Gut 1997; 40: 49-56

Alcoholic beverages produced by alcoholicfermentation but not by distillation are powerfulstimulants of gastric acid secretion in humans

S Teyssen, T Lenzing, G Gonzalez-Calero, A Korn, R L Riepl, M V Singer

AbstractBackground-The effect ofcommonly in-gested alcoholic beverages on gastric acidoutput and release of gastrin in humans isunknown.Aim and Methods-In 16 healthy humansthe effect of some commonly ingestedalcoholic beverages produced by fer-mentation plus distillation (for example,whisky, cognac, calvados, armagnac, andrum) or by alcoholic fermentation (beer,wine, champagne, martini, and sherry) ongastric acid output and release of gastrinwas studied. Gastric acid output wasdetermined by the method of intragastrictitration. Plasma gastrin was measuredusing a specific radioimmunoassay.Results-None of the alcoholic beveragesproduced by fermentation plus distillationhad any significant effect on gastric acidoutput and release of gastrin comparedwith control (isotonic glucose and distilledwater). Alcoholic beverages produced onlyby fermentation significantly (p<005)increased the gastric acid output by 57%to 95% ofmaximal acid output (MAO) andrelease of gastrin up to 5 l-fold comparedwith control. If beer, wine, and sherrywere distilled, only their remaining partsincreased gastric acid output by 53% to76% of MAO and increased release ofgastrin up to 4*3-fold compared withcontrol.Conclusions-(1) Alcoholic beverages pro-duced by fermentation but not by distil-lation are powerfil stimulants of gastricacid output and release of gastrin; (2) thealcoholic beverage constituents thatstimulate gastric acid output and releaseof gastrin are most probably producedduring the process of fermentation andremoved during the following process ofdistillation.(Gut 1997; 40: 49-56)

Keywords: alcoholic beverages, gastric acid output,gastrin, humans.

Although detailed epidemiological data on thefrequency of peptic ulcer disease associatedwith alcoholism are scanty, patients with pepticulcer disease are often advised to avoidalcoholic beverages. In addition, the patho-physiological mechanisms of damage to the

gastric mucosa by ingestion of pure ethanoland common alcoholic beverages are stillpoorly understood.An increased gastric acid and gastrin

response to alcoholic beverages could be apossible pathogenic factor in peptic ulcerdisease.' Intragastric instillation of 500 ml of1 4% and 4 0% (volvol) pure ethanol has asmall stimulatory effect on gastric acid outputwith a response equal to about 23% of thepentagastrin stimulated incremental gastricacid output (maximal acid output (MAO)).Higher concentrations of pure ethanol (up to40% vo/vol) have either no effect or a mildlyinhibitory one.2 None of the ethanol concen-trations tested increase plasma gastrin concen-trations'-9; for review see 10 l.

In contrast, some of the commonly ingestedalcoholic beverages are potent stimuli of gastricacid output and release of gastrin.2 Oral orintragastric instillation of beer causes a stimu-lation of about 95% of that produced by penta-gastrin (MAO). Red and white wine increasesgastric acid output up to 61% of MAO. Both,beer and wine, cause pronounced release ofgastrin. Beverages with a high alcohol con-tent, such as whisky (40% vol/vol) and cognac(40% vol/vol) do not stimulate gastric acidoutput or release of gastrin.2 6The search for the stimulatory substances in

beer shows that the powerful stimulants ofgastric acid output are produced during theprocess of alcoholic fermentation and thatthey are thermostable and anionic polar sub-stances with a molecular weight lower than 700Daltons.12-15 It was also found that the knownnon-alcoholic ingredients in beer and wine arenot responsible for the stimulatory action ofboth alcoholic beverages on gastric acid outputand release of gastrin.8

Until the present investigation, it was notknown why beverages with a high ethanolcontent (for example, whisky and cognac) donot stimulate gastric acid output and release ofgastrin, whereas alcoholic beverages with acomparatively low ethanol content (for example,beer and wine) have a stimulatory effect. Apossible explanation for the different effectsbetween alcoholic beverages with a high or lowethanol content on gastric function might betheir different production processes: beer andwine are produced by fermentation of carbo-hydrates (for example, glucose); whisky andcognac are produced by fermentation andsubsequent distillation.

