Anxiety, Hci Secretion and Peptic ulcer

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Anxiety, HC1 Secretion, and Peptic U lcer EtiologyGEORGE F. MAHL, Ph.D.

THIS paper reconsiders an anxiety hypothesisof peptic ulcer etiology, its relation to an oral-dependency hypothesis of peptic ulcer etiology, re-cent published comments (42) concerning an anx-iety hypothesis and its experimental basis, and itcites some further experimental observations rele-vant to this problem.Substantial direct and indirect evidence showsthat increased HC1 secretion is essential in pepticulcer etiology (8, 9, 11, 12, 13, 14, 24, 25, 26, 29,30 , 31, 32, 43, 47) and Wolf an d Wolff (47) andothers have shown how local vascular changes andmechanical factors might play a contributory rolein this disorder. There is, however, no conclusiveevidence as to the emotional processes that arepositively associated with these important physio-logic changes.

The most explicitly formulated viewpoint ex-pressed in the literature is that of Alexander (1 , 2,3 ) . It holds that the external or internal frustrationof intense oral-receptive and/or oral-aggressivedrives and the regression of these frustrated drivesto unconscious desires to eat or to be fed is thefundamental, unique psychologic process in pepticulcer etiology. Overt attitudes and behavior mightvary, but this process is reported to be invariablyfound upon analytic or detailed anamnestic studyof peptic ulcer patients (1, 3, 20, 23, 41, 45). It isinferred that the unconscious desires to be fed orto eat, produced in the manner indicated, are ac-companied by the gastric hyperfunction believed tobe essential for peptic ulcer development. For con-venience, this hypothesis will be referred to in thisarticle as an oral-dependency hypothesis of pepticulcer etiology.

There is also evidence from anamnestic study ofpersonality processes of ulcer patients (7, 10, 15, 44)and studies of the incidence of peptic ulcer in certainlife situations (36, 40) that chronic anxiety mightplay an important role in peptic ulcer etiology. Someof this evidence suggests that the source of theanxiety might not be critical (10, 15). There issome evidence that chronic anxiety is accompaniedby increased HC1 secretion (see below). On theFrom the Department of Psychology, Institute of Hu

Relations, Yale University.

basis of these studies it is proposed as a presentworking hypothesis that: a) the gastric hyperfunc-tion essential for peptic ulcer etiology is positivelyassociated with chronic anxiety; b) if these twoassociated processes persist peptic ulcer will develop;c) it is not essential what the source of the anxietyis , whether it is produced and maintained by en-vironmental stimulus conditions or by internal idea-tional or affective stimuli, whether these internalstimuli are conscious or unconscious, nor whetherthe anxiety is conscious or unconscious; d) while thepreceding factors might vary it is essential that thechronic anxiety be unrelieved by the developmentof adequate defense mechanisms or by changes inthe stimulus conditions. The assumptions in c) arethe ones in the proposal with a minimum of empiri-cal support. In the absence of critical positive ornegative evidence they are adopted now only fortheoretical reasons. They are specific assumptions tobe tested empirically. For convenience, this workinghypothesis will be called an anxiety hypothesis ofpeptic ulcer etiology.

Th e terms acute anxiety and chronic anxietyas presently used refer to a time continuum. Theyare temporal designations of the relative durationand/or frequency of anxiety responses. There areundoubtedly several important psychologic con-tinua that are some function of this time continuum,but exactly what these are and whether or not theycould be reliably measured is at present an openquestion.In this hypothesis and this paper, the writer doesnot distinguish between fear and anxiety . It is

usually stated tha t fear is objective anxi ety whi leanxiety is neurotic anxiety. For example, fearjudged by an observer to be appropriate to the stim-ulus conditions is called objective anxiety (fea r),while fear judged by an observer to be inappropriatefor the stimulus conditions is called neuroti c anx-iety (anx iety) . Th e criterion of appropriatene ss iswhat the observer would expect in response to thestimulus conditions. Thus if an internal stimulusto fear were repressed and the original conditionsof learning whereby that stimulus came to be fear-producing were unknown, one would use the termanxiety (neurotic anxiety). But if the stimulus forfear were conscious and the original conditions ofVOL. XII, NO. 3


