot theonly pathway to scientific truth, especially if they are serving a commercialpurpose as well as a scientific one. Biased results and conflicts of interest inpharmaceutically sponsored research—despite the fact that studies are usuallytechnically “well controlled”—are becoming a major bone of contention inAmerican medicine. Recent editorials in both the Journal of the AmericanMedical Association2–3 and theNewEngland Journal ofMedicine,4–5 the twomost prestigious and influential general medical publications in the UnitedStates, have decried the increasing influence of marketing pressures on thedirectionofmedicalresearchand,byimplication,medicalpractice.

One of the earliest but still applicable definitions of “science” is closeobservationofNature.Consider thisbitof “commonsense”observation:WhywouldNature expend somuchmetabolic energy to provide each one of usatbirth (and until at least age forty)with an ample supply of stomach acid andpepsinifitweren’treallynecessaryfordigestion?It’seasytoseetheharmthathypochlorhydriaandachlorhydriacancause, ifweknowenoughtolookfor it.It’s also easy to see remarkable recoveries from illnesses usually deemedchronic,incurable,orboth,usingthenaturaltreatmentsandtechniquesdescribedin this chapter. It is unfortunate thatmost physicians today are looking in thewrongdirectionwhenitcomestogastrointestinalhealth.

What’sActuallyGoingOnintheStomach?

WhenpatientscometotheTahomaClinicwithGIdistress(oroneofthemanydiseasesthatmayberelatedtoGIdysfunction,or,verylikely,both),oneofthefirst things we do is try to find out howwell their stomachs are working bymeasuring their gastric pH. While this measure, known as gastric analysis,wouldseemtobeanobviousfirststep,itisrarelyusedinconventionalmedicalpractice,evenincasesofGERD,whenhyperacidityisoftenpresumed.

Gastricanalysishasa longhistory inmedicine,goingbackat least to theearly nineteenth century. In most cases, the gastric contents were sampledthroughaslendertubethatwaspassedintothestomach.Oncepumpedoutofthestomach,thegastricjuicecouldthenbeanalyzedanditspHmeasured.Althoughthis technique can provide useful information regarding the pH and thecompositionofthegastricjuice,ithasobviouslimitationsineverydaypractice.

In fact, measuring the stomach’s acid-secreting capacity can be quitesimple.WeuseadevicecalledaHeidelbergcapsule,whichconsistsofatinypH

sensorandaradiotransmittercompressedintosomethingthatresemblesalargevitamincapsule.6–7

Although it sounds like amodern computerized instrument, variations ofthe Heidelberg capsule have actually been around since the 1960s. Whenswallowed, the sensors in thecapsulemeasure thepHof the stomachcontentsandrelaythefindingsbyradiosignaltoareceiverlocatedoutsidethebody.Acomputer and printer connected to the receiver records a continuous record ofgastric pH for as long as the capsule remains in the stomach (which can beseveralhourswithoutmuchdiscomfort).Sincethecapsuleistetheredtoalongthread, it can be easily removed from the stomach once the test is completed.(Heidelberg capsuleswithout tethers are sometimesused to evaluate the entireGItract.)

In a typical gastric analysis, after swallowing the capsule, the individualbeing tested ingests a solution of baking soda, which turns the gastric juicealkaline.AsthestomachliningcontinuestosecreteHCl,thepHgraduallyfallsbackintotheacidicrange.TherateatwhichthepHchangesfromalkalinebackto acidic through a series of bicarbonate challenges provides a very accuratemeasurementofthestomach’sabilitytoproduceHCl.

Stomach acidity can alsobe estimated indirectlyby analyzing samples ofhairformineralcontent. If thehair isdeficient ina largemajorityofminerals,particularly those known to be poorly absorbed in low acid states (e.g., iron,calcium, zinc), gastric hypochlorhydria or achlorhydria is a strong possibility.Thismethod isnotnearlyasaccurateorasdefinitiveasaHeidelbergcapsule,butitmayprovideusefulinformation,especiallyforyoungchildrenwhocannotswallowacapsule.

Theuseofacid-suppressingoracid-neutralizingmedicationspresumes anexcessofHClinthestomach,butmostphysiciansneverknowwhatthestateofacid secretion is in the stomach,because theynever look. In somecases, theymightmeasureesophagealpH,butaswehavenotedearlier,thistellsusnothingaboutwhat’sgoingoninthestomach.Itcanonlyconfirmthatacidhasindeedrefluxedintotheesophagus.

Physicianswho actuallymeasure gastric acidity in their heartburn/GERDpatientsoftenfindthatthepHishigherthanitshouldbe(higherpH=lessacid=relativelyalkaline).Ifmostphysiciansdidthis,perhapstheywouldthinktwiceaboutprescribingdrugsthatsuppressacidsecretionfurther.

ReducingRefluxviaDietaryandLifestyleChanges

Gastroesophagealrefluxhappensforalotofreasons.Acidsecretioncanbelow,high,ornormal.Thecommonthread that runs throughvirtuallyallcases isanLESvalvethatallowsthestomachcontentstobackupintotheesophagus.ThereasontheLESisn’tdoingitsjobcanoftenbetracedtothethingsweeat,drink,or smoke; to the drugs we take; and sometimes to our level of stress. ThefollowingfactorscanallweakentheLES,directlyirritatetheesophageallining,orsimplyforceacidicgastricjuicebackupthroughtheLESintotheesophagus:

• Some foods, including fats, chocolate, coffee, mints (especiallypeppermintandspearmint),sugar,onions,andsomealcoholicbeverages,can weaken the LES, making it more likely to open inappropriately(TLESRs).

•Otherfoods,includingacidiccitrusfruitsandtomato-basedfoods,spicyfoods, carbonated beverages, and coffee, can further irritate an alreadyinflamedesophageallining.

•Remembertheseriesofresearchstudiescitedinthelastchapterprovingthatcow’smilkcausesgastroesophageal reflux in infants?Manyadultsobserve that reflux is lessened or even disappearswhen food allergens(especiallycow’smilkanddairy,butmanyothers,too)areeliminated.

• Because a large volume of food in the stomach can increase thefrequency of TLESRs, overeating can cause reflux. Sufficient volumeand/orpressureofgaswill also force the stomachcontents through theLES.

•CertainmedicationscanweakentheLES.Theseincludebron-chodilatorsused to treat asthma (e.g., theophylline, albuterol, ephedrine),NSAIDs,certain types of blood-pressure-lowering drugs (e.g., calcium channelblockers, beta-blockers), the antianxiety drug Valium, the narcoticanalgesicDemerol, and nitroglycerine (and related drugs) used to treatcoronaryarterydisease(angina).Thesedrugsallfunction,inonewayoranother,torelaxmuscles,includingthosethatsurroundtheairwaysandbloodvessels,butalsothosethatcomprisemuchoftheGItract.

•Somemedicationscandirectlyirritatethegastrointestinallining,leadingto heartburn, esophageal and peptic ulcers, and leaky gut. These drugsinclude aspirin, NSAIDs (e.g., ibuprofen, naproxen, andmany others),

the antibiotic tetracycline, the cardiac antiarrhythmic drug quinidine,potassium chloride tablets, and iron salts. GI irritation is a major sideeffectofsomeofthesedrugs,causinggreatinjuryandseverelylimitingtheiruse.

• Activities suchas coughing,wheezing,bending from thewaist, heavylifting, straining at stool, and certain types of exercise can all increaseintra-abdominal pressure. The increased pressure can literally force thestomach contents through the LES, especially if the stomach is fulland/or the LES is already weakened. Heartburn is so much morecommon inpregnancybecause thegrowing fetus compresses theentireupperGItract.

•Gravitycanalsoplayanimportantrole.Refluxisfarmorelikelywhenwe lieonourbacksor sides thanwhenwestandupright,which isonereason why most serious reflux events occur during sleep. When westand,gravityhelpsdrawthestomachcontentsawayfromtheLES,butwhen we are reclining, stomach contents tend to remain in the upperportionofthestomach.

Once we are aware of which factors might be triggering our heartburn,eliminating them may be all that is required to relieve or prevent reflux. Ofcourse, breaking certain long-standing food and drug habitsmay not be easy.Nevertheless,understandingthehealthbenefitsthatcanaccruefromelimination—including heartburn relief, reducing the risks associated with GERD,elimination of acid-suppressing drugs, return of normal gastric function,improvednutrientabsorption,betterhealth,andlongerlife—mayprovidealittleextramotivation.

AvoidTheseFoodsandDrugsThatCanCauseHeartburn

LESWeakeners EsophagealIrritants

Foods Foods

•Fats •Citrusfruitsandjuices

•Chocolate •Tomato-basedfoods

•Coffee •Spicyfoods•Mints,especiallypeppermintandspearmint •Coffee•Carbonateddrinks•Sugar •Alcohol Drugs

•Onions •Aspirin•Foodallergies •NSAIDs •Tetracycline

Drugs •Quinidine

•Cigarettes •Potassiumchloridetablets

•Bronchodilators(e.g.,theophylline,albuterol,ephedrine)

•Ironsalts

•NSAIDs •Calciumchannelblockers(e.g.,Cardizem,manyothers)

•Beta-blockers(e.g.,Inderal,manyothers) •Diazepam(Valium) •Nitrates(e.g.,nitroglycerin) •Demerol

FirstSteps:HeadingOffHeartburnatHome

Thedietandlifestylechangeslistedbelowcanoftenbeextremelyeffectiveallby themselves in reducing and preventing reflux. For example, elevating theheadofthebedbysixinchesinordertoallowgravitytohelpkeepthegastriccontentsawayfromtheLESisalmostaseffectiveforhealingrefluxesophagitis

astakingZantac.8However, no matter what other herbal (or drug) treatments are

implemented, they should always be in addition to these dietary and lifestylechanges, not instead of them. It makes no sense to use drugs or naturaltreatmentsontheonehandandthenturnaroundandeatfoods,takedrugs,anddootherthingsthatpromoterefluxontheother.

• Avoid the foods and drugs shown in the table on page 136. (Foodallergieswill,ofcourse,varyfromindividualtoindividual.)

•Eatsmallermeals.

• Minimize activity that might increase intra-abdominal pressure, forexample,bendingorheavylifting.

• Wear loose-fittingclothingthatdoesnotsqueezetheabdomenandputaddedpressureontheLES.

•Limitfoodintake(especiallythefoodsinthetableonpage136)duringthehoursjustpriortobedtime.

•Elevatetheheadofthebedusingfour-toeight-inchblocks.

Itisregrettablethatthemarketersofanti-acidproductsareputtingoutthemessageintheiradvertisingthatwecanhaveourburritoandeatit,too.Allweneed todo ispopaPepcidor aPrilosec firstor aTurnsorMaaloxafterward.Andthephysicianswhoprescribetheseproducts,possiblyinveryhighdosestopeople with “intractable” heartburn, generally make little effort to get theirpatients to alter any possibly self-destructive behaviors.Most peoplewho buytheseproductsofftheshelfaregoingtofeelthatusingthemisalltheyneedtodo to rid themselves of “acid indigestion.” While some doctors may suggestchangesindietorbehaviorand/orhandoutbrochuresoutliningthestepslistedabove alongwith their prescriptions, it’s alwaysmuch easier—for both doctorand patient—to just prescribe a pill. This is especially true when the patient,primed by the flood of patentmedicine company ads, comes in demanding aprescription. Does anybody ever give a second thought to the potentialconsequencesofprofound,chronicgastricacidsuppression?Wesincerelydoubtit.

ReplacingHClandPepsin

Paradoxical as it may seem to those schooled in pharmaceutical medicine,replacing HCl in people with hypochlorhydria or achlorhydria can be a veryeffective way of eliminating heartburn/indigestion/GERD and other GIsymptoms,nottomentionthemanydiseaseslinkedtolowstomachacidity.

When I treat patientswithHCl, I alwaysmake clear thatwhile it can beextremely effective, it is not without its risks, and is, therefore, not foreveryone:*

•HClshouldonlybetakenbypeoplewhohavelower-than-normalgastricacid secretion, as determined by an objectivemeasure, such as gastricanalysis.

•ProblemsrelatedtosupplementaryHClarerare,buttheycanbeserious.People taking HCl should be carefully supervised by a physicianknowledgeableinitsuse.

•HClshouldneverbetakenbyanyonewhoisalsousinganykindofanti-inflammatory medication such as corticosteroids (e.g., Prednisone),aspirin,Indocin,ibuprofen(e.g.,Motrin,Advil),orotherNSAIDs.ThesedrugscaninitiatedamagetotheGIliningthatsupplementaryHClmightaggravate,increasingtheriskofgastricbleedingorulcer.

• HCl should usually be taken along with pepsin. It is presumed thatstomachsthatdon’tproduceenoughHClalsodon’tmakeenoughpepsin.Althoughthispresumptionhasrarelybeentested,IhavefoundthatHClreplacementusuallyworksbetterwithpepsin thanwithout it.Therearerareindividualswhoaresensitivetopepsin,andtheyshouldavoidtakingit.

Liquid,Tablets,orCapsules?

Although liquid HCl, which was used back in the early days of replacementtherapy,canstillbefound, it is justwhat itsounds like,concentratedacid inabottle, just likewe playedwith in high school chem lab. It is very dangerousstuffandisavailableforinternaluseinhumansonlybyprescription.LiquidHClmust be handled very carefully. It is difficult to transport and extremelydangerousifthebottleshouldbreakorspill.

“Modern” replacement HCl usually comes in more manageable forms

attached toa“carrier,”eitherbetaineorglutamic acid.Attaching theHCl toacarrieryieldsapowder—betainehydrochlorideorglutamicacidhydrochloride—thatcanbecontainedinacapsule.Typicallytheseproductsaresoldinhealthfoodstoresandcompoundingpharmacies,combinedwithpepsin.

My preference is for the capsule form of HCl.When we compare stoolspecimensfrompeoplewhohavetakenanadequatenumberofHClcapsulestothosewhotakediluteliquidHCl,capsuleuseleavesfarlessundigestedmaterial.This suggests that the people taking the capsules are digesting protein morecompletely. In some people taking themaximum dose ofHCl in liquid form,meat may still go virtually undigested. But when they switch to the capsuleform,meat(andotherprotein)digestionimmediatelyimproves.Inaddition,thecapsulesaresafertohandleandproducefewerunwantedsideeffects.

There’s no way to knowwhich form—betaine or glutamic acid HCl—isbestsuitedforagivenperson.Igenerallyfindthatifoneformcausesanysideeffects,itisworthwhiletryingtheother,sinceit’srarethatpeoplearesensitivetobothforms.However,sincethebetainemoleculeissmallerthantheglutamicacidmolecule,moreHCl can be concentrated in betaine capsules of identicalsize.

To minimize side effects, it is always best to start with one capsule ofbetaineHQcontainingabout650mg,withpepsin,intheearlypartofeachmeal.If there are no problems after two or three days, I recommend increasing thedose to two capsules in the early part of eachmeal; then after another two tothreedays,increaseitagaintothreecapsules.Weincreasethedosegraduallyinthisstepwisefashionuntiltherecommendeddose(fivetosevencapsulesforthe“average”adult) is reached.Whenpeoplehave to take severalcapsuleswithameal,Isuggesttakinghalfjustafterthefirstfewbitesandhalfmidwaythroughthemeal.