Department ofMedicine IV(Gastroenterology),University HospitalofHeidelberg atMannheim,Mannheim, GermanyS TeyssenT LenzingG Gonzalez-CaleroA KomM V Singer

Department ofMedicine,University HospitalofMunich,Kinikum Innenstadt,Munich, GermanyR L RieplCorrespondence to:ProfessorM V Singer,Department of Medicine IV(Gastroenterology),University Hospital ofHeidelberg at Mannheim,Theodor-Kutzer-Ufer,68135 Mannheim,Germany.Accepted for publication28 August 1996

49

Teyssen, Lenzing, Gonzalez-Calero, Korn, Riepl, Singer

In addition, the action ofcommonly ingestedbefore meal drinks (aperitifs and spirits otherthan whisky and cognac) on the stomach hadnot been studied until now.The aim of this study was to investigate in

non-alcoholic human volunteers the action ofsome alcoholic beverages with a high ethanolcontent produced by fermentation plus sub-sequent distillation, such as aperitifs and spirits,on the gastric acid output and release ofgastrin, and to compare their effects with thatof alcoholic beverages produced by fermen-tation, such as beer, champagne, sherry, andother aperitifs, because the action of thesealcoholic beverages on gastric acid output iscomparatively unknown. Some of these datahave been published in abstract form."6

Methods

SUBJECTSSixteen healthy young volunteers (nine men

and seven women, aged 21 to 31 years; bodyweight, 52 to 87 kg) were studied. All were ingood health, were not receiving medication,and were either teetotallers or drank less than20 g ofpure alcohol each day. Twenty per centwere smokers (not more than 10 cigarettes perday). None of the volunteers was Helicobacterpylori positive (tested by a '3[C] urea breathtest)."7 Fully informed written consent was

obtained from each subject, and the researchprotocol was approved by the UniversityHospital's Ethics Committee. The investigationwas carried out according to the principles ofthe revised declaration of Helsinki 1989.Each subject was investigated several times.

on separate days. The sequence of tests was

randomised, and not more than two tests per

week were performed in each subject with a

minimum interval of 48 hours between thetests.

STUDY DESIGN

Test meal stimulated secretionGastric acid output in response to variousliquid test meals was determined in 30 and 60

minute (see later) periods, respectively, byautomatic titration to pH 5*5 with 0-5 mol/lNaOH as previously described'8 with slightmodifications.'9 20 After an overnight fast (12hours, during which the subjects also avoidedsmoking), a two luminal nasogastric tube(AN 10; H G Anderson Products, New York,NY) was positioned in the most dependentpart of the stomach. The position was con-

trolled by the 'water-recovery test' describedby Hassan and Hobsley.2' The subjects were

sitting in a slightly recumbent position. Beforeinstillation of the first meal, the stomach was

rinsed with water (100-150 ml) and emptiedby aspiration; the intragastric titration was thenstarted.On each experimental day, five liquid meals

(volume 500 ml each, pH 5 5) were instilledinto the stomach in 30 or 60 minute intervals(see Fig 1A). After each period, the remaininggastric content was emptied, and the volumewas measured. Thereafter, the next meal wasinstilled. The first two meals of each studyconsisted of isotonic glucose (576% wt/vol):this has been shown to inhibit gastric emptyingwithout changing the acid secretory response."Thus, sufficient volume remained in thestomach for constant intragastric titration.Thereafter, 500 ml ofone ofthe liquid test mealswith a ethanol content less than 10% vol/vol(Table) was instilled into the stomach, and acidsecretion was measured for one 60 minuteperiod.When alcoholic beverages with an ethanol

content higher than 10% (vol/vol) were tested,a modification of the protocol was neededbecause intragastric instillation of 500 ml ofthese alcoholic beverages would not have beentolerable (Fig 1B). At the beginning of the testperiod, 125, 187, 250 or 300 ml (see Table),respectively of these meals was given intra-gastrically; 10 minutes later, 375, 313, 250or 200 ml, respectively, of isotonic glucose(5-76% wt/vol) was added to have enoughvolume for intragastric titration (500 ml). Therespective glucose control solutions were givenin a similar manner.To investigate the effect of the liquid test

meals after ending perfusion, the actual testperiod was followed up by two control periods