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MAHLlearning known to the observer, it would be termedfear (objective anxiety). While this distinctionserves a descriptive purpose, it obscures the theoret-ically more imp ortant fact that the two terms fearand anxiety refer to the same process within theorganismanticipation of or preparation for pain-ful stimulation ( danger ). It also obscures the im-portant functional identitythat what is called fear motivates the learning of behavior which re-duces this fear (33, 34, 38) in the same way thatwha t is called anxiety motivates the learning ofbehavior w hich reduces this anxiety ( defencesagainst anx iety ). Freud early pointed out thisidentity of fear and anxiety as intervenin gprocesses (17, pp. 343 f.) and later restated it(18, pp. 112 f.). While the descriptive distinctionhas value in classification, it seems cumbersomeand fruitless to maintain it in theoretical work.

It is impossible at the present time to make atruly critical evaluation of an anxiety hypothesisand an oral-dependency hypothesis of peptic ulceretiology solely on the basis of studies of the person-ality processes of ulcer patients. This is in part afunction of the differences in methods used to ob-tain the pertinent information. But it is primarilydue to the extreme difficulty (and it is a mu tualdifficulty) that one meets in handling the problemsof reliability and validity of judgments or inter-pretations of anamnestic or analytic material. Forexample, it is not yet known what the degree ofagreement in personality judgments or interpre-tations would be if: a), interview material were ob-tained from both controls and ulcer patients in sucha way tha t there was no differentially selective elici-tation of various affective processes or derivatives;b ) , all reference to somatic processes specifically re-lated to ulcer symptomatology were deleted fromthe material; and c), this interview material werethen studied and interpreted by two or more in-vestigators who did not know which material camefrom controls and which from ulcer patients andwho arrived at their interpretations of the samematerial completely independently of one another.When these methodologic controls are incorporatedwithin the framework of the psychoanalyticmethod, this method will realize its full power asan investigative procedure and the desired criticalevaluation of the role of various emotional processesin peptic ulcer, and other disorders, will then bepossible. In the meantime, all the writer could dois reiterate the findings cited above and profess amethodologic faith, but this would contributenothing towards making a critical evaluation.Since both hypotheses assume an increase in HC1MAY-JUNE, 1950

159secretion, direct studies of changes in HC1 secre-tion, accompanying the emotional processes em-phasized, aid in the evaluation of the two views.There is no experimental evidence, positive ornegative, concerning HC1 secretion associated withunconscious wishes to be loved, to be fed, or to eatas they appear in personality investigations.

There are observations of HC1 secretion duringconscious anxiety in humans and overt anxiety be-havior in dogs. All of these observations concernaffective responses to external stimuli. While theproblems of reliability and validity of judging theaffective processes in these circumstances are notas imposing as in the case of judging emotionalprocesses underlying affective derivatives, they stillexist in these studies and have not been handledwith complete adequacy in all of them.The writer found (27) that there was significantlygreater HC1 secretion in dogs during the experi-mental induction of chronic fear than during con-trol conditions, and that this increase was associatedwith conditioned fear behavior in the absence ofprimary pain stimulation as well as with fear be-havior evoked by both a conditioned fear stimulusand a primary pain stimulus. There was no in-

crease in HC1 secretion in the first hours of thefear-inducing procedure, and the one dog whodeveloped acute fear responses but not chronic fearbehavior was the only animal in 7 who did notshow a rise in gastric acidity. This suggested thehypothesis that increased HC 1 secretion accompanieschronic anxiety but not acute anxiety.In view of Szasz's recent published comments(42) concerning this study the following detailsof the experiment are briefly cited here.The chronic fear behavior was induced and main-tained in the dogs by using a modified conditioningprocedure in which they were repeatedly stimulated

in their living cages with a buzzer and a strongelectric shock; sometimes the buzzer was admin-istered alone and sometimes it was combined withthe shock. These stimuli were paired in three dif-ferent temporal patterns when they were giventogether, the occurrence of the reinforcing shockstimulus with the buzzer was semi-randomized,and the time intervals between successive stimula-tions were semi-randomized. Stimulation by thebuzzer alone occurred three times as often as didstimulation by the buzzer-shock combinations. Forany 24-hour period, the dogs were responding ata maximum directly to the shock for approximately90 seconds or z minutes, while they were respond-ing directly to the buzzer for approximately 1480seconds or 25 minutes.