ThemosteffectiveadultdoseofbetaineHClis5to7ofthe650milligramcapsulespermeal,withpepsin.(Alittlemoreoftheglutamicformisnecessarybecauseitdoesn’tcarryasmuchHCl).Itmakesintuitivesensetotakelesswithsmallmealsorsnacks,butit’shardtosetclearguidelinesonhowtoarriveattheproper dose. Individuals may have to experiment with different doses to seewhichonedoesthejobwithoutcausingdiscomfort.

WhenHClsupplementation isnot feasible,gradually increasingquantitiesof lemon juice (citric acid) or vinegar (acetic acid)will often relieve some orevenallsymptoms.Thisissupportedbythecommonpracticeinsomeculturesof treatinggastricdiscomfortwith lemon juiceorvinegar.Unfortunately,eventhough symptomsmaybe improved, actual nutrient digestion and assimilationarenotimprovednearlyasmuchaswithHClreplacement.

The doses of HCl recommended here may seem high, especially whencompared with the usual label recommendations. However, a normallyfunctioning stomach is quite capable of producingmuchmore. Thenwhy notgive even higher doses? The fact is that clinical experience shows that thesedosesworkquitewell.

SideEffects?

SideeffectsfromHClreplacementaregenerallymild,takingtheformofsomekindofGIdistress,likepain,burning,gas,orotherfeelingsofdiscomfort.Formost people, reducing or temporarily eliminating the dose relieves thesesymptoms. Paradoxically, adverse symptoms are most likely to occur inindividualswiththelowestlevelsofstomachacid.Thisisbecausethesepeoplearemost likely tohaveatrophicgastritis (a thinned-outstomach lining),whichmakesthemmuchmoresensitivetoevensmallquantitiesofHClthananormal,thickerstomachlining.

IsItWorking?

TomonitortheeffectivenessoftheHCl/pepsinreplacement(aswellasdigestiveenzyme replacement), I request repeated follow-up stool specimens to analyzehowwellproteinandotherdietarycomponents arebeingdigested. I also lookforimprovements inmineralabsorption,reflectedinhairandbloodtests.Withmany individuals, “before and after” blood tests for amino acids give strongindications of effectiveness.Most importantly, we monitor for both short-andlong-termsymptomimprovement.

PancreaticEnzymes

When the acidified food slurry known as chyme reaches the upper end of thesmall intestine (duodenum), the low pH triggers the release of the hormonesecretin.Secretin,inturn,stimulatesthepancreastoreleasebicarbonate,whichelevatesthepHofthestomachcontent.Alsoreleasedareagroupofenzymestodigest fats, carbohydrates, andany remainingundigestedproteins.Aswehavepointedoutearlier,ifgastricacidsecretionisdeficient,thepHofchymemaynotbelowenoughtotriggersecretinrelease.Consequently,thesubsequentrelease

of pancreatic enzymes may not occur efficiently. A weakened pancreas, afrequent occurrence with aging, can also lead to an enzyme deficiency.(Researchershavefound,andIhaveobservedrepeatedly, that individualswithdiabetesoftenhaveinadequatedigestiveenzymes,too.)

Indigestionorflatulencebeginninganhourormoreaftermeals—aboutthetime that chyme would be reaching the duodenum—is often a sign thatpancreatic enzyme secretion is not what it should be. Floating stools are arelativelyreliablesignthatfatsarenotbeingdigestedproperlyduetolowlevelsofpancreaticenzymes(fat floatsonwater).Othersigns includegreasy,smellystools;dryflakyskin;small,hardbumpsonthebackofthearm;andimpaireddark adaptation (“night blindness”). All these signs are frequently related toundigestedfoodsandresultingnutritionaldeficiencies.

If pancreatic enzyme secretion isn’t stimulated due to low gastric acidsecretion, HCl supplementation may be all that is required to remedy theproblem.”9–10However, inmost cases, enzyme supplements do the job better.The most common replacement is an extract of pancreatic tissue, known aspancreatine, that is taken from pigs, cows, or sheep. Alternatively, enzymesderivedfromplantscanbeused,althoughthey’relesssimilartonormalhumanenzymes than the animal forms. These include bromelain (from pineapple),papain(frompapaya),andothers.Whethertheplant-derivedenzymesareequalin efficacy to animal-derived pancreatin has not been adequately studied, so Iusuallyrecommendtheanimalforms(exceptforvegetarians).

In order to more closely simulate the natural process, it is best to takepancreaticenzymesat theendofameal. (Iknow that thebottle labelsusuallystatetheopposite.Idon’tagree!)Takingdigestiveenzymesaftermealsgivesthefood adequate time to undergo the “acid phase” of digestion, as happenswithnormaldigestivefunction.Iusuallyrecommendatrialoftwotofourcapsulesofpancreatin,bromelain,orpapainaftermeals.Ifthishelpstoimprovedigestion,thenIrecommendcontinuingtotakethem.

Keep inmind thatpancreaticenzymedeficienciesusuallyoccuralongsidehypochlorhydria or achlorhydria. Thus, if HCl replacement is indicated,pancreaticenzymereplacementprobablyisalso.

Digestive enzyme supplements are generally safe. The most importantpotential hazard is an allergic reaction,which usually takes the form of loosestoolsordiarrhea,althoughaskinrashorotherallergicsymptomsarepossiblebutrare.

Herbs,BitterandOtherwise

Awidevarietyofherbal remedies canproduce importantbeneficial effectsonGIfunction.Manyoftheseare“bitterherbs,”whichhavelongheldanimportantplaceinmanydifferentmedicaltraditions,becausetheystimulatedigestion.Asthe name suggests,when placed on the tongue, bitter herbs, or “bitters,” tastebitter.

Studies over the years have confirmed that bitters probably work byincreasingtheflowofavarietyofdigestivejuices,includingHCl,bile,pepsin,gastrin,andpancreaticenzymes.11–15 It almostgoeswithout saying thatbittersincreasethesecretionofsaliva.Theymayalsohelpheadoffrefluxbyincreasingthe tone of the LES. It is unclear whether we even need to swallow a bit ofbitters to obtain its benefits. Some research suggests that it may only benecessarytotastethem.16

It is thought that bittersmay have a “priming” effect on digestion in themouth,esophagus,andstomach.Wemayhaveevolvedthisresponseasameansof protecting ourselves frompoisons, since poisonous substances often have abitter taste. Those poisons that don’t get spit out immediately might getdeactivatedbyacid andenzymes in the stomach.However theywork, though,modern studies confirm the usefulness of bitter herbs like gentian root andwormwood (artemisia) in stimulating the secretion of gastric acid, bile, andpancreaticenzymes.17–18

Not surprisingly, it’s hard to find good published scientific researchevaluating the therapeutic use of unpatentable/unprofitable bitters. OneuncontrolledstudywasrecentlyconductedinGermany,whereherbalmedicineistakenfarmoreseriously.Theresearchersevaluatedtheeffectofgentianrootcapsulesin205peoplewithlossofappetite,heartburn,constipation,flatulence,abdominalpain,nausea,anddyspepsia.TheyreportedarapidreturnofappetiteanddramaticreliefoftheirGIsymptoms.19

AmongthemostcommonlyusedbitterherbsinWesternmedicineare:

•Barberrybark(Berberisvulgaris)

•Caraway(Carumcarvi)

•Dandelion(Taraxacumofficinale)

•Fennel(Foeniculumvulgare)

•Gentianroot(Gentianalutea)

•Ginger(Zingiberofficinale)

•Globeartichoke(Cynarascolymus)

•Goldensealroot(Hydrastiscanadensis)

•Hopsflowers(Humuluslupulus)

•Milkthistle(Silybummarianum)

•Peppermint(Menthapiperita)

•Wormwood(ArtemisiaabsinthiumL.)

•Yellowdock(Rumexcrispus)

Bitters are normally taken in very small doses, just enough to evoke astrong taste of bitterness. Bitters are almost always available in natural foodstores in liquid form. Sometimes they’re derived from just one or two of theherbalsabove;oftenthey’recombinationsofseveral.

For best results, the recommended dose (which varies according to theconcentrationoftheparticularproduct)is“takenstraight”ordissolvedinaslittlewateraspossibletomaintainthebittertaste.(That’sthepoint!)Bittersshouldbesippedbeforemeals.Moststudieshaveshownthat,inordertostimulatestomachacidaswellasdigestiveprocessesingeneral,itisbesttotastethebitterness.

Bitters generally work best in mild to moderate cases ofheartburn/indigestion/bloating, since in these cases it’smore likely that there’ssomestill-functional stomach liningavailable tobe stimulated.Becausebittersworkprimarilybystimulatingthesecretionofgastricjuices,theymayhavenoeffectifthestomachliningisseverelyatrophied.

Eveninseverecasesofheartburn/GERD,bittersmightbehelpful,but it’sbest to consult a physician skilled and knowledgeable in both herbal andnutritionalmedicinebeforeusingthem,since,incasesofLESmalfunction,evenalittlemoreacidcanaggravatesymptoms.

SinceI’mlessexpert inherbalmedicinethanmycolleagueKerryBone,Irefer readers interested in learning more about bitters to his writings on thistopic,includinghisnumber-one-in-its-fieldtextbook,PrinciplesandPracticeofPhytotherapy(writtenwithSimonMills)andvariousarticles(see“HowtoTakeBitters”).

VitaminB12

Incasesofachlorhydria,itisanestablishedfactthatvitaminB12isneitherwelldigested nor well absorbed. When stomach function is normal, vitamin B12digestionandabsorptionarealsonormal.Butfortheentire“in-between”group,rangingfromseriouslylowstomachacidtoonlyaslightproblem,there’sgreatvariability in B12 digestion/absorption and even greater controversy aboutwhethersupplementalvitaminB12isuseful,necessary,orjustified.SincetestingforvitaminB12statusisrelativelyexpensiveandnotnecessarilyprecise,Itakeapracticalapproach.

HowtoTakeBitters

ByKerryBone,MCPP,FNHAA,FNIMH

The main bitter herbs used in Western herbal medicine are gentian andwormwood.Fora reflexeffect,bittersdonotusuallyhave tobegiven inhighdoses.Enoughtopromoteastrongtasteofbitternessisusuallysufficient.Thisistypically5to10dropsofthe1:5tincturesoftheaboveherbsinabout20mLofwater.(Bittersareoneexceptionwheredropdosesareappropriate.)Sincebittershaveaprimingeffectonupperdigestivefunctionandworkbyavisceralreflex(whichisslow)theyarebesttakenabout15minutesbeforemeals.Also,bittersworkbestiftheyaresippedslowly,toprolongthestimulationofthereflex.Thiscanbedifficultforsomepeople,butwillgiveoptimumresults.

For a direct effect on the gastric mucosa, higher doses need to be used.About300to600mgofgentianrootbeforemealswouldbeanappropriatedose.Be careful of such high doses of gentian taken in liquid form, since they cancausenauseainsomepeople.

One question which has vexed herbalists is whether the taste of bittersgiven in liquid form can be masked,* and yet their reflex activity still bepreserved.This isprobably thecase, since themaskingagentswill change theconscious perception of bitterness, but the bitter taste buds will still bestimulated.

(“TheStoryofBitters,”NutritionandHealingnewsletter,December1998)

Whenever testing demonstrates any degree of low stomach acid, Irecommenda“trialseries”ofvitaminB12injections,whichcanbeperformedathome. There aremany reasons for this approach.Most importantly, it is safe.Theonlywayto“overdose”onvitaminB12istofillyourbathtubanddrowninit!Itisinexpensive:Usually,vitaminB12,alongwithneedlesandsyringes,costsless than one dollar per injection (if done at home). In fact, a trial series oftwenty to thirty injections is considerably less expensive than a single test forvitamin B12. Lastly, it is almost always obvious to the individual involvedwhethervitaminB12injectionsareusefulornot.

A“positive” response tovitaminB12manifestsas improvement inoneormore of the following: energy, sleep pattern, “nervousness,” and anxiety. In anegativeresponse,noneofthesechange.Iftheresponseisnegative,thevitaminB12 injectionsarediscontinuedafter the trial series. If the response ispositive,they are continued, with the frequency adjusted to self-perceived need, oftenonceortwiceweekly.

In twenty-four years of following this pattern, it has become absolutelyclear that there is a sharp difference between hypochlorhydric women andhypochlorhydricmenintheirresponsestovitaminB12injections.Sixtypercentto70percentofwomenreportthattheyfeelbetterwiththem,andcontinuethemformonthsorevendecades.Bycontrast,only20percentto30percentofmennoticeanydifference.

SincevitaminB12andfolicacid(folate)aresofrequentlyfoundtogetherinbiochemical pathways, we always add a small amount of folic acid to thevitaminB12 injections.Also, because absorption of other B-complex vitaminscandeclinerapidlyafterageseventy,wealsoaddaB-complexinjectiontothevitaminB12/folicacidinjectionsinolderpeople.BothfolicacidandB-complexinjectionsarequitesafewhengivenintramuscularly(IM).

OtherHelpfulHerbsandNutrients

DeglycyrrhizinatedLicorice(DGL)

Before theacid-suppressingdrugscamealong,perhaps themosteffectivedrugfortreatingpepticulcerwascarbenoxolone,whichwasasyntheticderivativeof

theancienthealingherb licoriceroot.Thevalueof licorice*forhealingpepticulcerswasfirstdocumentedduringthe1940sintheNetherlands.Althoughquiteeffective,theuseoflicoricewaslimitedbyserioussideeffects,primarilyfluidretention,highbloodpressure,potassium loss, andconsequentheartproblems.Carbenoxolonealsohadthesesamelimitations.

The ingredient in licorice that is largely responsible for these unwantedadverse effects is now known to beglycyrrhizin, which closely resembles thehormonecortisoneinitsstructureandactivity.Justascaffeinecanberemovedfromcoffee,97percentof theglycyrrhizincanalsobe removed from licorice.What’s left, a product called deglycyrrhizinated licorice (DGL), retains thehealingpropertiesoflicoricebutlosesitsmostimportantsideeffects.DGLhasbeenshowntobeeffectiveintreatinggastricandduodenalulcers,anditworksaswellinthisregardasTagametandZantac,withfarfewersideeffects(andnoacidsuppression).20–22 Inanimalstudies,DGLhasevenbeenshowntoprotectthestomachliningagainstdamagecausedbyaspirinandotherNSAIDs.23–25”

Although only a small minority of those suffering from heartburn,indigestion, bloating, gas, or GERD actually have peptic or gastric ulcers,evidencesuggeststhatDGL’smechanismofactionmakesitalsoveryusefulforheartburn/indigestion/GERD. The therapeutic effect of licorice (and DGL)—sometimescalled“cytoprotective”—appearstoderivefromitsabilitytorestorethe integrity of the gastric and intestinal lining. It does this by enhancing thesecretion of protective mucus in the gastric and duodenal linings. Recall thatmucussecretedbycellsintheGIlininghelpsformthebarrierthatprotectsthatliningfromcontactwithHClandotherdigestivejuices.

Researchshowsthat licoriceraises theconcentrationofcompoundscalledprostaglandins,whichpromotemucus secretion, stabilize cellmembranes, andstimulate new cell growth, all leading to the healing of ulcers.26† This is theexact opposite effect of drugs like aspirin and the NSAIDs, which suppress“bad” prostaglandins and lead to the formation of ulcers. Thus, DGLmay behelpfulforpeoplewhoareexperiencinggastricdistressbecausetheyaretakingNSAIDs.