Alcoholic beverages produced by alcoholic fermentation or distillation

Ethanol content Given volumeTest meal (% vol/vol) (ml) pH Production process

Beer (Eichbaum Pilsener) 4-9 500 5-5 alcoholic fermentationWhite wine (Kinheimer Hubertuslay)* 10 0 500 5-5 alcoholic fennentationChampagne (Pommery Drapeau sec) 12-0 300 5-5 alcoholic fermentationMartini Bianco 15-0 250 5-5 alcoholic fermentationHarveys Bristol Fino Sherry 16-5 250 5-5 alcoholic fermentationRemaining part (=supernatant) of distilled sherry 0 500 5-5 alcoholic fermentationRemaining part (=supernatant) of distilled wine 0 500 5-5 alcoholic fermentationRemaining part (=supernatant) of distilled beer 0 500 5-5 alcoholic fermentationScotch whisky (Ballentines)* 43-0 125 5-5 distillationCognac (Remy Martin)* 40 0 125 5-5 distillationCalvados Hors d'Age 40-0 125 5-5 distillationArmagnac Cles Des Ducs 40-0 125 5-5 distillationBacardi Superior Gold Rum 37-5 125 5-5 distillationPemod Fils 40-0 125 5-5 distillationCointreau 40 0 125 5-5 distillationCampari 25-0 187 5-5 distillationDistilled sherry 16-5 250 5-5 distillationDistilled wine 10-0 500 5-5 distillationDistilled beer 4-9 500 5-5 distillation

*Results are taken from reference 2.

50

Akoholic beverages and gastric acid secretion

in which isotonic glucose was administered for30 minutes each (data not shown).Blood samples (6 ml) for determination

of gastrin were drawn at 30 minute inter-vals during the control periods and at 10minute intervals during administration ofthe test solutions (Fig 1). The blood wascollected in ice chilled EDTA tubes containing400 KIU aprotinin (Trasylol) per ml of blood.The samples were centrifugated immediatelyat 4°C, and the plasma gastrin was frozenat -20°C. Plasma gastrin was measuredusing a specific radioimmunoassay (BectonDickinson and Company, Orangeburg, NewYork, USA).Blood samples (4 ml) for ethanol concen-

trations were drawn once at the end of thesecond control period before the test solutionswere given, during the test period in 10 minuteintervals, and during the last two controlperiods in 15 minute intervals. Serum concen-trations of ethanol were determined by thealcohol-dehydrogenase method (Blutalkohol,C F Boehringer & Sohne GmbH, Mannheim,Germany).

Pentagastrin stimulated secretionTo determine the maximal acid output (MAO)and to ensure that gastric acid output waswithin normal limits (that the subjects wereneither hyposecretors nor hypersecretors), apentagastrin test (6 ,ug/kg subcutaneously) wasperformed in each subject. Gastric acid outputwas measured by intragastric titration. Duringthe 60 minute basal period, two meals ofisotonic glucose solution (500 ml each) wereadministered intragastrically. After sub-cutaneous exogenous administration of penta-gastrin, another two isotonic glucose solutionswere administered at 30 minute intervals.

TEST MEALS

Before instillation of the liquid meals (seeTable), the pH of each solution was adjusted

500 mlA ci C2 Test meal C3 C4

plus 125 to 375 ml

ci 3 C2glucose solution

C2~~~~(ad 500 ml)

125 to 375 mlTest meal

* 0

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0 10 30 50 60 75 90

to 5-5 by addition of HCL or NaOH in theappropriate amount. In the upper part ofTableall tested alcoholic beverages produced by theprocess of alcoholic fermentation are listed. Inthe lower part of Table all tested alcoholicbeverages produced by the process of alcoholicfermentation and subsequent distillation arelisted. Beer, wine, and sherry were distilled bythe method of 'patent-still' (synonym: 'con-tinuous or coffey-still-method'). For a detaileddescription of the process of fermentation anddistillation see specific reports (for examplerefs 22-25).