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i6oWhen the shock occurred it typically producedrapid circling of the cage, tetany, barking, andfrequently urination and defecation. There was asignificant increase in circling the cage, crouching,and trembling in response to the buzzer alone (27,Table 2) and the dogs developed specific phobicbehavior to their cages and the cage area of theexperimental room (27, Table 1). In addition,nonsystematic observations indicated that 6 of thedogs showed a decrease in general activity level,a decrease in amou nt of time spent sleeping, andan increase in the time spent maintaining one posi-

tion in their cages. Some of the dogs would leavetheir limbs in awkward positions when they weremanipulated by E. (Two dogs showed this; theexact number was not stated in the original report.)It was common for the dogs to tremble outsidetheir cages as well as in them and to startle toextraneous noises. No signs of hostile behavior to-wards E or the other dogs appeared.Szasz (42) attempted to reinterpret the behaviorof these dogs and concluded that they were notfearful dogs because they did not react in an adaptive way, but that they were paralyzed byfear, overwhelmed, massively disintegrated and

regressed dogs. He reached this conclusion by goingthrough the following process. He casually men-tioned the buzzer stimulation and failed to mentionthe conditioned fear responses to the buzzer, Heemphasized the shock stimulus and the shock re-sponse, the limb maintena nce behavior, and thelack of hostile behavior. Thus he selectively citedthe less frequent shock stimulus and response andthe atypical limb maintena nce behavior, and heselectively omitted citing the more frequent buzzerstimulation and conditioned behavior to it and themore typical phobic behavior. Yet all of the datacited here except the exact number of dogs whoshowed the limb maintena nce behavior wereavailable in the original report of the study.Normally one would regard the conditioned fearbehavior to the buzzers, the avoidance behavior tothe cage, and the silent wa iting in the cage, as prepara tion for dang er, as the adaptive behaviorthat meets Szasz's criterion of fear and which hedenied had occurred. These dogs were not paralyzedby fear or by overwhelming stimuli as Szasz in-sisted. They continually attem pted to cope withthe situation but the situation was intentionallyarranged so that nothing the animals could do ina manipulative or instrumental sense would suc-cessfully reduce their anxiety. When the dogs con-

tinued to react with anticipation of pain stimulationand continued to attempt to avoid the anxiety-pro-

ULCER ETIOLOGYducing environment but were unsuccessful in re-ducing their anxiety, then their gastric acid levelssignificantly increased. When a dog failed to de-velop chronic anticipation of pain stimulation, hisacid level failed to increase. How this is related tothe problem at the human level is considered in thediscussion.

Szasz did not consider the fact that the increasedHC1 secretion was associated with a significantincrease in the nonresting heart rate of these dogs(27, Table 8). If he had, he would have seen thedifficulty of trying to account for both of these auto-nomic changes by his misinterpretation of theanimal's behavior as regression. There was no mass autono mic regression in the sense of the vegeta-tive retreat postulated by Alexander (2 ), for thenonresting heart rate increased; it did not de-crease.Gantt (19) reports that Nick, the dog he studiedmost extensively, showed fasting gastric samplesconta ining free HC1 after the onset of his ex-perimen tal neurosis. Ga ntt did not report controlmeasures of this particular autonomic response butrefers to Pavlov's findings that the dogs in hislaboratory showed no free HC1 in their fasting