SinceDGLbecameavailableintheUnitedStatesinthe1980s,hundredsofindividualssufferingfromheartburn,indigestion,bloating,gas,andevenGERDhaveadvisedmethatregularDGLusebringsthemasmuchasormoresymptomreliefthanantacidsoracidblockers.However,it’svery importanttorememberthatneitherDGLnoranyothersymptomreliever(withtheexceptionofbittersin some cases) actually helps correct the usual causes of these symptoms, amajoroneofwhichislower-than-adequatestomachacid-pepsinsecretion.Only

replacementHCl-pepsin(alongwithothernaturalmeasures)canhelpnormalizeboth symptoms and digestive function, restoring the normal flow of nutrientsintothebody.

For best results, DGL tablets should be thoroughly chewed and thenswallowedwithas littlewateraspossible, since ithelpshealbydirectcontactwiththecellsofthegastrointestinallining.Forthisreason,DGLisbesttakenonan empty stomach. I usually recommend thoroughly chewing and swallowingtwoDGLtabletsthreetofourtimesdailywithnofoodonehourbeforeorafterameal.Itcanbeusedevenmoreoftenifit’sadditionallyhelpfultodoso.

VitaminC

The value of vitamin C for health is well known, and the idea of vitamin Csupplementation is now widely accepted (although there’s still considerabledisagreement on the amounts to be taken). Many people associate vitamin Cwith such benefits as relief of the common cold and protection against heartdisease and certain cancers. Less appreciated is the protective role vitamin Cplays in the health of the stomach, where it provides vital protection againstgastric cancer.Many studies have confirmed that low levels of vitaminC areassociated with a high risk of gastric cancer and that high intake of foodscontaining vitamin C (as well as vitamin E, beta-carotene, and others) isassociatedwithreducedincidenceofgastriccancer.27–32

VitaminC from food is normally secreted (or passively diffuses) directlyinto the stomachcavity,where it is converted toascorbicacid, alsoknownasascorbate. Thus, normal gastric juice contains both vitamin C and ascorbicacid.31Ascorbicacidappearstoexertitsprotectiveeffectsherebyatleastthreeroutes:

• Inhibiting the formation of N-nitroso compounds. Ascorbic acidinterferes with the chemical conversion of nitrites from food tocarcinogenic N-nitroso compounds such as nitrosamines. As wediscussed in chapter 5, nitrosamines and related compounds commonlyformedinthestomacharethoughttobeamajorcauseofstomachcancer.Ascorbicacidinterfereswiththisreaction.33-35

• Retarding the growth ofH. pylori. Colonization ofH. pylori in thestomachmakesusvulnerabletochronicgastritisandeventuallytogastriccancer. Vitamin C in gastric juice helps retard the growth of this

pathogenic bacteria and, in some cases,may be enough to eradicate italtogether.36-38

• Scavenging free radicals. Reactive oxygen species, better known asoxygenfreeradicals,arerecognizedtocausecancerandotherdestructivechangesalloverthebodybydamagingDNA.Asanantioxidant,ascorbicacidfromvitaminCscavengesthefreeradicalsinthestomach,limitingtheharmtheycando.39

TakingvitaminC

Manyindividualswithheartburn/indigestionreportthattheascorbicacidformofvitaminCisastomachirritant,butthatthevarious“ascorbate”formsofvitaminC are well-tolerated. These include sodium ascorbate,* calcium/magnesiumascorbate, and multiple-mineral ascorbates. Sodium ascorbate andcalcium/magnesium ascorbate are usually available as powders; multiple-mineralascorbatesastablets.Higherquantitiesofcalcium/magnesiumascorbateandmultiple-mineral ascorbates can contribute to “loose bowels,” but sodiumascorbateislesslikelytodoso.

Iusuallyrecommendaminimumtotalof1to3gramsofvitaminCdaily,takentwoorthreetimesperdaywithmeals.If“loosebowel”isnotaproblem,it’sadvisabletotakemore.

OtherUsefulNaturalProducts

Wehavedescribedonlysomeofthemajornaturalsubstancesthatcanbeusedtohelp prevent or heal upper GI dysfunction. There are many, many more,including:

L-glutamine,VitaminA,andZinc

L-glutamine,anaminoacid,hasmanyfunctions inourbodies.Forexample, itservesastheprincipalenergysourcefortheliningcellsoftheupperGItract.Ifmore energy is supplied to these cells, they have a better chance of stayinghealthyorreturningtohealthiftheyaredamaged.Morethantwodecadesago,electron microscope studies of biopsy specimens showed that vitamin A

stimulated healthy growth of intestinal lining cells. Zinc (which is oftenmarginallydeficientinourdiets)hasbeenproventopromotetissuehealing.Forthesereasons,fordecadesI’veincludedthesethreenutrientsinanyprogramthatattempts to improve or heal gastrointestinal function, alongwith the ascorbateformofvitaminC,andnowwithDGL.Althoughthere’snosystematicresearchon this combination,many have reported that it works even better than DGLalone.

QuantitiesofDGLandascorbaterecommendedareasnotedpreviously.Tothisareaddedeachday1000mgofglutamine,40,000IUofvitaminA(notbeta-carotene),and30mgzinc(fromzincpicolinate).

ASpecialCircumstance

Very occasionally, individuals with heartburn/indigestion/bloating/gas have atestthatunequivocallyshowsverylowstomachacid,buttheycannottakeevenalittlereplacementHCl-pepsinwithoutstomachpain(notesophagealrefluxpain).Thisoccursincaseswherethestomachliningissothin(moreseveredegreesofatrophicgastritis)thatitcannotwithstandevenalittlereplacementacid.Inthosecases,useofDGL,ascorbate,L-glutamine,vitaminA,andzincinthequantitiesnotedaboveforsixtoeightweeksusuallyenablestheseindividualstocautiouslystartHCl-pepsinreplacement.

Turmeric(Curcumin)

Turmericisabrightyellowherbusedinpreparingnumerousverytastydishes,includingmanycurries. It alsohas a longhistory inmany folk cultures in theMiddleandFarEastasatreatmentforgastrointestinalandotherdisorders.Whatlittle systematic research there is on turmeric has been conducted primarily inAsia and suggests that it acts as amild irritant that stimulates the secretionofdigestive juices, such as saliva andmucus, bothofwhich canhelpprotect theesophagus and stomach against gastric acid. It may also have antioxidantproperties40–43 and improve gall bladder function.44 A randomized, double-blind,placebo-controlledtrialfromThailandfoundthattakingturmeric(two250mgcapsulesfourtimesaday,aftermealsandatbedtime)significantlyimprovedcommonsymptomsofdyspepsiasuchasheartburn,gastricpainordiscomfort,belching, gas and flatulence.45Other research suggests that turmeric treatmentcanhelphealgastriculcers.46

Capsaicin

Capsaicinis theingredientthatmakesredpeppers“hot.”Althoughit iswidelybelieved that hot peppers cause indigestion, in fact, quite the opposite can betrue.Studieshaveshownthatcapsaicinprotectsthegastricmucosalliningfromdamage caused by aspirin, alcohol, and probably other potentially harmfulagents.47–48 Capsaicin apparently works by activating a built-in “neuralemergency system” in the stomach consisting of certain sensory nerves in thestomach lining.This leads to enhanced local blood flowandprotectivemucussecretion.49–50However, since capsaicin can irritate already inflamed tissue, itshouldnever be used by individualswithmore severe acid reflux (e.g., refluxesophagitis)orGERDexceptinconsultationwithaphysicianwhoisskilledinnutritionalandbotanicalmedicine.

Ginger

Ginger is a traditional herb that has featured prominentiy in the cooking andmedicineofChina,India,andotherculturesinAsiaforthousandsofyears.Theunderground root of the Zingiber officinale plant, ginger is made into teas,candies, or capsules, and is added to food. As a “medicine,” ginger has beenusedto“cleanse”thebody,inpartbyimprovingdigestion.Specifically,gingerhasbeenusedtotreatcolds,fever,chills,seasickness,menstrualpains,andotherdisorders. Modern scientific research confirms that ginger can protect the GItract inmuch the sameway that capsaicin and turmeric do.51–52 I recommendgingerforitsabilitytorelievenauseafromnearlyanycause,especiallyincasesof nausea due to motion sickness, which is well documented.53–56 Recentresearch has also demonstrated that ginger can help prevent atherosclerosis,possiblybyinhibitingtheoxidationoflow-densitylipoprotein(LDL,the“bad”)cholesterol.57–58

EssentialFattyAcids

Essentialfattyacids(EFAs)canhelphealgastricandduodenalulcers.59–64SinceEFAsareoneofthemostcommonnutritionaldeficiencies,Irecommendeatingfish,unroasted nuts and seeds (roasting nuts and seeds removesmost of theirEFAcontent), and saladoils. Inmanycases, anEFAsupplement is advisable,

especially for thoseofuswhohavedryskin. (Dryskin isusuallycausedbyadeficiencyinEFAs,notbyadeficiencyinskinmoisturizers.)Sinceourdietsareusually more deficient in omega-3 fatty acids (which are generally anti-inflammatory) than in omega-6 fatty acids (which are generally pro-inflammatory), I advise supplementation with oils containing a majority ofomega-3 fatty acids. Flaxseed and walnut oils are the principal single oilscontaining both omega-3 and omega-6 in a favorable balance. There are alsomanyblendedoilsavailablewithsimilarfavorableomega-3/omega-6fattyacidbalance. And never forget to take vitamin E whenever taking essential fattyacids.

Chamomile

The herb chamomile has anti-inflammatory properties, which explains itstraditionaluseforhelpingsootheirritatedorinflamedmucousmembranesinthedigestive tract. Sipping chamomile tea can help relieve heartburn by soothingesophagealinflammation.

Lactase

Lactoseintolerance(theinabilitytodigestthemilksugarlactose)iscausedbyadeficiency in the enzyme lactase. It can cause many digestive problems,including gas, cramps, and diarrhea. For many reasons (including, but notlimitedto,increasedriskofcataracts,ovariancancer,andprostatecancer),itisbesttoavoidmilkanddairyproductsaltogether,andthat’swhatIrecommend.However, some lactose-intolerant individuals prefer to consume themanyway.For these individuals, supplements of lactase (lactose-digesting enzyme) areavailable. Research has shown that lactase preparations can reduce pain,bloating, and other symptoms associated with lactose intolerance.65 Since alllactaseproductsarenotequallyeffective,itmaybebesttotrymorethanoneifnecessary.66

Probiotics

Supplements containing “friendly” bacteria can be very helpful for promotinghealthydigestion,becausetheyfavorablyaltertheintestinalmicroflorabalance,inhibitingthegrowthofharmfulbacteria(includingH.pylori),boostingimmune

function, and increasing resistance to infection. Beneficial bugs such asLactobacillus acidophilus and Bifidobacterium bifidum secrete enzymes,including lactase, that aid in digestion.67–71 Stool tests are available to tell uswhethertheLactobacilluspopulationofthebowelsisadequateornot.Thesecanbeorderedwiththehelpofanynutritionallyorientedphysician.Ifprobioticsarefoundtobeneeded,askthatphysicianforarecommendation,sincetherearesomanyprobioticproductsavailablethatareviewisnotpracticalhere.

Artichoke

Besides making a healthy and delicious food, artichoke is also a plant withimportantmedicinalqualities.Indouble-blindstudies,extractsofartichokehaverepeatedly demonstrated benefits to people with indigestion. Artichoke isparticularlyusefulwhentheproblemislackofbileproductionbytheliver.Asabonus,artichokecanhelp lowercholesterol levelsandprotectLDLcholesterolfromoxidation,amajorfactorinthedevelopmentofatherosclerosis.72-77Whentakingartichokeextracttoenhanceliverfunction,itisbesttotakeasupplementthatcontains500to1000mgperdayofthemainactiveingredientinartichoke,cynarin.

Mastic,theNaturalH.pyloriKiller

MasticisarareandremarkableproductthathasbeenastapleofmedicineintheMediterraneanandMiddleEast regions for thousandsofyears,but isvirtuallyunheardofinWesternmedicine.Sinceancienttimes,mastichasbeenvaluedforitsabilitytosafelyrelieveawiderangeofdigestivedisordersfrombadbreathtopeptic ulcers. Now known to have broad spectrum antimicrobial properties, ithas recently been found to kill various bacteria, including H. pylori, theorganismresponsibleformostcasesofatrophicgastritisandpepticulcer.

The only problemwithmastic has always been that it is rarer than gold.Masticresin,whichcontainsthemedicinallyactiveingredients,isproducedonlybythemastictree,knownasPistacialentiscusvarchia,whichgrowsinjustonetinyspotontheentireplanet,thesoutherncorneroftheGreekislandofChios.Theremustbesomethingmagical inthesoilofsouthernChios,because,whenmastictreesthatgrowherearetransplantedtoandcultivatedinotherplaceswithsimilarclimates,theygrowwellbutneverproducetheirtherapeuticresin.

InthetimeofColumbus,masticwashighlyvaluedbecauseitwasthebest

available treatment for all kinds of GI distress, including the deadly diseasecholera.Thisexplains theunusualrewardoffered toColumbusandhiscrewiftheycouldfindanewsourceofmasticintheirexplorationsoftheNewWorld.In fact, they did find a close relative ofPistacia lentiscus, which produced aresinthelocalnativestoldthemwasgoodfortreatingstomachaches.

In recent times, the vast majority of mastic from Chios is shipped tolocationsintheMiddleEast,whereitremainsanimportanttherapeuticagentinavarietyofGIdisorders.Notsurprisingly,whatlittlesystematicresearchthereis onmastic comes from this area.Onedouble-blind trial from Iraq comparedmastic (1 g/day) with placebo in the treatment of thirty-eight patients withduodenal ulcer,whichwas confirmed by endoscopic examination.78After justtwoweeksoftreatment,symptomsimprovedsignificantlyin80percent(sixteenoutoftwenty)ofthemastic-treatedpatients,comparedwith50percent(nineoutofeighteen)ofthosereceivingtheplacebo.Evenmoreimportantthansymptomrelief,though,wasthefactthatulcerhealingwasverifiedendoscopicallyin70percentofthemasticgroup,butjust22percentoftheplacebogroup(seeFigure7-1).79Mastichasalsobeenreportedtobeeffectiveinhealinggastriculcersinfiveofsixpatientswithinfourweeks.80

Figure7-1.Superiorsymptomaticreliefandendoscopicallyverifiedhealinginduodenalulcerpatientstreatedwithmasticorplacebofortwoweeks.P<0.01.AdaptedfromAl-Habbaletal.,1984.

At least part of mastic’s therapeutic power probably derives from itsantimicrobialproperties.Numerousinvestigatorshavedemonstrateditsabilitytokill a broad spectrum of bacteria, as well as disease causing yeasts and otherfungi.81–83 Chewing mastic gum for five days has been reported to reducebacterialdentalplaqueformationby41.5percentinpeoplewhowereinstructednottobrushtheirteethduringtheexperimentalperiod.Bykillingbacteriainthemouth, chewing mastic is also used to help “sweeten” the breath. Due to itsmalleability,strength,andantibacterialability,masticgumhasalsobeenusedto

filldentalcarries.Mastic’sabilitytokillH.pylori,asreportedintheNewEnglandJournalof

Medicinein1998,84hasfinallybroughtittotheforefrontofGItherapiesintheUnitedStates,aswellasprovidedamechanismofactionforitslong-recognizedulcer-healing properties. The report described test-tube research showing thatmastickilledseveral strainsofH.pylori, includingsome thatwere resistant toconventionalantibiotics.