CALCULATIONS AND STATISTICSAll statistical analyses were performed onincremental responses, that is, on observedgastric acid response minus response to intra-gastric isotonic glucose. To calculate the onehour incremental gastric acid output, the valueobtained during the second 30 minute controlperiod of intragastric glucose administrationwas multiplied by two, and this value wassubtracted from the observed one hour gastricacid response to a given stimulus. This onehour incremental gastric acid output inresponse to the various test substances wascalculated for each experiment and eachsubject, and these individual values were usedfor statistical analysis.MAO was calculated by adding the two 30

minute outputs produced by subcutaneousinjection of pentagastrin. To compare thegastric acid response to pentagastrin with thatto the different test meals, the incrementalMAO - that is, observed MAO in response topentagastrin minus acid output during intra-gastric instillation of isotonic glucose - wascalculated.The integrated gastrin response for each

dose of stimulant was calculated by the formuladescribed by Taylor et al.26 All statisticalanalyses were performed on the integratedresponses of gastrin.The differences between the various treat-

ments were evaluated using analyses of variance(ANOVA). p Values of <0 05 were consideredsignificant. Data are reported as means (SEM)unless stated otherwise.

-ResultsEach subject had a normal gastric acidsecretory response to pentagastrin. The meanbasal gastric acid output in response to 500 ml

C3 C4 isotonic glucose solution (5-8% wt/vol) was10-7 (1-7) mmol/h. The mean MAO was 28-1(2 3) mmol/h, and the mean incremental MAOwas 17-4 (1-6) mmol/h (mean (SEM), n=16).

Intragastric instillation of 500 ml distilledwater did not significantly stimulate gastric

__,_, _, acid output above basal (Fig 2).120

Time (min)Figure 1: Schematic representation ofthe experimental procedure applied when 500 ml (A)and 125 to 375 ml (B) of the test solution were given (see Table). Cl to C4=controls=500 mlof 5 76% (wt/vol) glucose each. For a detailed description of the protocol, see text. (-) Bloodsamples for gastrin determination; ( ) blood samples for determination of alcoholconcentrations.

Alcoholic beverages produced byfermentationOf the alcoholic beverages produced only byfermentation tested, beer and champagnewere the most potent stimuli of gastric acidoutput causing 85% and 95%, respectively,

51

Teyssen, Lenzing, Gonzdlez-Calero, Korn, Riepl, Singer

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Figure 2: One hour incremental gastric acid output (mmol) in response to different alcoholic beverages produced byfermentation or distillation. For comparison, the mean one hour maximal acid output (MAO) in response to pentagastrin isalso shown. Results are means (SEM) ofsix subjects and of 16 subjects forMAO. *p<0 05 compared with both distilledwater and isotonic glucose (5 76% wt/vol) control solution (n= 16).

of incremental MAO. The distillate of beerdid not significantly increase gastric acid output,whereas the remaining part of the distilled beerstill caused an increase in gastric acid output ofabout 64% of incremental MAO (Fig 3).The one hour incremental response to

Martini Bianco was 570/o of incremental MAO.The one hour incremental gastric acid re-

sponse to sherry was 83% of incremental MAO.The distillate of sherry did not cause any signi-ficant increase in gastric acid output, whereasthe remaining part of the distilled sherry stillcaused an increase in gastric acid output ofabout 76% of incremental MAO (Fig 3).The one hour incremental gastric acid

response to wine was 61% of incrementalMAO (results are taken from ref 2). Thedistillate of wine did not cause any significantincrease in gastric acid output, whereas theremaining part of the distilled wine still causedan increase in gastric acid output of about 54%of incremental MAO (Fig 3).