gastric samples and then infers that their occurrencein Nick was due to the experimentally producedbehavior disorder. Since Nick showed considerablechronic anxiety behavior, the observation of freeHC1 in his fasting gastric samples agrees with thefindings of the writer. Confidence in this agreementis limited, however, by the inadequacy of usingPavlov's observations as controls. Cannon (6) citesa report by LeConte that the HC1 secretion of dogswas inhibited immediately following their introduc-tion into a strange laboratory. Since this is a caseof acute anxiety, this observation is consistent withthe hypothesis that increased HC1 secretion accom-panies chronic anxiety but not acute anxiety.Most of the direct studies of HC1 secretion duringanxiety have been made with humans. Some reporteither a negative or a varying relationship betweenthese two variables. Beaumont (4) reported that theacid secretion of Alexis St. Martin was inhibitedduring fear. In this pioneering work, however,Beaumont's references to emotions and HC1 secre-tion are largely incidental and nonspecific. Floyerand Jennings (16) obtained fractional secretorycurves from medical students while they were as-sembled in a room and awaited the announcementof the results of their M.B. examinations. Theyconcluded that the curves were all within the range

of the results of their M.B. examinations. Theyjects appeared to be tense and apprehensive. TheseVOL. XII . NO. 3


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MAHLinvestigators did not take any control measures onthe same or different subjects, however, and theinference that there was no increase in HC1 secre-tion that could be attributed to the experimentalsituation is open to question for this reason. Thevariability of no rm al secretory curves is con-siderable and may be great enough to mask effectsdue to the experimental situation used by Floyerand Jennings. It is also possible that the HC1 secre-tion stimulated by the test meal was as great orgreater than that which might be stimulated bysuch an anxiety-producing situation. If this were thecase, and if the two excitatory processes are notadditive, then fasting samples, not fractional secre-tory curves, would have to be studied to determinethe effect of the experimental situation. Wolf andWolff (47) report an observation in which fear andalarm were associated with inhibition of HC1 secre-tion. This is cited later.

Wittkower (46) reports that the relationshipbetween anxiety and HC1 secretion varies fromperson to person. He states that hypnotically inducedfear states in his subjects were accompanied byincreased acid secretion in some cases and by de-creased acid secretion in other subjects, but thatwhichever type of change did occur in any particu-lar subject was consistently shown by that subject.It is difficult to evaluate these reports because onlyvery brief illustrative material is presented.

Several studies in humans have reported resultssuggesting that there is a positive relationship be-tween anxiety and HC1 secretion. Thus Bennett andVenables (5) found that when they hypnotized aveteran pilot of World War I and suggested thathe was flying in foggy weather over enemy terri-tory and was about to make a forced landing thesubject's secretory curve was greater at the beginn ingand the end of the test meal cycle than under con-trol conditions. The test meal response of a studentinvestigated by Miller, Bergheim, and Hawk (35)was greater while he was taking an examinationthan when he was resting quietly. During a ten-dayperiod in which he was afraid of being attackedby some Chicago gangsters, Hoelzel (21) foundthat the acidity of his own fasting gastric juice wastwice as great as it normally was. Mittelman andWolff (37) stated that the acid secretion of theirsubjects was higher during stress interviews inwhich anxiety and conflict were aroused than dur-ing nonstress interviews. Wolf an d Wolff (47 )found that the individual they studied extensivelysecreted much m ore HC1 dur ing protracted periodsof stress and anxiety than he usually did. Theyalso cite an instance in which an alarm response ofMAY JUNE, 1950

fear and feelings of helplessness were associated withdecreased HC1 secretion. They imply that the HC1inhibition in the cases of the alarm responses is amanifestation of feelings of helplessness and abjec-tion and that the excitation of HC1 secretion in thecases of protracted anxiety is a manifestation ofanxiety, hostility, resentment, guilt, and conflict.But the alarm reactions and the chronic anxietyreactions also differ with respect to the acute-chroniccontinuum, and in this respect they agree with thehypothesis that HC1 secretion is positively associatedwith chronic anxiety but not acute anxiety.The results of these direct experimental studiestend to support the hypothesis that increased HC1secretion is positively associated with chronic butnot with acute anxiety. Further studies at thehuman level, however, are needed before one canadequately evaluate an anxiety hypothesis of pepticulcer etiology.Such studies would also aid in resolving a con-tradiction between an anxiety hypothesis of pepticulcer etiology and the unqualified extension ofCannon's hypothesis of the emergency function ofemotions to chronic emotional behavior. The formerpredicts increased HC1 secretion during chronic

anxiety, while the latter predicts inhibited or de-creased HC1 secretion during such emotional re-sponses.Present Experiment