In addition to its antimicrobial actions, mastic appears to offer furtherprotection to theGIsystemfromknownirritants.Thiswasdemonstrated inanexperiment in which mastic was found to protect laboratory animals againstdamage caused by a variety of drugs known to injure the GI tract (aspirin,phenylbutazone, alcohol, and reserpine), as well as by physical stress (coldrestraint) and mechanical stress (ligation of the pylorus). The protectivemechanisminvolvedhereisnotyetknown.85Mastichasnoknownsideeffectsofanysignificance.

Mastic is available as capsules, powder, toothpaste, and as mouthwash(masticoil).Puremasticresin,directfromthetree(knownas“teardrops”),andessentialmasticoilarealsoavailable.*Theresincanbechewedlikegum,whiletheoilcanbeaddedtofoods.Powderedmasticresincanalsobeaddedtofoods.Forexample,inTurkeyicecreamismadewithmasticpowder.

Mastichasbeenavailable in theUnitedStates for less than twoyears.Sofar,theonlyexperienceIhavehadwithitsuseisforthosewithH.pylori-relatedpeptic ulcers. In several cases, 500 mg, three times daily, has been veryeffective.However,as the last fewparagraphs imply,masticmayalsobeveryuseful forH. pylori-related atrophic gastritis. In such cases, it is theoreticallypossible that using mastic to eliminateH. pylori would allow at least partialregeneration of the stomach lining, perhaps restoring HCl-pepsin production(and overall stomach function) toward normal. However, more research andclinicalobservationareneededbeforefirmconclusionscanbedrawnregardingthispoint.

WhentoSeekMedicalHelp;WhentoDoItYourself

Before heartburn, indigestion, bloating, and gas progress tomore serious acidreflux and GERD, they are almost always treatable by the various all-naturalmeans discussed earlier. It is always best to start out with a combination ofdietary changes, drug avoidance, and lifestyle modifications. These will

frequentlyeliminatesymptomsandpromotehealing,particularlyinthoseofusunderageforty-fivetofifty.

Nearlyallofushavehadoccasionalepisodesof indigestion from“eatingthewrong thing,” emotional upset, or “stuffing ourselves” at Thanksgiving. Ifindigestionisveryoccasionalortheprobablecauseisobvious,thereisnoneedtobeconcerned.Butifindigestionbecomesfrequentandpersistent,especiallyifaccompaniedbyheartburn,bloating,andconstipation,itisdefinitelywisestnotto ignore it.Whileonlya fractionof thosewith indigestionwilldevelopmoreserious acid reflux/GERD with esophageal damage, we don’t want this tohappentoyou!Itisalwaysmuch,mucheasiertopreventGERDthantotreatit.

Step1:IdentifyandEliminatetheCause(s)

Elsewhereinthischapterandbook,wehavewrittenaboutmanyoftheknowncausesofindigestionandheartburn.Thefirststepinaself-helpprogramaimedateliminating indigestionshouldalwaysbe to identifyandeliminatecauses, ifpossible.MostofthecommoncausesarelistedinTable7-1.Remember,causesvaryfrompersontoperson,andwhataffectsoneofusmaynotaffectanother.Youmayneedtoeliminateonlyoneofthesepossiblecauses,acombinationofseveralofthem,orevenallofthem.

Step2:BitterstoStimulatetheStomach

IfStep1isn’thelpful,thenweshouldtrystimulatingourstomachstoworkontheir own again. Bitters are safe, natural stomach stimulants that can restorenormal stomach function in many cases. It is always preferable to try bittersbeforemovingontoreplacementtherapywithHClandpepsin.

Step3VinegarorLemonJuice

Ifindigestionpersists,tryswallowingonetotwotablespoonsfulofcidervinegarorlemonjuiceinaslittlewateraspossibleduringtheearlypartofameal.Ifthislessens or eliminates indigestion and/or heartburn, then it is reasonable toconcludethatsymptomsarearesultofinsufficientstomachacid.

Step4:DigestiveEnzymes

Sometimesdigestive enzymesor “plant enzymes” (e.g., pancreatin, bromelain,papain) takenwithmealswill relieve indigestion.Takingdigestiveenzymes iscertainlysafe,andsomephysiciansadvisecontinuingusingthemindefinitelytoimprovedigestionandrelievesymptoms.Itisveryimportanttounderstandthatsymptoms of heartburn/indigestion are usually not due to digestive enzymedeficiency, but instead result from low stomach acid production.As symptomrelievers, digestive enzymes are definitely preferable to antacids or acid-blockingdrugs.Butdigestive enzymesdonothave the sameeffectonproteinandmineraldigestion/assimilationasHCl-pepsindoes.

Whyisthissuchanimportantpoint?Let’sverybrieflyreviewthenormaldigestiveprocess.Wechewfood,mixingitwithenzymespresentinsaliva.Weswallow,droppingthefoodintothestomach,whereit’sthoroughlymixedwithacid, pepsin, and other stomach secretions. This “acid phase” of digestionusuallylastsforuptoanhour.Thefoodisthenpropelledfromthestomachintothe upper small intestine,where itsacidity stimulates the release of hormonesthat,inturn,stimulatethereleaseofpancreaticdigestiveenzymes,bicarbonate,andbile.Thesemixwithfood,changingthepHfromacidtoalkaline.Thisstartsand continues the “alkaline phase” of digestion. Both the acid and alkalinephasesofdigestionarenecessarytooptimallydigestandassimilatenutrients.Ifwe correct symptoms due to lack ofacid by usingalkaline enzymes,wemayfeel better, but we really have not fixed the problem or restored normaldigestion.

Step5:TestStomachAcidLevel

If either cider vinegar/lemon juice or digestive enzymes correct or improveindigestion/heartburn, it is time to consider consulting a physician who canperform a test for hypochlorhydria.We regret to report that,while these testswere once quite common, most physicians (especially “board certified”gastroenterologists) long ago quit testing for stomach acid production. Thesespecialists,whoarefirmbelieversinthequestionableconventionalwisdomthatsuppressing stomach acid secretion is therapeutically necessary andbeneficial,uniformlyridiculetheideaofHCl-pepsinreplacementtherapytomakeupforadeficiency in stomach function. This attitude ismuch easier to assume if yourefuse even to measure stomach acid secretion. Fortunately, many of thesephysicians do perform stool tests, which can expose inadequate digestiveenzymesecretion.We’resorrytobeforced(byfacts)towritethatvery,veryfew“board-certified” gastroenterologists or internal medicine specialists perform

teststomeasurelevelsofstomachacidsecretion.

Step6:TestforSeriousGastricorEsophagealDisease

For more severe heartburn/indigestion, it is frequently best to consult agastroenterologist first to be checked (usually with a gastroscope) for pepticulcer,GERD,esophagitis,Barrett’sesophagus,orotherseriousconditions.Oncea diagnosis is made, there is usually time to consult a physician who isknowledgeable in using natural treatments before resorting to antacids or(especially)acid-blockingdrugs.

WhatAboutSelf-TreatmentwithHCL-Pepsin?

For thevastmajorityof indigestion/heartburn sufferers, a brief “trial” ofHCl-pepsinislikelytobeharmlessandwilloftenbringsymptomrelief.However,Irecommend consulting a physician skilled and knowledgeable in natural andnutritionalmedicinebeforeembarkingonsucha“trial.”

For readers ofDr.Wright’s Book of Nutritional Therapy (1979) andDr.Wright’s Guide to Healing with Nutrition (1984), this recommendation mayseemabit of a surprise. Inboth thesebooks, instructionsweregiven forverycautious HCl-pepsin self-trials. However, in the year 2001, there are many,many more of us “just getting into” natural medicine and self-care. A muchgreaterproportionof“newbies”have taken,orare still taking,medication thatcould adversely interact with HCl and pepsin supplements. The samemedications (mostly anti-inflammatories, but other medications, too) canseriouslyweaken the stomach lining to the point where it cannot handle HCleven if it is really needed. So, if you have indigestion, heartburn, bloating, orgas, and have unsuccessfully tried all the steps noted above, please considerconsultingaknowledgeablephysicianforguidance.

ShouldAntacidProductsEverBeUsed?

We have strongly advocated treating the cause of indigestion and heartburn(which is very likely to be low stomach acid, variably associated with otherfactors)ratherthantreatingthesymptoms.Aswe’vewrittenmanytimes,eventhough antacids and acid-blockers may relieve symptoms, they are the exact

oppositeofwhatisreallyneededbothtotreatsymptomsandtorestorenormalfunction.

We have presented alternatives that, used singly or in combination, canrelieve symptoms without eliminating the very important “acid phase” ofdigestion.Theseshouldalwaysbetriedfirst, inpreferencetoalkaline-inducingantacidsandacidblockers.Butwhatifthatisnotpossibleordoesnotwork?Touse an extreme example, what if we are stuck on a desert island sufferingindigestion and heartburn (too many coconuts?), with no available remediesexceptforanunlimitedsupplyofacidblockersandantacids?Whattodo?

Throwtheacidblockersintotheoceanandrelyinsteadontheantacidsuntilrescuersarrive!*Thereason?AntacidsneutralizeacidandraisethepH,butthatis all they do. If we avoid aluminum-containing antacids, and rely instead onthoseinwhichthemineralcontentismostlycalciumand/ormagnesium,weareonlybrieflyinterferingwiththenormaldigestiveprocessandprobablydoingnofurtherharm.Thatisnotatallthecasewithacidblockers,whicharemuchmorecomplexmolecules, designed to throwmolecular “monkeywrenches” intoourbodies’ enzymaticmachinery.While these drugs indeed achieve the particulareffect desired by their drug company creators, they also have a variety ofunwanted,andusuallyunanticipated,effects.Ifantacidsoracidblockersaretheonlyalternatives,antacidsaredefinitelypreferable.

WeaningYourselfoffAntacidsandAcidBlockers

Ifyou’represently takingantacidsoracidblockers, I recommendswitching tonatural, lessharmfulmethodsofdealingwith indigestionandheartburn.Sincethere is no “withdrawal” from acid blockers or antacids, it is safe to just stopthemandswitch tonaturalalternatives,as longassymptomsarecontrolled.Incasesofmild-to-moderate indigestionorheartburn, there’susuallynoproblemwith switching. Inmore seriouscases,particularly if there’s severeacid refluxwithongoingesophagealdamage,it’swisesttowithdrawfromacidblockersorantacidsonlyinconsultationwithaknowledgeablephysician.

FindingaPhysicianWhoWillTreatIndigestionNaturally

It is unfortunate that in today’s medical climate, which is dominated by thepharmaceutical and managed care industries, it has become routine forphysicians to reach for their prescriptionpadat the first signofheartburnandwrite the name of the most potent acid suppressor they know. Because asignificantportionof theirknowledgebasederives frompatentmedicine salesreps, medical journals supported by patent medicine company advertising, orpatent medicine company sponsored conventions, the average “conventional”medical doctor in theUnited States knows virtually nothing about the naturaltreatment of digestive disorders. Tomany of these doctors, natural treatmentssound like the latest food fad: “HCl to prevent acid indigestion? Give me abreak!” Moreover, those “conventional” medical doctors who may be a littlemoreopen-minded, are all toooften intimidatedby their statemedical boards,medicalsocieties,orotherpeergroups,allofwhomstilldisapproveof“naturalremedies.”

Fortunately, like therestofus, increasingnumbersofmedicaldoctorsarebeginning to see through the smoke and mirrors offered up by thegovernment/patent medicine company complex. Many of these doctors havetakenituponthemselvestolearnaboutnaturaltreatmentsforindigestionandtorecommend these to their patients in preference to expensive, patented, andpotentiallydangerouspharmaceuticalproducts.

Thequickestandmostefficientwaytofindaknowledgeable,open-mindeddoctor is to locate one who is a member of the American College forAdvancement in Medicine (ACAM). All members of this professionalorganizationareskilledandknowledgeableintheprescriptionanduseofvariousnutritional, herbal, and botanical products. ACAMmembers have studied andlistened to discussionsbydozensof experts (even includingmyself [JVW]onoccasion)concerningthebiochemistry,effects,andusesofthesesubstances.ForareferraltoanACAMdoctornearyou,contactACAMat:

AmericanCollegeforAdvancementinMedecineTelephone:1(800)532–3688

Address:23121VerdugoDrive/Suite204,LagunaHills,CA92653Internet:http://www.acam.org

OtherMedicalAlternatives

Although the AMA would probably like you to believe otherwise, there are

qualified medical professionals who have letters other thanM.D. after theirnames. Many of these doctors, known as naturopaths, along with a fewnaturally-orientedosteopaths,tendtohaveafarbetterunderstandingofnormaldigestivefunctionandhowtohelprestoreit,andtheyusuallyhaveconsiderablymoreexperienceinusingnaturalalternativesthantheaverage“regular”M.D.

NaturopathicPhysicians

Naturopathic medicine is based on the belief and observation that the humanbody possesses enormous power to heal itself when given the correct naturalmaterialsandenergies.

After earning an undergraduate degree (B.A. or B.S.), including pre-medical requirements such as chemistry, biochemistry, biology, and physics,naturopathic physicians go on to a four-year, graduate-level, accreditednaturopathic school of medicine, where upon graduation, they earn an N.D.degree.N.D.’sareeducatedinallthesamesciencesasM.D.s,althoughwithlessemphasis on drugs, radiation, and surgery, and much more emphasis onnutrition, botanical remedies, manipulation, homeopathy, acupuncture,psychology, andotherholistic andnontoxic therapies.Naturopathicphysiciansplace strong emphasis on disease prevention, lifestyle change, and optimizingwellness.

Before licensure, naturopathic physicians must complete at least four-thousand hours of study in specified subject areas, and then pass a series ofrigorousprofessionalboardexams.

Although naturopathic physicians can be found in every U.S. state andCanadian province, they’re currently licensed by state boards only in Alaska,Arizona,Connecticut,Hawaii,Maine,Montana,NewHampshire,Oregon,Utah,Vermont,andWashington,IntheDistrictofColumbia,naturopathicphysiciansmust register to practice. In Canada, naturopaths are licensed in BritishColumbia,Manitoba,Ontario,andSaskatchewan.

To locate a naturopathic physician, contact theAmericanAssociation ofNaturopathicPhysicians(AANP)at:

AmericanAssociationofNaturopathicPhysiciansTelephone:(703)610-9037Fax:(703)610-9005PostalAddress:8201

GreensboroDrive,Suite300McLean,Virginia22102

Internet:http://www.naturopathic.org/

OsteopathicPhysicians

After earning an undergraduate degree (B.A. or B.S.), doctors of osteopathicmedicine graduate from a four-year osteopathic medical school with a D.O.degree.Theirtrainingandaccreditationissimilartothatwhichmedicaldoctorsreceive. Most osteopaths are primary care physicians, but many specialize insuch areas as internal medicine, surgery, pediatrics, radiology, or pathology.Residencies in these areas typically require an additional two to six years oftrainingbeyondmedicalschool.

Although many D.O.’s are members of the AMA, generally they differfromM.D.’sintheiremphasisonthe“wholeperson”andapreventiveapproachto the practice of medicine. Rather than treating specific symptoms, as manyconventional “allopathic”M.D.’s usually do, aD.O. is trained to focus on thebody’s various systems—particularly the musculoskeletal system—and howtheyinteractwitheachother.AlthoughD.O.’scananddoprescribeconventionaldrugs, they are more likely to be open to and knowledgeable about naturalremedies.

Osteopaths are licensed in all U.S. states and Canadian provinces topractice medicine and prescribe drugs. To find an osteopath, a good startingpoint is the American Osteopathic Association (AOA) or the CanadianOsteopathic Association. However, it’s always wisest to ask any osteopath’sofficewhetherthephysicianusesnaturaltherapies,asthemajoritystilldonot.