Alcoholic beverages produced by distillationOf the selected alcoholic beverages producedby distillation (calvados, armagnac, cointreau,

and bacardi) none significantly changed gastricacid output compared with controls (Fig 2).

Plasma gastrin concentrationsBeer and champagne as well as martini, sherry,and the rest (remainder) of distillated beer,wine, and sherry significantly increased plasmagastrin concentrations up to 5-1-fold comparedwith control. Their one hour integrated gastrinresponses are shown in Figures 4 and 5.Plasma gastrin concentrations in response to

alcoholic beverages produced by distillationand distillated beer, wine, and sherry were not

significantly changed compared with control(isotonic glucose solution and water; Figs 4and 5).

Serum alcohol concentrationsSerum alcohol concentrations in response tothe different alcoholic beverages (Table) peakedwithin 20 to 50 minutes (in respect to theiralcoholic concentrations up to 19 1 mmol/l)and did not reach basal values within two

hours after ingestion of the various alcoholicbeverages (data not shown).

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Figulre 3: One houir incremental gastric acid ouitpuit (mmilo) inl responise to beer, zine, anid sheriw, their distillates anid theirremaining parts (-supernatants). For comparison, the mean onie houir miiaxiiial acid ouitpuit (AA 0) in tresponse topentagastnt? is also showni. Results are means (SEM) of six subjects and of 16 suibjects for AMAO. *p<005 compared zit/iboth distilled water and isotonic glucose (5 76% wt/vol) control solution (n=-16).

DiscussionThe important new findings of this study are:(1) alcoholic beverages that are produced onlyby fermentatiQn, such as champagne, beer,white and red wine,2 6 7 sherry, and martini arestrong stimulants of gastric acid output andrelease of gastrin in healthy, non-alcoholichumans.

(2) Alcoholic beverages produced by fer-mentation and subsequent distillation, suchas whisky and cognac,2 5 Pernod, Bacardi,and other spirits such as armagnac, calvados,cointreau do not stimulate gastric acid outputand release of gastrin.

(3) The distillation of beer, wine, and sherryresults in the loss of their effect on gastric acidoutput and release of gastrin. This finding isproof that the distillation process is responsiblefor the loss of the stimulatory action of thesebeverages.The finding that oral or intragastric instil-

lation of beer is a potent stimulus of gastric acidoutput (>95% of MAO) and release of gastrinis confirmation of earlier studies by otherinvestigators3 and ourselves.' Until now, itwas not known that champagne is a verypowerful stimulus of gastric acid output (950

of MAO). This powerful action of champagnedoes not depend upon its content of CO,."

In earlier studies,2 5-' we have shown thatred and white wine, which are produced byalcoholic fermentation, are also powerfulstimulants of gastric acid output and releaseof gastrin. In this study, we observed thatsherry, which is produced on the basis ofwine, is almost as potent as beer and cham-pagne (83% of MAO). When sherry is dis-tilled, no significant stimulatory action of thedistillate on gastric acid output and releaseof gastrin is observed, whereas the remainingpart (=supernatant) is still a potent stimulus.Thus, the distillation process is responsible forthe loss of the stimulatory action of thisbeverage.

Alcoholic beverages, produced by fer-mentation plus distillation, such as ap&ritifsand spiritis, had no stimulatory action ongastric acid output and release of gastrin. Theethanol content of beverages produced bydistillation is high (above 40%0 vol/vol). It hasbeen shown that intragastric instillation of 40%(vol/vol) pure ethanol does not stimulate gastricacid output and release of gastrin'2; thus,ethanol is excluded as a causal factor for the

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53

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Teyssen, Lenzing, Gonzailez-Calero, Korn, Riepi, Singer

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Figure 4: One hour integrated plasma gastrin response (pM) to different alcoholic beverages. Results are means (SEM)ofsix subjects. *p<0 05 compared with both distilled water and isotonic glucose (5 76% wt/vol) control solution(n= 16).