L The ProblemThe study with dogs (27) showed that afterchronic anxiety had been developed, increased HC1secretion was associated with acquired anxiety(conditioned anxiety). If an anxiety hypothesis ofpeptic ulcer etiology has any validity for humansit must be demonstrated that acquired chronicanxiety in humans is accompanied by increasedHC1 secretion.The theoretical hypothesis of the study then is:Acquired chronic anxiety in humans is accompaniedby increased HC1 secretion.The experimental hypothesis of the study is:The gastric acidity of young human males is greaterwhen they are undergoing the stress of the under-graduate examination period, if they react to thiswith anxiety over a period of days, than before orafter the period.It is assumed that such acquired anxieties asfear of failure, fear of loss of prestige and status,fear of loss of parental approval, etc., are aroused

during the examination period. In the study ajudgment of the degree of the arousal of such


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acquired anxieties asmanifested in overt behaviorand overt statements ismade independently of themeasurement of thegastric samples. It is assumedthat under theconditions of this study changesinthe acidity of fasting gastric contents is an indexof changesin therate of HC1 secretion.Contradictory conclusions were reached by Floyerand Jennings (16) and Miller, Bergheim, and Hawk(35) concerning theeffect of similar anxiety-pro-ducing situationson HC1 secretion. This contradic-tion ismore imagin ary th an real, however, becauseof the inadequate procedure used by the formerand th efact that th elatter investigated onlyonesubject. T he present study will have thesecondaryeffect of helping to resolve this contradiction.II. Experimental Procedure

Subjects: Eight undergraduate male universitystudents volunteered assubjects forthe experiment.At thetime hevolunteered, each subject kne wofthe nature ofthe study an d tha t it involved intuba-tion. Thesubjects ranged in agefrom 21 to 25years.Method of Measurement: Control and experi-mental fasting gastric samples were obtained by

aspirating the stomach contents throug h a Levintube.* Thetube waspassed nasally for some sub-jects, orally forothers, depending upon the wishofthe subject. In either case, it waspassed by thesame means for both theexperimental andcontrolmeasures for each subject. Five m inutes after th etube was passed, the stomach contents were aspiratedas completely as possible. The criterion forstomachemptiness wasthat point at which each of threesuccessive aspirations yielded 2cc . orless of fluid.Th is wasdone to clear thestomach of anyfluidsthat mayhave been secreted on a conditionedre-sponse basis before theexperimental an d controlsessions, when the subjects would norma lly haveeaten breakfast or a mid-morning snack or wouldbe anticipating lunch,or fluids that may have beensecreted as a result of the trauma of intubation.The stomach wasagain aspirated at the end of atwenty-minute period. Thefasting fluid obtainedat this time constituted the test sampleofthe controland experimental conditions.Itwas titrated against.1 N N a O H for free HC l and total acid, u singTopfer 's reagent an dphenopth alein respectivelyasindicators for theend-points.Conditions of Measurement: a) CONTROL MEAS-*The writer wishes to express hisgratitude to John R.

Williams, M. D., andHarvey R.Dunsmore, M. D.,ResearchFellows, Yale University School of.Medicine, for intubatingthe subjects.

ULCER ETIOLOGYURES. The control fasting gastric samples weremeasured from two tofour weeks before the ex-amination period for 5subjects andfrom threetofive weeks after theexam ination periodfor 3 sub-jects. They were split in this way to control forany adaptation tosuccessive intubations. Th e datesfor th econtrol measures were a rrange d sothatn osubject had any pressing academic tasks at thet ime. During the twenty-minute control test period,the subject and E carried on a conversation. Edirected it to theextent that he kept it centeredabout the subject's h obby in terests andactivities,otherwise he remained as passive as possible. Allow-in g for thevarying degrees of discomfort due tothe presenceofthe tube, allof the subjects appearedrelaxed an dundisturbed during this period.T hecontrol test sample thus contained those gastricfluids secreted during aninnocuous twenty-minuteconversation which occurred during a relativelystress-free period of the school year.