AmericanOsteopathicAssociationTelephone:(800)621–1773

Fax:(312)202–8200PostalAddress:142E.OntarioStreet,Chicago,IL60611–2864

Internet:http://www.am-osteo-assn.org

CanadianOsteopathicAssociationPostalAddress:575WaterlooStreet,London,Ontario,N6B2R2

Telephone:(519)439–5521

CompoundingPharmacists:BacktotheFuture

Another excellent source of information and useful therapeutic products is thegrowing number of compounding pharmacies in the United States.

Compoundingpharmacists can prepare naturalmedications andherbs for eachpatient according to their doctor’s prescription in the form best suited to thepatient’s individual needs. Although they cannot diagnose illnesses, they canoffervaluableadvicetobothphysiciansandpatients.

In the centuries before the patent medicine industry took over themanufacturing of nearly all drugs, all pharmacists were compoundingpharmacists.Asrecentlyastheearly1940s,mostdrugsandnaturalcompoundswereprepared thisway.By the1990s,mostpharmacistshadbeenrelegated totheroleofpillcounters.

Aseveryoneknows,thecurrentsystembasicallyworkslikethis:thedoctorwritesaprescriptionforastandardizedcommercialdruglikePrilosecandeithercallsthepharmacistorgivestheprescriptiontothepatient,whothenhandsittothepharmacist at the local drug store.Thepharmacist,whokeeps a supplyofPrilosecpillsonhand,readstheprescription,grabsaboxofftheshelf,sticksalabelwiththepatient’snameanddosinginstructionsonit,fillsitwithpills,andhandstheboxtothepatient.Inmanycasesavendingmachinecoulddothejobjust aswell (some“advanced”pharmacies actuallyhavemachines that do thiswithpopulardrugs.)

Fortunately, compounding pharmacies have been undergoing a rebirth,caused by rapidly growing public demand for more natural and moreindividualizedhealthcare,andbyeconomicnecessity for the traditional, smallpersonal-service pharmacy. Consumers are increasingly dissatisfied with“nothing but drugs” and are seeking out natural remedies in ever-increasingnumbers. Many drug-prescribing doctors are increasingly frustrated with thelimited selection of “approved” drug preparations and are working withcompounding pharmacists in growing numbers to develop unique preparationsand “delivery systems.” Many small, traditional, personal-service pharmacieswereliterallybeingdrivenoutofbusinessbycost-cuttinginsurancecompanies,managedcareorganizations,andHMOsthatsigncontractswithgiantdrugstorechainstoprovidemassivequantitiesofdeeplydiscounteddrugs,orevenopeningtheir ownmail-in drug outlets.With rapidly increasing consumer demand, thepath to economic survival for smaller personal-service pharmacies becameobvious:areturntotraditionalpharmaceuticalcompounding.

Today’s compounding pharmacists can produce literally “whatever thedoctor orders,” usually in a variety of forms that best suits the individualpatient’s needs. The pills, capsules, creams, and other forms produced by acompoundingpharmacistarevirtuallyindistinguishablefromthemass-producedvariety, except that they usually do not comewith the chemical colorings andshapes the pharmaceutical industry uses to distinguish its products from the

competition and discourage “counterfeiting.” As an added “bonus,” acompounding pharmacist can leave out all unnecessary chemical flavors,preservatives,andadhesives(inpatchproducts),aswellascoloringchemicals,andcanindividualize“bases”accordingtoapatient’sallergiesandsensitivities.

Thequalityofindividuallypreparednaturalhormonesordrugsproducedbyacompoundingpharmacistisgenerallyexcellentforseveralreasons:

• Compounding pharmacists are often more extensively educated thanpharmacistswhoare just“pill-counters.”They’ve takenspecial traininginmoderncompoundingmethods.

• They have that extra motivation borne of having to satisfy eachindividual customer for their individualized prescription. A primarymotivation formany noncompounding pharmacists is keeping a “third-partypayer”happy.“Happiness”forthird-partypayersalwaysmeansthelowest price possible, with “patient satisfaction” a very secondaryconsideration.

• Every compounding pharmacy is licensed and inspected by its StatePharmacyBoard,justlikeallotherpharmacies.

•Materialsusedbycompoundingpharmaciesarethesamequalityusedbythemajor pharmaceutical companies. All materials used are subject toFDAinspectionandtheagency’sGoodManufacturingProcedurescode.

It’snosurprisethattheFDAandthepharmaceuticalindustrywouldliketoseecompetitionfromcompoundingpharmacistseliminated,andtheyhavemadesignificanteffortstosquashthisvaluablehealthresource.Sofar,thisrepressionhas been stalled in Congress and the courts, thanks to the vigorous efforts ofrepresentatives of the compounding pharmacists, knowledgeable medicalprofessionals and consumers, andothers concernedwith preservingoneof thelastoutpostsofhealthcarefreedomintheUSA.

HowtoLocateaCompoundingPharmacist

Compounding pharmacies are located all over the country, and finding onenearbyisnotdifficult. If there isnocompoundingpharmacynearby,nearlyalltransactionscanbecarriedoutviamail,phone,and/orfax.

Theeasiestwaytolocateacompoundingpharmacististocontacteitherthe

ProfessionalCompoundingCentersofAmerica,Inc.(PCCA)ortheInternationalAcademyofCompoundingPharmacists(IACP).

PCCA provides compounding pharmacists with support in the form oftraining, equipment, chemicals, and technical consultation on difficultcompoundingproblems.Atpresent,morethannineteen-thousandcompoundingpharmacists in the United States, Canada, Australia, and New Zealand aremembers of PCCA. For information about PCCA, including a listing ofcompoundingpharmacists,youcancontactthemat:

ProfessionalCompoundingCentersofAmericaTelephone:(800)331–2498

Fax:(800)874–5760Postaladdress:9901SouthWilcrestDrive,Houston,TX77099

Internet:http://www.pccarx.com/TheLACPcanbecontactedat:

InternationalAcademyofCompoundingPharmacistsTelephone:(800)927-4227

Fax:(281)495-0602PostalAddress:POBox1365,SugarLand,TX77487

Internet:http://www.iacprx.org/

*It’snothardtobelievefromthemanufacturer’spointofview,though.Withitspatentabouttorunoutandwithevenmorepowerfuldrugscomingdown thepipeline,Prilosec isaperfectcandidate to joinZantac,Pepcid,andtheother“has-been”acidsuppressorsondrugstoreandsupermarketshelves—atrulychillingprospect!

*ThereareoccasionswhentherisksrelatedtoHClreplacementmaybehigherthanwewouldlike.Inthesecases,aslongasthepotentialbenefitsoutweightherisks,Imaystillrecommendthetreatment.However,beforestarting,Ialwaysexplainthepossiblerisks,benefits,andprecautions.OncepatientsstartonHCl,Ialwayscarefullymonitorthecourseoftherapy.

*Forexample,withtheintensesweetenerstevia.—JVW

*Licoricerootshouldnotbeconfusedwithlicorice-flavoredcandy,whichmayormaynotcontainlicoriceextract.

† Prostaglandins are further categorized as “anti-inflammatory” (frequently thought of as “good”prostaglandins)and“pro-inflammatory”(frequentlythoughtofas“bad”prostaglandins).

*Thereisconcernthattakingintoomuchsodiumcancausehighbloodpressureinsomepeople.However,researcherswho have compared sodium chloride, sodiumbicarbonate, and sodium ascorbate have found

that only sodium chloride (table salt) raises blood pressure and sometimes causes edema. Sodiumbicarbonateandsodiumascorbatedonot.

*Sources ofmastic-based products includeLifeEnhancement Products, Petaluma,California,www.life-enhancement.com; Francesco Sirene, Spicer, Peachland, British Columbia, Canada,www.silk.net/sirene/spices.htm; Liberty Natural Products, Portland, Oregon, www.libertynatural.com;Allergy Research Group/Nutricology.com, 30806 Santana Street, Hayward, California 94544,www.nutricology.com.

* In this example,weare temporarily ignoring the adverse effectsof acidblockerson fish and all otheroceaniclifeforms.

APPENDIX1

IsDepressiontheResultofanAminoAcidandNeurotransmitterDeficiency?

Depression is never caused by a deficiency of drugs! After working withindividuals suffering from depression, I am convinced that a considerableproportion of “clinical depression” is caused simply by a deficiency ofneurotransmitters, which are (mostly) made from amino acids.(Neurotransmittersarethemoleculesthat“carrythemessages”fromoneneuron[nervecell]tothenext.)

If an individual’s history includes a “favorable response” to anantidepressant medication, we can be quite confident that a combination ofnutritional therapies centering on essential amino acids will eliminate thedepressionevenbetterthanthepatentmedicationdid,andwithvirtuallynosideeffects.Even if thepatentableantidepressantdrug iscurrentlybeing taken, theuse of an individualized combination of essential amino acids and othernutritional therapies will almost always allow a gradual “tapering off” of thepatentmedicationwithoutrecurrenceofthedepression.

Fordepressed individualswho’venot takenpatentmedications, this sametreatmentislikelytobejustaseffectiveinahighpercentageofcases.

How can this be? Doesn’t it take millions and “kazillions” of dollars,hundreds to thousands of researchers, and decades to develop effectivetreatments for major individual (and “public-health”) problems such asdepression? That’s certainly true if we’re focusing on patentablemedications,butifwefocusinsteadonthebiochemistryofourbodies(inthiscaseourbrainsand nervous systems), and work with what happens naturally (“follow theoriginalblueprints”),it’sreallynotthathardtodoorunderstand.

FreudandElectroshock

Formostofthefirsttwo-thirdsofthetwentiethcentury,medicalstudents(your

author included) were taught that the mental condition called depression is aproblemofpsychologicalorigin.Inmostmedicalschoolpsychiatrydepartmentsfromthe1920sthroughthe1950s,SigmundFreudreignedsupreme.AllmedicalstudentsweretaughtFreud’stheoriesof“ego,superego,andid,”“oral,anal,andsexual,” the “Oedipus complex,” and so on. Depressed individuals weresubjected to psychoanalysis, in which they were instructed in how to (forexample) blame their “controlling” mothers and “distant” fathers for theirpresentdepressedstate.

For “major” depressions beyond the reach of Freud and psychoanalysis,“electroshock” therapy (ECT, electroconvulsive therapy)was sometimes used.Asdepressionhadnot(andtothisdayhasnot)beenshowntobeduetoalackofconvulsion-causing high-voltage electricity in the brain, ECTwas not terriblyrationalorhelpfulbutwasusedanywayforlackofanythingbettertodo.

PatentMedications

Within a remarkably short time after the marketing of the first “moderngeneration” of patented antidepressant medications, Sigmund Freud’sexplanations for depression underwent an abrupt decline in popularity; ECTfaded intowell-deservedobscurity. It suddenlybecame fashionable (yes, thereareasmany“fashions”inmedicineasinanyotherfieldofendeavor)todescribedepressionasa“biochemicalillness.”(Ifnot,howcouldanyonejustifytheuseofpatentmedications—chemicals—to“correct”a“psychological”problem?)

MonoamineOxidaseInhibitors

Oneofthefirstcategoriesofpatentedchemicalantidepressantsweremonoamineoxidase(MAO)inhibitors.Aprincipaleffectofthesechemicalsistoinhibittheenzymeafterwhichthey’renamed,monoamineoxidase.SinceMAOisactiveinthe normal breakdown of certain neurotransmitters (including dopamine,norepinephrine, epinephrine, tyramine, tryptamine, and 5-hydroxytryptamine,alsoknownasserotonin),inhibitionofMAOresultsinhigherlevelsofalltheseneurotransmitters. If these neurotransmitters aren’t broken down as much asusual, theywill,ofcourse,accumulateathigherlevelsandstayat thesehigherlevels as long as theMAO inhibitor drug is taken.Depressionwas apparendyimprovedbyraisinglevelsoftheseneurotransmitterswithMAOinhibitors.Butas patentable molecules never before found present in human bodies, MAOinhibitorshadalongandlamentablelistofunwantedsideeffects.

TricyclicAndidepressants

Thenextmajorcategoryofpatentedantidepressantchemicalstoappearwasthetricyclics (named because of the three-ring-shape of their molecules). Themechanism(ormechanisms)ofactionof thevarious tricyclicswasn’tasclear,butonemajortextbookofthetimenotedthatthesedrugsblockedthe“reuptake”of theneurotransmitternorepinephrinebynervecells (paralleling theactionofthe“SSRI”drugsnotedlater).Whileblockingneurotransmitterreuptakedoesn’tincreasethelevelof thatneurotransmitter, itdoesallowitdoits jobfor longerthanitordinarilywould.

NeurotransmittersandTheirCycles

Let’s digress for a brief description of neurotransmitter production and thenormal “neurotransmitter reuse cycle.” The very large majority ofneurotransmitters aremade by nerve cells (neurons) from amino acid startingmaterials (“precursors”). For example, the essential amino acid phenylalanineand the nonessential amino acid tyrosine are processed by neurons to makedopamine, epinephrine (also called adrenaline), and norepinephrine(noradrenaline).Theessentialaminoacidtryptophanisaprecursoroftheaminoacid 5-hydroxytryptophan (5-HTP) and the neurotransmitter serotonin. Thenonessential amino acid histidine is precursor of histamine (which is aneurotransmitter as well as a participant in allergic reactions). One majorexception to the “neurotransmitters are made from amino acids” rule isacetylcholine, which is made in neurons from choline, a naturally occurringmetaboliteoflecithin.

Onceproduced,neurotransmittersarestoredintheneuronsthatmadethemuntilthey’reused.“Use”consistsofreleaseintothespace(thesynapse)betweenthe “producing” or “stimulating” neuron and an adjacent “receiving” neuron.(All neurons can be “stimulating” or “receiving” or both, depending on thecircumstances.) Released into synapses from the “stimulating” neurons thatproducedthem,neurotransmittersthenstimulatetheadjacent“receiving”neuroninto action. But the neurotransmitters aren’t physically transported into the“receiving”neurons.Instead,somemoleculesstimulatethe“receiving”neuron’souter membrane, and then (in one of nature’s many, many cycles) the largemajorityarereabsorbedbytheneuronsthatproducedtheminthefirstplace,andstored again for the next use. Only a small percentage of secretedneurotransmittermoleculesare“brokendown”andmetabolizedawayeachtime

they’reused.Remember how MAO inhibitors are thought to act? The enzyme

monoamine oxidase “waits” in synapses for the secretion of monoamineneurotransmitters, such as those named earlier, and “breaks down” a smallproportionofthemsotheycanneitherbereabsorbedintotheneuronsthatmadethemnorcontinuetostimulatethe“receiving”neurons.Apparendy,eventhoughthisenzymebreaksdownonlyasmallpercentageofneurotransmitterseachtimethey’resecreted,blockingthatsmall-percentagebreakdownisenoughtoproduceaclinicaleffect.

SelectiveSerotoninReuptakeInhibitors

The 1990s rage in antidepressant patent medications has centered on the“selective serotonin reuptake inhibitors” (SSRIs), the prototype of which isProzac.(WerememberalltoowellastatementfromthefrontpageoftheWallStreetJournal,whichstatedthattherewasa“goldmine”[phraseactuallyused]indrugsthatworkedbyalteringserotoninlevelsinourbodies.)Rememberthatneurotransmitter cycle? SSRIs work by selectively blocking the reabsorption(reuptake)of theneurotransmitterserotoninintotheneuronsthatproducedandsecreted it.The effect is to leave the serotoninmolecules in the synapse for agreater-than-natural time period, where, of course, they will continue tostimulate the “receiving”neurons for longer than isnormal.Since serotonin isgenerally a “mood-elevating” neurotransmitter, the individual taking the SSRIwill likely feel less depressed. Unfortunately, the list of unwanted SSRI sideeffectsislongandserious.