non-stimulatory action of alcoholic beveragesproduced by distillation on the stomach.During the distillation process of alcoholic

beverages, inhibiting substances are generated,or stimulatory substances are removed as far as

gastric acid output and release of gastrin are

concerned. We favour the hypothesis thatduring the distillation process non-alcoholicsubstances, which have been generated duringalcoholic fermentation and which stimulategastric acid output and release of gastrin, are

removed. The fact that the distillate of sherry,beer, and wine no longer stimulates gastricacid output and release of gastrin but therest of sherry, beer, and wine still does isstrong evidence for this hypothesis. We donot know whether the same inhibitory sub-stance or substances are produced in allbeverages tested and as a consequence are

responsible for the non-stimulatory action ofthese beverages on gastric acid output andrelease of gastrin.During previous years, we have looked

intensively for the stimulatory substances inbeer.8 1215 None of the known stimulants ofgastric acid output present in beer eitheralone or in combination could be implicated.8Among the various preproducts of beer tested,only those products produced after theaddition of yeast - that is, after the onset offermentation - had any capacity to stimulate

acid secretion. Fermented glucose was themost potent stimulant.8 To identify this meta-bolic product of yeast, fermentation of glucoseextracts obtained from fermented glucose bydifferent extraction methods (for example,ethylacetat extraction and eluate of anionexchange resin) were tested for their ability tostimulate acid secretion or gastrin release.'2-15Preliminary results suggest that the powerfulstimulants of gastric acid output are thermo-stable and anionic polar substances with a

molecular weight lower than 700 Daltons. Wespeculate that these substances are removedduring distillation.

In conclusion, this study shows for the firsttime that alcoholic beverages produced by fer-mentation but not those produced by alcoholicfermentation plus distillation are powerfulstimulants of gastric acid output and release ofgastrin in healthy, non-alcoholic humans. Thestimulatory non-alcoholic constituents of thosealcoholic beverages that stimulate gastric acidoutput and release of gastrin are most probablyproduced during the process of fermentation ofcarbohydrates and removed during the follow-ing process of distillation. Their pronouncedsecretory effect on the stomach is perhapsmediated greatly but not exclusively by gastrinrelease.

Both, the inhibitory and, predominately, thestimulatory mechanisms of alcoholic beverages

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Figure 5: Onie hour in2tegrated plasma gastnniz responise (pM) to beer, wvine, anzd shernw, their distillates and thleir remainingparts (=supematants). Resiults are mizeanis (SEAI) of slix sinbjects. *p<00.5 comiipared wzith both distilled zater and ifsotonlicglzucose (5 76% wt/ivol) conitrol soluitionz (ni=16).

on gastric acid output and release of gastrinremain to be further elucidated.

1 Chan' ST, Tevssen S, Singer MV. Alcohol and gastric acidsecretion in humans. Gu.t 1993; 34: 843-7.

2 Singer MV, Leffmann C, Evsselein VE, Calden H,Goebell H. Action of ethanol and some alcoholicbeverages on gastric acid secretion and release of gastrinin humans. GastrreLterologc 1987; 93: 1247-54.

3 McArthur K, Hogan D, Isenberg JI. Relative stimulator-effects of commonly ingested bev-erages on gastricsecretion in humans. Gastiroenterology 1982; 83:199-203.

4 Singer .MAV, Calden H, Evsselein \VE, Goebell H. Bierstimuliert sehr stark, seine Inhaltsstoffe Athanol undAminosauren hingegen nur schwach die Magensaure-sekretion des Menschen. Z Gastroenterol 1983; 21:439-40.

5 Singer MV, Evsselein VE, Goebell H. Beer and wine butnot whisky and pure ethanol do stimulate release ofgastnn in humans. Digestino 1983; 26: 73-9.

6 Lenz HJ, Ferrari-TavlorJ, IsenbergJI. Wine and five percentethanol are potent stimulants of gastric acid secretion.Gastroterology3, 1983; 85: 1082-7.

7 Petersen WL, Bamett C, Walsh JH. Effect of intragastricinfusion of ethanol and wine on serum gastrin concen-tration and gastric acid secretion. Gastroes.terology 1986;91: 1390-5.