b) EXPERIMENTAL MEASURES. These were obtaineddur ing the final exam ination period. The y weremade on the morning of a day on which eachsubject had to take what heregarded as a difficultexamination. The exam ination itself was to betaken in the afternoon. The hour of the experimentalsession was matched tothat of thecontro l sessionto controlfor any hourly variationsinHC l secretionthat might occur . During th e twenty-minuteex-perimental test period E and the subject agai ncarried on aconversation. This no w took the formof a stress interview in contrast to the relativelynonemotionally toned discussion of the control con-dition. E centered it about the following questionsfor each subject:

1. Had thesubject ever failed any kind of anacademic examination before andwhat werethe consequences?2. Did the subject realize th e importance ofdoing well on today's examination intermsofbeing admitted to a graduate or professionalschool or obtaining a job? (Seven of the 8subjects were pre-professional students.)

3. H ow didthe subject's p arents usually reacttohis no t doing well on examinations and incourses?4. How would hisstanding ontoday's exam ina-tion affect hiscourse grade and howwouldthis affect hiscompetitive status w ith his stu-dent friends?5. How hard had thesubject work ed in prepar-

in g for today's examination? Did hefeelsuf-ficiently well prepared?VOL. XII, NO. 3


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MAHLAt the end of this experimental period, E dichoto-mized the subjects into two groups on the basis ofthe degree of anxiety motivation shown by them.These are recorded as Hi gh Anxie ty and LowAnxiety. This is a judgm ent of observable, overtanxiety behavior and verbalizations made duringthe interview on the experimental day. It was re-corded immediately at the end of this period, priorto titration of the gastric sample obtained at thatt ime.

The experimental test sample thus contains thosegastric fluids secreted during an interview touchingupon aspects of the current stress stimulation of thefinal examination period.For both the control and experimental measures,no food was eaten by the subjects after midnightof the previous night and no water was taken fortwo hours prior to the aspiration of the gastricsamples.

Two of the 8 subjects were judged by E to fallin the Low Anxiety category. These judgeme ntswere made for the following reasons. Subject 6was a premedical student who had already beenaccepted for the following year's entering class atone of the most sought-after medical schools in thecountry even though he had not yet completed thefirst semester of the fourth year of his undergraduatecourse. In the midst of the stress interview helaughed and asked, W hat are you trying to do,get me worried ? He stated that since he wasalready accepted for medical school all he had todo was pass his courses and that he could fail hisexaminations and still do this. Subject 2 was nota preprofessional student, was a member of theuniversity hockey squad, and spent more time dis-cussing the progress of the hockey team than hispending examination and his concern over it; hewas planning to go on a skiing party in the midst

TABLE 1.FRE E HCL AND TOTAL ACID MEASURES, EXPRESSED IN CLINICAL UNITS, DURING CONTROLANDEXPERIMENTAL CONDITIONS

Subject12345678

%stP

Con.00090000

1 . 13

Free HClExp.175303 4746

00

19.620.4

Con.Exp.+ 17+ 5 30+ 2 5 7+ 4 6

00

+18.519.82.467< O 3

Con.165112 05417610.5

6

Total acid

Exp.2 76 1I I431653

9728.42 0

Con-Exp.+ 11+ 5 60+ 2 3+ 1 1+ 49- 8+ 1+ 17-923.22.168


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6precision and are of unknown reliability the dif-ference in anxiety level between the twogroupswas pronounced.

Since thegroup as awhole showed significantlyhigher gastric acidity values during the stress periodthan in thecontrol period, onewould predict thatthis increase would begreaterfor the High Anx-iety group than for the LowAnxiety group.The following breakdown of thedata yieldsre-sults that are in agreement with this prediction.