Nature’sAlternatives

It appears that bothMAO inhibitors andSSRIs (and possibly the tricyclics aswell) exert a major proportion of their antidepressant activity by artificiallyincreasing the number of neurotransmitter molecules in the synapses betweenneurons,andpossiblyprolongingtheirlengthofactivity.Howdoesnaturedothesamethingwithouttheuseofpatentablemolecules?

Very simply: by making more neurotransmitters in the first place, andputtingmoreofthemintothesynapses.Iftherearemoreneurotransmittersmadeandsecretedintothesynapsesbythe“producing”neurons,thenthe“receiving”neuronswillbestimulatedbetter(betterbecausetherearemoreneurotransmittermolecules) and longer (longer because it takes a longer time to reabsorb a

greaternumberofneurotransmittermolecules),anddepressionwillberelieved,ornothappeninthefirstplace!

Whenworkingwithan individualwithdepression, Iprefer torecommendindividualizedcombinationsofalleightessentialaminoacids. (Whensuppliedwithallotheressentialnutrients—vitamins,minerals,essentialfattyacids—ourbodies can usually take these “eight essentials” and turn them into all thehundreds of other amino acids—and most of the neurotransmitters—that ourbodies require.) However, for purposes of preliminary illustration, we’ll firstconsidertheuseofsingleessentialaminoacids,tryptophanandphenylalanine.

Tryptophan is metabolized into serotonin, the previously noted “moodelevating”neurotransmitter.Onemightimmediatelysuspectthatbytakingextraquantities of tryptophan, an individual could raise his or her own levels ofserotonin and consequently lessen or abolish depression in some cases,especiallythosecasesaffectedbySSRIdrugs.Thatsuspicionwouldbecorrect:Inthelastyeartryptophanwasavailableforpublicpurchase,nearly14millionindividuals bought nearly $200 million worth of tryptophan capsules (atapproximately$15perbottleversusover$100perbottleforsomeSSRIs),andthe“growthcurve”fortryptophansaleswasclimbingexponentially.Byraisinglevels of serotonin following “Nature’s way,” and without side effects,tryptophanpurchasersweremakingaseriousdentinthemarketforProzacandotherpatentedSSRIs.

Atthispoint,we’llpausetoreflectonthewordsofoneofourhighlypaidpublicservants:

“… Pay careful attention to what is happening [with dietary supplements] in the legislativearena … there could be created a class of products to compete with approved drugs … theestablishment of a separate regulatory category for supplements could undercut exclusivity rightsenjoyedbyholdersofapproveddrugapplications.”

—DavidAbrams,FDADeputyCommissionerforPolicy,

D-C-ATanSheet11,July19,1993

Clearly, the use of an unpatentable amino acid to (in many cases) relievedepression effectively, inexpensively, andwithout side effects just isn’t “FDApolicy,”andsomethinghadtobedone.Byinexplicablecoincidence,justasthesituation was looking grim for the profits of manufacturers of SSRIs, the“tryptophan contamination episode” occurred, and tryptophan was removedfromtheopenmarket.Permanently.

Idonotmakelightofthe“tryptophancontaminationepisode.”Nearlyfortypeople died, hundreds were made seriously ill, and some have still not

recovered. But once the cause of the problemwas found (at theMayoCliniclaboratories and elsewhere), tryptophan never returned for public purchase.(Presendy,it’savailableonlybyprescriptionthroughcompoundingpharmaciesatapproximately three times thepriorprice.Asnoonehasbecome illordiedfrom prescription tryptophan, one might wonder why an over-the-counterversionofthisessentialaminoacidshouldbedangerous.Butthat’satopicmorethan adequately addressed by FDA Deputy Commissioner Abrams, or hissuccessors.)

Back to neurotransmitters: Phenylalanine is converted by neurons intonorepinephrine(andepinephrine).Someindividualshavefoundthattakingextraquantitiesofphenylalaninerelievestheirdepressionandeven“energizes”them.Although individuals with the genetic disease phenylketonuria (PKU) cannottoleratephenylalanine,intherestofus(over99percent),noserioussideeffectsof phenylalanine ingestion have been reported, and phenylalanine has had (sofar)no“contaminationepisodes.”Manyindividualsusethenonessentialaminoacidtyrosineforthissamepurpose:Tyrosineisametaboliteofphenylalanineonthe“pathway”tonorepinephrineandepinephrine.

Obviously, individual aminoacids suchas tryptophan,phenylalanine, andtyrosine can be used to safely raise levels of neurotransmitters and relievedepression.WhydoIinsistonindividualizedcombinationsofalleightessentialaminoacidsinstead?Putsimply,it’sbecause,atthepresenttime,“we”(science)don’tknowenoughabouttheincrediblecomplexitiesofbrainbiochemistry!(Forexample,howmanyofushavereadorheardabouttheuseoftheessentialaminoacidthreonineasatreatmentfordepression?AccordingtoDr.EricBraverman,whenhewasworkingwith thefamousDr.CarlPfeifferat thePrincetonBrainBioCenter,itwasfoundthatthreoninewashelpfulfor18percentofdepressedindividuals.) But even though “science” doesn’t know asmuch as it needs toaboutwhichessentialaminoacidsdowhat (andhowtheydowhat theydo) inthebrain,Naturedoesknow.

So how do I presume to know precisely (or even semiprecisely) exactlywhatNatureknowstogetthejobdone?HowdoIpresumetoknowexacdytherightamountofeachessentialaminoacidforeachdepressedindividual?

I don’t know. I ask, every time. And the answer is different for everyindividual.

Beforethisbeginstosoundjusttoopreposterousforwords,Iimmediatelyadmitthatthe“asking”isdonebyveryconventionalmeans:abloodtest.

As part of the laboratory evaluation of individuals suffering fromdepression, I request a “fasting plasma essential amino acid” determination.(TestingisdoneeitheratMeridianValleyLaboratories,Kent,Washington[253-

859-8700;http://www.meridianvalleylab.com],forwhomIamaconsultant,oratMetaMetrixLaboratories,Norcross,Georgia [770-446-5483],withwhom I amnotaffiliated.)Veryfrequendy,thetestreportshowsthattwo,three,ormore—occasionally all eight—essential amino acids are lower than the normal range.Less frequendy, one or two of the essential amino acids are higher than thenormal range. Using a previously determined “optimum” number for eachessential amino acid (an “optimum” derived from testing many nondepressedindividuals), a calculation is performed to determinewhat percentage of eachaminoacidislikelytohelp“balance”allessentialaminoacidsat“optimum”forthat individual. (Another thing“science”hasverylittleknowledgeabout is theeffects of “relative balance” of one amino acid to another; once again, I amguidedbyNature andwhat’s foundnaturally in nondepressed individuals.)Ofcourse,thecalculationyieldsdifferentresultsforeverydepressedindividual,asnotwohaveexactlythesamebloodtestresults.

Next, I recommendaquantityof thebalanced-for-that-individualblendofall eight essential amino acids, ranging from a minimum of 5 to a usualmaximum of 15 grams daily. (Tryptophan presently must be prescribedseparately and added by each individual to his or her own individualizedcombination, as the companies that supply individualized amino acidcombinations cannot legally do so. The “tryptophan problem” can also behandledbyworkingwithacompoundingpharmacist,butthissolutionisusuallymoreexpensive.)

HOWLOWSTOMACHACIDMIGHTCAUSEDEPRESSION

lowstomachacid

reducedabsorptionofessentialaminoacids

neurotransmitter(serotonin,norepinephrine)deficiency

depression

Fiveto15grams?That’s…5,000to15,000mgaday!Isn’tthattoomuch?The previously-termed “RDA” (officially, “recommended daily

allowance”;unofficiallyandirreverently,“recommendeddeficiencyallowance”)

for“gramsofcompleteprotein”rangedfrom50to60gramsdaily,dependingonwhetherornotone lived in India (nokidding!).Remembering that abalancedcombinationofalleightessentialaminoacidsisequivalentgram-for-gramwith“completeprotein,”it’sobviousthat5to15gramsisasmallfractionofeventheRDA,andwon’t“overdose”anyone,especiallyifatestshowsdeficiencybeforestarting.Inmyexperience,5gramsdailyisanabsoluteminimum,and10to15gramsdailyismorelikelytobeeffective,andalsomorequickly.

Althoughthere’snowayatpresenttomeasuredirectly,theoverwhelminglikelihoodis that lowlevelsofoneormoreessentialaminoacidsresult in lowlevels of one or more neurotransmitters, with resulting varying degrees ofdepression. It’s also overwhelmingly likely that normalizing low levels ofessential amino acids contributes gready to the elevation of levels of theneurotransmitters of which amino acids are precursors (remember, choline toacetylcholineisamajorexception),andthustothedisappearanceofdepression—especially (but not limited to) those depressions “favorably” influenced bypatentablemedicationsthatalsoactonneurotransmitters!

Howoftendoesthisnatural“individualizedcombinedessentialaminoacid”treatment approach to depressionwork?Although I have no research grant tohelpcompileexactstatistics,experienceshowsthatitwillhelpover50percentofdepressedindividuals,whichisequaltoorbetterthanthenumbersgenerallyclaimed for antidepressant drugs.All it takes to predict success is the “fastingplasmaessentialaminoacid”test.Ifnoessentialaminoacidsarelow,replacingthem is not very likely to be helpful; the lower the essential amino acids, themorelikelythatnormalizingthemwilldothejob.

What,NoSt.John’sWort?

Aidedmightilybythemedia,manyhavetheimpressionthatSt.John’sWortisthemajor“alternative”treatmentfordepression.Although,thereisnodoubtthatSt. John’sWort is often effective, it should actuallybeoneof the last naturaltreatmentstotry.

A basic principle of nutritional and natural medicine is always use therelevant essential nutrients first, before turning to or adding other naturaltreatments,whetherherbaloranyothertype.Thereasonissimple:Sinceeveryessentialnutrienthasdozensofpurposesinourbodies,ifwehaveaneedforanessential nutrient for one purpose we happen to know about, the chances arenearly 100 percent that we have a need for that essential nutrient for otherpurposes,whichwemayormaynotknowabout.Justasweshouldalwaysuse

zinc and essential fatty acids for the prostate beforewe add sawpalmetto,weshould always explore the use of essential amino acids (and other essentialnutrients) for depression before turning to or adding St. John’s Wort. To beclear:IamnotopposedtotheuseofSt.John’sWort.Iaminfavor,aslongasallessentialnutrientsare“covered”first.

WhyAretheEssentialAminoAcidsLow?

As we discuss in detail in this book, the usual reason is poordigestion/assimilation,withhypochlorhydria(lowstomachacid)mostfrequentlypresent.

InSummary

Forthereasonsstatedabove,Iamconvincedthatinalargepercentageofcases,depressionistheresultofaneurotransmitterdeficiencywhichismostoftendueto low stomach acid. In over 50 percent of cases, depression is treatable bysupplying (relatively) large quantities of the essential amino acids needed byeach depressed individual, alongwith any supporting nutrients ormetabolites.Ultimately, correction of depression in these cases can be achieved bycompensatingforfaultydigestion.

APPENDIX2

AreOurFacesRed?AcneRosaceaandLowStomachAcid

OneofDavidFlanagan’sproblemswasobvious.Hisentirefacewasshinyand pinkish red,more pink around the edges andmore red and shiny on andaround his nose and the central areas of his face. There were a few smallnodules scattered at random on his forehead, cheeks, and chin, and anunfortunatelylargeroneontheendofhisnose.

“I’m here from Chicago,” he said. “And you can see why! I’ve had thisrosacea’ thingsince Iwas twenty-twoor twenty-three,and I’mforty-onenow.I’vehadmoretetracyclinethanIcanremember,andithelpswhenItakeit,butit’sbeenhelpinglessandlessthelastfewyears.Iaskedmydermatologistaboutcortisone ointment or cream, but she said if I kept using it for a chronic skinconditionlikethis,myskinwouldjustthinout.She’striedotherantibiotics,buttheydon’tevenworkaswellasthetetracycline.Somyfacejustkeepsgettingredder and redder, and now I just use the tetracyclinewhen the pimples”—hepointedtohisnose—“getparticularlybad.”

“Likenow?”“Yeah,thoughIhaven’tgottenasmanybadoutbreaksasI’vegottenolder.”“Anyotherproblemswithyourhealth?”“Notreally.”“Anyheartburn,gas,indigestion?”“Yeah,butnomorethanalotofotherguysmyage.Besides,thathappens

morewhenIovereat.”“Tired?”“Idon’tthinkso.‘CourseI’mnotasfullofenergyaswhenIwasyounger.”I asked other questions about possible symptoms; his answers were

negative.Afterhisphysicalexam,wereturnedtomyoffice.“So,whatvitaminsshouldItake?That’swhyI’mherefromChicago.My

wifesaysyourclinicdoesalotwithvitaminsandmineralsandherbsandall,andthat’sanapproachIhaven’t tried. If Ineed tostaya fewdays, that’sOK,I’mstayingwithmybrotherhereinSeattle.”

“You’lljustneedadayortwoatmost,”Isaid.“You’llneedtohaveyourstomachtested…”

“Mystomach?Therosacea’sonmyface.”“Iknow.Butyourfaceisreflectingagastrointestinalproblem.”“Heckofareflection…soifrosacea‘reflectsagastrointestinalproblem,’

howcomenoonetoldmethatbefore?Besides, thisgasandheartburnthingisminor,andjuststarted.I’vehadthisrosaceathingforyears.”

“Idon’tknowwhynoonetoldyou,”Isaid.“Ihaveanarticlepublishedin1948 that says ‘every dermatologist knows’ about stomach malfunction—specificallylowornostomachacid—incasesofrosacea.”

“Nostomachacid?What’sthatgottodowithmyface?”“What’stetracyclinegottodowithyourface?”“Killsgerms,Iguess.”“Wherearethegerms?”“Inthesepimplethings.”“Howaboutalltheredskininbetweenthepimples…orwhenyoudon’t

evenhavepimples?Therednessofyourskindoesn’tgoawaythen,doesit?”“Notreally,Iguess.Sowherearethegerms?”“Don’t know for certain, but I can guess. When you swallow the

tetracycline,wheredoesitgo?”“Mystomach.…”“Andintotheintestinesafterthat.Biggestreservoirofbacteriainthewhole

body, the intestines, especially the colon. And if we don’t have stronghydrochloric acid produced by our stomachs, the entire pH—the acid-alkalinebalance—of the intestines and colon is shifted more alkaline. When thathappens,“unfriendly”germsaremorelikelytogrow.”

“Andmaybethat’swhytetracyclineworks,atleastsome?”“That’s my guess. It’s also probably why several hydrochloric acid and

pepsincapsulestakenwitheverymealhelpcontrolrosaceaaswellasorbetterthantetracycline.”

“BecausethehydrochloricacidchangesthepH—theacidity—backtowardsnormal,andthe‘unfriendly’germscan’tgrowaswell?”

“Exactly right.Andwegetevenbetter resultswhenweuseLactobacillusacidophilus—thoseare‘normal’acid-lovingbacteria—aswell.”

“That’scertainlyadifferentapproach.”