8 Singer MV, Tevssen S, Eysselein VE. Action of beer and itsingredients on gastric acid secretion and release of gastrinin humans. Gastroehiterolov 1991; 101: 935-42.

9 Chittenden RH, Mendel LB, Jackson HC. A further studsof the influence of alcohol and alcoholic drinks upondigestion, sith special reference to secretion. Ai_7nPl si'0l1898; 1:164-209.

10 Singer MV, Leffmann C. Alcohol and gastric acid secretionin humans: a short reviess. Scanid Gastro .terol 1988; 23(suppl 146): 11-21.

11 Chari ST, Tevssen S, Singer MV'. What controls should beused in studies of acute effects of alcohol and alcoholicbeverages on the stomach and the pancreas? S&anid 7

Gastrooeerol 1993; 28: 289-95.12 Teyssen S, Singer MV, Evsselein VE. Fermentation

of carbohvdrates by yeast is the major step for thepox erful stimulators action of beer on gastric acidsecretion in humans. [Abstract]. Alcohiol Alcohlol 1991; 26:261.

13 Tevssen S, Spies KP, Schlattmann B, Singer MV. Beer andfermented glucose are poss erful stimulants of gastric acidsecretion in humans. Which metabolic product of glucoseis responsible for this effect? [Abstract]. Alcohol Alcohol1992; 27 (suppl 1): 45.

14 Tevssen S, Gonzalez-Calero G. Schafer M. Schaff M,Singer MV. Partial purification of the poverfulstimulants of gastric acid secretion present in beer andfermented glucose. [Abstract]. Alcohol Alcohol1993; 28:241.

15 Teressen S, Gonzalez-Calero G. Brust A, Riepl RL,Singer MNV. Effect of some purificated ingredients ofbeer and fermented glucose on gastric acid secretionand release of gastrin in humans. [Abstract]. Alcoholl'sill1994; 18:30.

16 Tevssen S, Gonzalez-Calero G, Lenzing T, Brust A,Singer MIV. Effect of some aperitifs, champagne and beeron gastric acid secretion in humans. [Abstract]. Alcoholl'so1994; 18: 31.

17 Graham DY, Klein PD, Evans DJ, et al. Campylobacterpylori detected non-invasivelv bv the 'C-urea breath test.Lanicet 1987; ii: 1174-7.

18 Fordtran JS, WValsh JH. Gastric acid secretion rate andbuffer content of the stomach after eating, results innormal subjects and in patients wvith duodenal ulcer.(ClilzIczvest 1973; 52: 645-57.

19 Maxwell V, Evsselein VE, Kleibeuker J. Reeds T, WValsh JH.Glucose perfusion and intragastric titration. Dilg I)s Sci1984; 29: 321-6.

20 Lam SK, Isenberg JI, Grossman MlI, Lane WX'H,Walsh JH. Gastric acid secretion is abnormallx sensitive

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C)

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Teyssen, Lenzing, Gonzdlez-Calero, Korn, Riepl, Singer

to endogenous gastrin released after peptone test mealsin duodenal ulcer patients. Clin Invest 1980; 65:555-62.

21 Hassan MA, Hobsley M. Positionierung of subject and ofnaso-gastric tube during a gastric secretion study. BMJ1970; 1: 458-60.

22 Angelino SAGF. Beer. In: Maarse H, ed. Volatile compoundsinfoods and beverages. New York: 1991.

23 Gattermann L. Die Praxis des organischen Chemikers. 43.Auflage. Berlin: W De Gruyter, 1982: 35-57.

24 Organikum. Organisch-Chemisches Praktikum. Heidelberg:VEB Deutscher Verlag, 1988: 35-52.

25 Siegel S, Siegel S, Lenger H, et al. Handlexikon derGetrAnke. Band 1 (1986) und Band 2 (1989). Linz:RudolfTrauner Verlag.

26 Taylor IL, Byrne WJ, Christie DL, Ament ME, Walsh JH.Effect of individual L-amino acids on gastric acidsecretion and serum gastrin and pancreatic poly-peptide release in humans. Gastroenterology 1982; 83:272-8.

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