“Almost always works, though. Also, we add injections of vitamin B12,which isn’t absorbed aswell when our stomachs aren’tworking, orwhenwehave ‘bacterial overgrowth’ in the intestines. And as long as we’re injectingvitaminB12,weputtheotherBvitaminsinthere,too,especiallyvitaminB2.”

Likemostpeoplewithacnerosacea,Mr.Flanaganhadverypoorstomachfunction.Aftertwoyearsofreplacementhydrochloricacid-pepsincapsuleswithmeals,Lactobacillus acidophilus, andB12 withB complex injections, he flewbackinfromChicagotovisithisbrotheragain,andcamebytoshowusthathisskinwasalmostnormal“forthefirsttimeintwentyyears.”

NOTES

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7. Anon.Diarrhea, skin reactions, and headache following omeprazole(Losec,Astra)therapy.CurrProb.1991;June(31).

8. Ricci RM,DeeringKC. Erythema nodosum caused by omeprazole.Cutis.1996,57:434.

9. Buckley C. Pityriasis rosea-like eruption in a patient receivingomeprazole.BrJDermatol.1996,135:660–661.

10. KrausA,Flores-SuarezLF.Acutegoutassociatedwithomeprazole.Lancet.1995,345:461–162.

11. LindquistM,EdwardsIR.Endocrineadverseeffectsofomeprazole.BrMedJ.1992,305:451–452.

12.Prilosec(omeprazole).PrescribingInformation.2000:Merck&Co.,WestPoint,PA19486.

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4.HaleP.Personalcommunication.AstraMerck,Wayne,PA.1997.

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5. Prilosec (omeprazole).Prescribing Information.2000.Merck&Co.,WestPoint,PA19486.

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8.Lanzon-MillerS,PounderRE,HamiltonMR,etal.Twenty-four-hourintragastric acidity and plasma gastrin concentration in healthysubjects and patients with duodenal or gastric ulcer, or perniciousanaemia.AlimentPharmacolTher.1987,1:225–237.

9. Solcia E, Rindi G, Havu N, Elm G. Qualitative studies of gastricendocrinecellsinpatientstreatedlong-termwithomeprazole.ScandJGastroenterolSuppl.1989,166:129–137.

10.LambertsR,CreutzfeldtW,StruberHG,BrunnerG,SolciaE.long-termomeprazoletherapyinpepticulcerdisease:gastrin,endocrinecellgrowth,andgastritis.Gastroenterology.1993,104:1356–1370.

11.CreutzfeldtW,LambertsR.Ishypergastrinaemiadangeroustoman?ScandJGastroenterolSuppl.1991,180:179–191.

12.MertzH.Helicobacterpylori:Itsroleingastritis,achlorhydria,andgastric carcinoma. In:Holt P, Russell R, eds. ChronicGastritis andHypochlorhydria in the Elderly, pp. 69–82. Boca Raton, FL: CRCPress.1993.

13. Brunner G, Creutzfeldt W, Harke U, Lamberts R. Therapy withomeprazole in patients with peptic ulcerations resistant to extendedhighdoseranitidinetreatment.Digestion.1988,39:80–90.

14. LambertsR,CreutzfeldtW,StockmannF, JacubaschkeU,MaasS,BrunnerG.Long-termomeprazoletreatmentinman:effectsongastricendocrinecellpopulations.Digestion.1988,39:126–135.

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17. KoopH,KleinM,ArnoldR.Serumgastrinlevelsduringlong-termomeprazoletreatment.AlimentPharmacolTher.1990,4:131–138.

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Absorption in theMonogastric GI Tract (Advances in ExperimentalMedicineandBiology,Vol.249).NewYork:PlenumPress,1993.

7. Bezwoda W, Charlton R, Bothwell T, Torrance J, Mayet F. Theimportanceofgastrichydrochloricacidintheabsorptionofnonhemefoodiron.JLabClinMed.1978,92:108–116.

8. Jacobs P, T B, Charlton R. Role of hydrochloric acid in ironabsorption.JApplPhysiol.1964,19:187–188.

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10.EkenvedG,HalvorsenL,SolvellL.Influenceofaliquidantacidontheabsorptionofdifferent ironsalts.ScandJHaematolSuppl.1976,28:65–77.

11. O’Neil-Cutting MA, Crosby WH. The effect of antacids on theabsorption of simultaneously ingested iron. JAMA. 1986;255:1468–1470.

12. SkikneBS,LynchSR,Cook JD.Role of gastric acid in food ironabsorption.Gastroenterology.1981,81:1068–1071.

13.IvanovichP,FellowsH,RichC.Theabsorptionofcalciumcarbonate.AnnInternMed.1967,66:917–923.

14.CarrollH.Personalcommunication.15.Ibid.16. LazloJ.Effectofgastrointestinalconditionsonthemineral-binding

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19.PedrosaM,RussellR.FolateandvitaminB12absorptioninatrophicgastritis. In: Holt P, Russell R, eds. Chronic Gastritis andHypochlorhydria in theElderly, pp.157–169.BocaRaton,FL:CRCPress.1993.

20. Russell RM, Golner BB, Krasinski SD, Sadowski JA, Suter PM,Braun CL. Effect of antacid and H2 receptor antagonists on theintestinal absorption of folic acid. J LabClinMed. 1988, 112: 458–463.

21.Ibid.22.PedrosaM,RussellR.FolateandvitaminB12absorptioninatrophic

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23. Krasinski SD, Russell RM, Samloff IM, et al. Fundic atrophicgastritis in an elderly population. Effect on hemoglobin and severalserumnutritionalindicators.JAmGeriatrSoc.1986,34:800–806.

24.SteinbergWM,KingCE,ToskesPP.Malabsorptionofprotein-boundcobalamin but not unbound cobalamin during cimetidineadministration.DigDisSci.1980;25:188–191.

25.SaltzmanJR,KempJA,GolnerBB,PedrosaMC,DallalGE,RussellRM. Effect of hypochlorhydria due to omeprazole treatment oratrophicgastritisonprotein-boundvitaminB12absorption.JAmCollNutr.1994,13:584–591.

26.Ibid.27.MarcuardSP,AlbernazL,KhazaniePG.Omeprazoletherapycauses

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28. Koop H. Metabolic consequences of long-term inhibition of acidsecretionbyomeprazole.AlimentPharmacolTher.1992;6:399–406.

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30.WoodR,Serfaty-LacrosniereC.Effectsofgastricacidityandatrophicgastritisoncalciumandzincabsorptioninhumans.In:HoltP,RussellR, eds. Chronic Gastritis and Hypochlorhydria in the Elderly, pp.187–204.BocaRaton,FL:CRCPress,1993.

31. SturnioloGC,MontinoMC,RossettoL,etal. Inhibitionofgastricacidsecretionreduceszincabsorptioninman.JAmCollNutr.1991,10:372–375.

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34.MaltbyE.Thedigestionofbeefproteinsinthehumanstomach.JClinInvest.1934,13:193–207.

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37.SoperH.Theclinicalsignificanceofindicanuria.AmJDigDisNutr.1936,3:564–565.

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46. Cater REd. The clinical importance of hypochlorhydria (aconsequenceofchronicHelicobacterinfection):Itspossibleetiologicalrole inmineral and amino acidmalabsorption, depression, and othersyndromes.MedHypotheses.1992,39:375–383.

47. Champagne E. Effects of pH onmineral-phytate, protein-mineral-phytate, and mineral-fiber interactions. Possible consequences ofatrophic gastritis on mineral bioavailability from high-fiber foods. JAmCollNutr.1988,7:499–508.

48. Champagne E. Possible consequences of reduced gastric acidsecretiononmineralbioavailability fromhigh-fiberdiets. In:HoltP,RussellR,eds.ChronicGastritisandHypochlorhydriaintheElderly,pp.171–186.BocaRaton,FL:CRCPress:1993.

49. Champagne E. Effects of pH onmineral-phytate, protein-mineral-phytate, and mineral-fiber interactions. Possible consequences ofatrophic gastritis on mineral bioavailability from high-fiber foods. JAmCollNutr.1988,7:499–508.

50.ChampagneET.Lowgastrichydrochloricacidsecretionandmineralbioavailability.AdvExpMedBiol.1989,249:173–184.

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11.PeuraD,GuerrantR.Achlorhydriaandentericbacterialinfections.In:HoltP,RussellR,eds.ChronicGastritisandHypochlorhydriaintheElderly,pp.127–142.BocaRaton,FL:CRCPress.1993.

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13. GoldinB,GorbachS.Bacterialovergrowth inatrophicgastritis. In:HoltP,RussellR,eds.ChronicGastritisandHypochlorhydriaintheElderly,pp.143–156.BocaRaton,FL:CRCPress.1993.

14. Theisen J, Nehra D, Citron D, et al. Suppression of gastric acidsecretion in patients with gastroesophageal reflux disease results ingastric bacterial overgrowth and deconjugation of bile acids. JGastrointestSurg.2000,4:50–54.

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19. LewisSJ,FrancoS,YoungG,O’KeefeSJ.Alteredbowel function

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20. Thorens J, Froehlich F, Schwizer W, et al. Bacterial overgrowthduring treatment with omeprazole compared with cimetidine: Aprospectiverandomiseddoubleblindstudy.Gut.1996,39:54–59.

21. GoddardAF,SpillerRC.Theeffectofomeprazoleongastric juiceviscosity,pHandbacterialcounts.AlimentPharmacolTher.1996,10:105–109.

22. PatelTA,AbrahamP,AsharVJ,BhatiaSJ,AnklesariaPS.Gastricbacterialovergrowthaccompaniesprofoundacidsuppression.IndianJGastroenterol.1995,14:134–136.

23.GoughA,AndrewsD,BaconPA,EmeryP.Evidenceofomeprazole-induced small bowel bacterial overgrowth in patients withscleroderma.BrJRheumatol.1995,34:976–977.

24.SaltzmanJR,KowdleyKV,PedrosaMC,etal.Bacterialovergrowthwithout clinical malabsorption in elderly hypochlorhydric subjects.Gastroenterology.1994,106:615–623.

25. FriedM, Siegrist H, Frei R, et al. Duodenal bacterial overgrowthduring treatment in outpatientswith omeprazole.Gut. 1994, 35: 23–26.

26. Theisen J, Nehra D, Citron D, et al. Suppression of gastric acidsecretion in patients with gastroesophageal reflux disease results ingastric bacterial overgrowth and deconjugation of bile acids. JGastrointestSurg.2000,4:50–54.

27.Prilosec(omeprazole).PrescribingInformation.2000,Merck&Co.,WestPoint,PA19486.

28.StevensJ.It’sajungleinthere.BioScience.1996,46:1–5.29. MertzH.Helicobacterpylori: Its role ingastritis,achlorhydria,and

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30. NIH Consensus Conference. Helicobacter pylori in peptic ulcerdisease.NIHConsensusDevelopmentPanelonHelicobacterpyloriinPepticUlcerDisease.JAMA.1994,272:65–69.

31.TheEUROGASTStudyGroup.AninternationalassociationbetweenHelicobacter pylori infection and gastric cancer. Lancet. 1993, 341:1359–1362.

32.ParsonnetJ,FriedmanGD,VandersteenDP,etal.Helicobacterpyloriinfectionandtheriskofgastriccarcinoma.NEnglJMed.1991,325:

1127–1131.33. Logan RP,WalkerMM,Misiewicz JJ, Gummett PA, Karim QN,

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34.KuipersEJ,PenaAS,MeuwissenSG.[Helicobacterpyloriinfectionascausalfactorinthedevelopmentofcarcinomaandlymphomaofthestomach;reportWHOconsensusconference].NedTijdschrGeneeskd.1995,139:709–712.

35. KuipersEJ,UyterlindeAM,PenaAS,etal.Long-termsequelaeofHelicobacterpylorigastritis.Lancet.1995,345:1525–1528.

36.KuipersEJ,UyterlindeAM,PenaAS,etal.IncreaseofHelicobacterpylori-associated corpus gastritis during acid suppressive therapy:implications for long-term safety. Am J Gastroenterol. 1995, 90:1401–1406.

37. KuipersEJ,LeeA,Klinkenberg-KnolEC,MeuwissenSG.Reviewarticle:Thedevelopmentofatrophicgastritis-Helicobacterpyloriandtheeffectsofacidsuppressivetherapy.AlimentPharmacolTher.1995,9:331–340.

38. Kuipers EJ, Thijs JC, Festen HP. The prevalence ofHelicobacterpylori inpepticulcerdisease.AlimentPharmacolTher.1995,9:59–69.

39. Solcia E, Rindi G, HavuN, ElmG. Qualitative studies of gastricendocrinecellsinpatientstreatedlong-termwithomeprazole.ScandJGastroenterolSuppl.1989,166:129–137.

40.KuipersEJ,LundellL,Klinkenberg-KnolEC,etal.AtrophicgastritisandHelicobacter pylori infection in patients with reflux esophagitistreatedwithomeprazoleorfundoplication.NEnglJMed.1996,334:1018–1022.

41. Parsonnet J. Helicobacter pylori in the stomach—a paradoxunmasked.NEnglJMed.1996,335:278–280.

42.HanssonLE,NyrenO,HsingAW,etal.Theriskofstomachcancerinpatientswithgastricorduodenalulcerdisease.NEnglJMed.1996,335:242–249.

43.Prilosec(omeprazole).PrescribingInformation.2000,Merck&Co.,WestPoint,PA19486.

44.39.SolciaE,RindiG,HavuN,ElmG.Qualitativestudiesofgastricendocrinecellsinpatientstreatedlong-termwithomeprazole.ScandJGastroenterolSuppl.1989,166:129–137.

45. Jansen JB, Klinkenberg-Knol EC,Meuwissen SG, et al. Effect of

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46.Lanzon-MillerS,PounderRE,HamiltonMR,etal.Twenty-four-hourintragastricacidityandplasmagastrinconcentrationbeforeandduringtreatment with either ranitidine or omeprazole. Aliment PharmacolTher.1987,1:239–251.

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48.Prilosec(omeprazole).PrescribingInformation.2000,Merck&Co.,WestPoint,PA19486.

49.FrestonJW,BorchK,BrandSJ,etal.Effectsofhypochlorhydriaandhypergastrinemiaonstructureandfunctionofgastrointestinalcells.Areviewandanalysis.DigDisSci.1995,40:50S-62S.

50.Prilosec(omeprazole).PrescribingInformation.2000,Merck&Co.,WestPoint,PA19486.

51.LambertsR,CreutzfeldtW,StruberHG,BrunnerG,SolciaE.long-term omeprazole therapy in peptic ulcer disease: Gastrin, endocrinecellgrowth,andgastritis.Gastroenterology.1993,104:1356–1370.

52.CreutzfeldtW,LambertsR.Ishypergastrinaemiadangeroustoman?ScandJGastroenterolSuppl.1991,180:179–191.

53. MertzH.Helicobacterpylori: Its role ingastritis,achlorhydria,andgastric carcinoma. In:Holt P, Russell R, eds. ChronicGastritis andHypochlorhydria in the Elderly, pp. 69–82. Boca Raton, FL: CRCPress.1993.

54. Jansen JB, Klinkenberg-Knol EC,Meuwissen SG, et al. Effect oflong-term treatment with omeprazole on serum gastrin and serumgroup A and C pepsinogens in patients with reflux esophagitis.Gastroenterology.1990,99:621–628.

55. Brunner G, Creutzfeldt W, Harke U, Lamberts R. Therapy withomeprazole in patients with peptic ulcerations resistant to extendedhighdoseranitidinetreatment.Digestion.1988,39:80–90.

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57. Pounder R, Smith J. Drug-induced changes of plasma gastrinconcentration.GastroenterolClinNorthAm.1990,19:141–153.

58.KoopH,Naumann-KochC,ArnoldR.Effectofomeprazoleonserumgastrin levels: Influence of age and sex. Z Gastroenterol. 1990, 28:603–605.

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60. MertzH.Helicobacterpylori: Its role ingastritis,achlorhydria,andgastric carcinoma. In:Holt P, Russell R, eds. ChronicGastritis andHypochlorhydria in the Elderly, pp. 69–82. Boca Raton, FL: CRCPress.1993.

61.FrestonJW,BorchK,BrandSJ,etal.Effectsofhypochlorhydriaandhypergastrinemiaonstructureandfunctionofgastrointestinalcells.Areviewandanalysis.DigDisSci.1995,40:50S-62S.

62. Bloomfield A, PollandW Anacidity with cancer of the stomach.Gastric Anacidity: Its Relation toDisease, pp. 125–136.NewYork.MacMillan.1933.

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64.SvendsenJH,DahlC,SvendsenLB,ChristiansenPM.Gastriccancerrisk in achlorhydric patients. A long-term follow-up study. Scand JGastroenterol.1986,21:16–20

65. Heatley R, Sobala G. Acid suppression and the gastric flora.Baillière’sClinGastroenterol.1993,7:167–181.

66.Ibid.67. StockbruggerRW,CottonPB,EugenidesN,BartholomewBA,Hill

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68.SoybelD,ModlinI.Implicationsofsustainedsuppressionofgastricacidsecretion.AmJSurg.1992,163:613–622.

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70. Elder JB,GanguliPC,Gillespie IE.Cimetidine andgastric cancer.Lancet.1979,1:1005–1006.

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73. MollerH,NissenA,MosbechJ.UseofcimetidineandotherpepticulcerdrugsinDenmark1977–1990withanalysisoftheriskofgastriccanceramongcimetidineusers.Gut.1992,33:1166–1169.

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75. WormsleyKG.Therapeuticachlorhydriaand riskofgastriccancer.GastroenterolJpn.1989,24:585–596.

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INDEX

Abrams,David,170absorption,56aceticacid,140acetylochoine(ACh),48,168achlorhydria,27,40,105andallergies,112andaminoacids,78andanemia,60andcalciumabsorption,66andfolateabsorption,67andHelicabacterpylori,90andreplacingHCl,138andrheumatoidarthritis,119andstomachcancer,97andvitaminB12acid-alkalinebalance,15,25acids,29barriersto,15,39,83blockersof,11,14,25,158neutralizersof,25reductionof,11acid-suppressingdrugs,11,25,26adverseeffectsof,21andaminoacids,78andironabsorption,63acidtriggers,14,50,82Aciphex,19,28acne,16,41adenocarcinoma,90adrenaline,168Advil,138Age-RelatedEyeDiseaseStudy(AREDS),73

albuterol,110,136alkalis,25,29Alka-Seltzer,19,26allergies,21,41,116aluminum,25hydroxide,26,63magnesiumhydroxidesulfate,26Alzheimer’sdisease,26AmericanAssociationofNaturopathicPhysicians(AANP),160AmericanCollegeforAdvancementinMedicine(ACAM),159AmericanCollegeofCastroenterology(ACG),11AmericanMedicalAssociation(AMA),11,34AmericanOsteopathicAssociation,161aminoacids,14,16,38anddepression,165andgastricatrophy,41andprotein,78Amphojel,26anacidity,40anemia,41.Seealsoiron-deficiencyanemiaantacids,13,25,63,158antiaging,16antibodies,116antioxidants,150anxiety,38artemisiaabsinthium,142,144artichoke,152ascorbicacid,147aspirin,136,138asthma,16,21,99,104andgastricatrophy,41andgastroesopagealrefluxdisease(GERD),21,109andtreatinglowstomachacid,33andvitaminB12,68atherosclerosis,68atrophicgastritis,11,41,52,140.

Seealsogastricatrophyandallergies,116andaminoacids,78andB12absorption,69andcalciumabsorption,65andHelicobacterpylori,90andhypergastinemia,95andmastic,152andnutrients,56andperniciousanemia,70andrheumatoidarthritis,120andstomachcancer,93,97andzincabsorption,72autoimmunediseases,115,121Axid,19,27,48

bacterialovergrowth,39andaminoacids,78andB12absorption,69andfolateabsorption,67andstomachcancer,95,97badbreath,90,152bakingsoda,26barberrybark,143Barrett’sesophagus,36,157bases,25,29belching,16,21berberisvulgaris,143beta-blockers,136betainehydrochloride,16,139betazolehydrochloride,65bicarbonate,14,141andcholera,85andHelicobacterpylori,90andstomachprotection,53Bifidobacteriumbifidum,152bile,14,50,87,142,152bitters,142

bloating,16,21,84,146Boone,Kerry,144Braverman,Eric,171Bray,GeorgeW.,101,104,112breastenlargement,28bromelain,141,155BromoSeltzer,26bronchodilators,110,136

calcium,25,38,64ascorbate,148carbonate,26,63–65channelblockers,136chloride,65citrate,65malate,66CanadianOsteopathicAssociation,161capsaicin,150caraway,143carbenaxolone,145carbohydrateabsorption,87cardiovasculardisease,68,80Carroll,Harvey,66carumcarvi,143celiacdisease,116chamomile,151Champagne,ElaineT.,81chiefcells,47cholecystokinin(CCK),50choleraandtheacidbarrier,84andfolateabsorption,67andmastic,153choline,168chronicindegestion,13.Seeindegestionchyme,46,141cimetidine,27,64

citricacid,140colorectalcancer,80,96compoundingpharmacists,161constipation,16,27,84conventionalmedicine,10,25,102copper,38corticosteroids,138cortisone,146coughing,136cramps,151Crockett,J.A.,108curcumin,149Cutler,Bobby,Rebecca,andDavid,99cynarascolymus,143,152

dairyproducts,135dandelion,143Dcells,47deglycyrrhizinatedlicorice,145Demerol,136depression,16,21andaminoacids,165andgastricatrophy,41andproteindigestion,38andtreatinglowstomachacid,33andvitaminB12,68dermatitis,41diabetes,16andallergies,117anddigestiveenzymes,141andgastricatrophy,41andlowstomachacid,39diaphragm,53diarrheaandtheacidbarrier,84andfolateabsorption,67andhistamineH2-receptorblockers,27andprotonpumpinhibitors,28

dietarychanges,134,154digestion,44digestiveenzymes,16,155juices,142secretions,14dopamine,167,168Dr.Wright’sBookofNutritionalTherapy,157Dr.Wright’sGuidetoHealingwithNutrition,157duodenalulcersandessentialfattyacids,151andHelicobacterpylori,90andlicorice,146andmastic,153duodenum,14,46,141Duracid,26dysentery,67,84dyspepsia,18,84

E.coli,40,89eczema,41Enterochromaffin-like(ECL)cells,47enzymes,14,16,141,155ephedrine,110,136epinephrine,167,168epithelialcells,45esomeprazole,28esophagitis,36,157esophagus,19.Seealsoloweresophagealsphincter(LES)valvedamageto,22andgastroesophagealrefluxdisease(GERD),21,109ulcersof,36andupperGItract,45essentialfattyacids(EFA),151

famotidine,27fastingplasmaessentialaminoacidtest,171

fatabsorption,87fatigue,13,33,60,68fennel,143ferricsalts,61ferroussalts,61fiber,80fingernails,79flatulence,67,84,141.SeealsogasFloyer,John,104foeniculumvulgare,143folicacid,66,145foodallergies,39,135FoodandDrugAdministration(FDA),11–12,19,34freeradicals,148Freud,Sigmund,166functionalgastricatrophy,42fungalovergrowth,39

Gaby,Alan,122gallbladder,14,50,121,150gallstones,41gas,16.Seealsoflatulenceandgastroesopagealrefluxdisease(GERD),21andlactase,151andlicorice,146gastricadenocarcinoma,52,147analysis,133atrophy,41,67.Seealsoatrophicgastritismotility,51reflux,109ulcers,90,146,151gastrin,47,50,91,142gastroesophagealrefluxdisease(GERD),19,21,25,157gastrointestinal(GI)tract,21,44gastroplication,131Gaviscon,26Gcells,47Gelusil,26

gentianalutea,143gentianroot,142,143ginger,143,150globeartichoke,143glomerulonephritis,117glutamicacid,139glycyrrhizin,146goldensealroot,144Goodpasture’ssyndrome,117gout,28Grave’sdisease,39,41,117gutflora,15.Seealsointestinalmicroflora

hair,117,134Hashimoto’sthyroiditis,117headache,28heartburn,11,13andtheacidbarrier,84causesof,23andchamomile,151chronicconditionsof,21andgastroesophagealrefluxdisease(GERD),21andhistamineH2-receptorblockers,27andlicorice,146andloweresophagealsphincter(LES)valve,24relievingsymptomsof,28andseriousconditions,36andstomachacid,22asasymptom,19Heidelbergcapsule,133Helicobacterpylori(H.pylori),27,53,89,148,152,154hemeiron,61hemoglobin,60hiatalhernia,49,53histamines,26,48,168histidine,168histocompatibilitylocusantigens(HLA),103Hitchcock,JonandSara,124

hoarseness,21hopsflowers,144hpochlorhydria,78H2-receptorblockers,48humuluslupulus,144hydrastiscanadensis,144hydrochloricacid(HCl),11,16,25,107hyperacidity,11,38,90,133hyperchlorhydria,90hypergastrinemia,52,95,120hyperplasia,95hypochlorhydria,40andallergies,112andanemia,60andasthma,105andB12absorption,72anddepression,173andHelicobacterpylori,90andreplacingHCl,138andrheumatoidarthritis,118andstomachcancer,97testingfor,156

ibuprofen,136,138immuneresponses,39impotence,28indigestion.Seealsochronicindigestionandartichoke,152anddigestiveenzymes,141andlicorice,146andstomachacid,22Indocin,138inflammatoryboweldisease,116inflammatorysensitivity,116insomnia,21,38InternationalAcademyofCompoundingPharmacists(IACP),164International Foundation for Functional Gastrointestinal Disorders

(IFFGD),

12intestinalflora,15.Seealsoprobioticsintestinalhyperpermeability,115intrinsicfactor,69iron,38,60iron-deficiencyanemia,60.Seealsoanemiaironsalts,136

kidneyfailure,25Koch,Robert,85

lactase,151Lactobacillusacidophilus,152,176lactoseintolerance,151lansoprazole,28lecithin,168lemonjuice,140leucine,78L-glutamine,149licoriceroot,92,146lifestylechanges,134,154ligands,63litmuspaper,29lowacidity,40loweresophagealsphincter(LES)valve,20,24,45,110,134lupus,16,39,41,115,117lymphoma,90

Maalox,19,26,137MacDonald,ElaineandTom,55maculardegeneration,55,73magnesium,25,26,63,148malnutrition,16,38Marshall,Barry,92mastic,152medications,134menthapiperita,144Mi-Acid,26

milk-alkalisyndrome,25milkofmagnesia,26milkthistle,144Mills,Simon,144minerals,14,16,41monoamineoxidase(MAO)inhibitors,167motilityenhancers,28Motrin,138mouth,45mucouscells,47,53multiplesclerosis,16,115,117Mylanta,26,67

naproxen,136NationalInstituteofDiabetesandDigestiveDiseases,18NationalInstitutesofHealth(NIH),11naturopathicmedicine,159nausea,27,150neurotransmitters,165neutralizes,25Nexium,19,28nightblindness,141nitazidine,27nitrates,97nitroglycerine,136N-nitrosocompounds,147noradrenaline,78,168norepinephrine,78,167,168nutrients,14,38,44,56,141omeprazole,28osteopathicphysicians,159,160osteoporosis,16,21,26,33,41

pancreas,14,49,142pancreatin,141,155pantoprazole,28papain,141,155parietalcells,47

Parnelli,VincentandTheresa,73Parsonnet,Julie,93Pepcid,19,27andHelicabacterpylori,94andhistamines,48andreflux,137andzincabsorption,72peppermint,144pepsin,16,38andasthma,107andB12absorption,69andbitters,142andreplacingHCl,138pepticulcers,27,146,152,157peptides,38,78peristalsis,45perniciousanemia,70,96Pevacid,11,19,28Pfeiffer,Carl,171pH.Seeacid-basebalancepharmacists,compounding,161phenylalanine,38,78,168,170phyticacid,80Pizzoli,Vincent,Monica,99pneumonia,85potassiumchloride,136Prednisone,138Prilosec,11,19,28andachlorhydria,42andtheacidbarrier,85andasthma,111andB12absorption,70,71andbacterialovergrowth,87anddietaryfiber,81andgastrinlevels,52,95andreflux,137salesof,22andulcers,91

PrinciplesandPracticeofPhytotherapy,144probiotics,16,151.SeealsointestinalfloraProfessionalCompoundingCentersofAmerica(PCCA),164Profonix,19,28Propulsid,28prostaglandins,146proteins,38,41,78protonpumpinhibitors,26,47Prozac,78pseudoephedrine,110

quinidine,136

rabeprazole,28ranitidine,27reflux,19,24andasthma,109anddigestion,45andheartburn,36reducing,134relievingsymptomsof,28regurgitation,21rheumatoidarthritis,16,21,116andallergies,115,117andgastricatrophy,41andlowstomachacid,39andtreatinglowstomachacid,33Riopan,26Rolaids,13,19,26,81rosacea,16rumexcrispus,144

saliva,45,53,88,142salmonella,40,67,85scleroderma,117secretin,141selectiveserotoninreuptakeinhibitors(SSRI),168

serotonin,78,167,168Serzone,78silybummarianum,144Sjogren’ssyndrome,117skin,21,28,41,141smoking,134sodium,25ascorbate,148bicarbonate,26,29,63hydroxide,29somatostatin,47sorethroat,21sphincter.Seeloweresopagealsphincter(LES)valveSt.John’sWort,173staphylococcus,89stomach,16,46stomachcancer,12,50,52,95,97andgastricatrophy,41andHelicobacterpylori,90stools,141stress,134swallowing,21symptoms,30

Tagamet,14,19,27andB12absorption,71andcalciumabsorption,66anddietaryfiber,81andfolateabsorption,67andHelicobacterpylori,94andhistamines,48andironabsorption,64andnitriteconcentrations,97andulcers,91andzincabsorption,72taraxacumofficinale,143Tempo,26tetracycline,136,176

theophylline,110,136threonine,171transientLESrelaxations(TLESR),46tricyclic,167tryptamine,167tryptophan,38,78,169tuberculosis,84Tums,13,18,19,26andcalciumabsorption,65anddietaryfiber,81andmilk-alkalisyndrome,26andreflux,137turmeric,149typhoid,84tyramine,167tyrosine,38,78,170

ulcerativecolitis,16,41,115,116ulcers,12,24upperGItract,44upsetstomach,21,84U.S.DepartmentofAgriculture(USDA),67

valine,78Valium,136Vibriocholerae,40vinegar,140vitamins,14,16,41A,149B12,68,107C,147E,151vomiting,27wheezing,21,136wormwood,142,144

yellowdock,144

Zantac,19,27

andtheacidbarrier,85anddietaryfiber,81andfolateabsorption,67andHelicabacterpylori,94andhistamines,48andreflux,137zinc,38,72,73,149zingiberofficinale,143,150Zollinger-EllisonSyndrome(ZES),96Zoloft,78