MEAN CONTROL-EXPERIMENTALDIFFERENCES INACIDITY EXPRESSEDINCLINICAL UNITS

Lo w HighAnxiety Anxiety pgroup groupFree HC1Total acid -3-5 +24.7+256

.9O>.8o

DiscussionThe present results agree with the findingsofthe previous study (27)with dogs andwiththe

ULCER ETIOLOGYincrease in HC1 secretion predicted by an anxietyhypothesis of peptic ulcer etiology. To theextentthat conscious chronic anxiety and concomitantincreased HC1 secretion are important inthis etiol-ogy, these results support an anxiety hypothesis.Theydo notdirectly confirm thehypothesis, how-ever, since onemust still infer that peptic ulcerswould develop if the anxiety and theassociatedincreased HC1 secretion were protracted. The studyis also limited by itslack of study ofmechanicaland vascular factors.

Szasz (42) raised theoretical objections to ananxiety hypothesisofpeptic ulcer etiology.Hesaysthat because anxiety isomnipresentit isinadequateand meaningless simply to correlate somaticpro-cesses with anxiety per se; he says that theonlyadequate correlation for psychosomatic theory isthat between somatic processes and the way inwhich the ego defends itself against anxiety arisingfrom specified stimulus conditions.

There are two important questions involved here.First, areanxiety andHC1 secretion positivelyas-sociated regardlessof the stimulus conditions?Th easpect of this question that is most importantforpeptic ulcer etiology iswhether or notanxiety aris-ing from varying concomitant affective processes e.g. hostile wishes, incestuous wishes, fear of notbeing loved) aswell asfrom external stimuli(e.g.reality danger situations, threatening parentalfig-ures) is positively associated with HC1 secretion.What evidence thereisavailable on this point refersalmost completely toanxiety produced byexternalstimulus conditionsand it suggests that regardlessof themanner inwhich theanxiety isproduced itis associated with increased HC1 secretion. Whetheror not thisistrueforall sourcesofanxiety, internalor external, isaproblem for future investigation andnot one simply to be dismissedapriori.Itis assumedfor thepresent for dieoretical purposes that thesourceofanxiety is notcritical,but theautonomicpatterns may become very complex when additionalaffects areinvolved. This assumption will bemod-ified inaccordance with experimental findings.

The second principle question iswhat therela-tive roleofanxiety and the defense reactions againstit might be in peptic ulcer etiology. Here Szaszhas confused thedifferential roleofanxiety incon-versionand theother defense mechanisms, on theone hand,and itsrole inpsychosomatic disorders,on theother. In theformer, anxiety is ofprimaryimportance as a motive fordefense and itsauto-nomic concomitants are not of major importancebecause conversion symptoms or other defensemechanisms can maintain theanxiety at areduced

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MAHLlevel. In the case of peptic ulcer, however, it isproposed that anxiety is not successfully reduced bythe defense mechanisms and that the resultingchronic anxiety and its autonomic concomitantsthen become of major importance.

Although he emphasized a different emotionalprocess in peptic ulcer development, Alexander (2)clearly pointed out that in the vegetative neurosesthe essential factors are the physiologic aspects ofchronic emotions per se. His point in the sectionon vegetative neuroses is that in these disorders thechronic autonomic excitation is not the result'ofconversion of repressed emotions (warded-off im-pulses) but are the physiologic aspects of these re-pressed emotions themselves.

The writer is proposing, in addition, that in thevegetative neuroses, the motive for the defensemechanisms ( the warding-off impulses ) also be-comes chronic and that its physiologic concomitantsthen become important. (Of course, in some in-stances anxiety might also be the unsuccessfully warded-off impulse. )

Reluctance to consider the autonomic concomi-tants of anxiety per se in peptic ulcer etiology ap-pears to the writer to be a joint result of the historicaldevelopment of psychodynamic theory and the factthat psychosomatic theory early adopted Cannon'shypothesis of the emergency function of emotionsand unqualifiedly extended it to chronic emotionalprocesses without considering the fact that hishypothesis was based on studies of acute emotions.In the development of psychodynamic theory, em-phasis was placed on anxiety as a motive for defensemechanisms and the elucidation of these defensemechanisms was the primary task undertaken. Butanxiety has physiologic concomitants and when itbecomes chronic these physiologic concomitants cancontribute to the psychosomatic disorders. Cannon'shypothesis predicts inhibited HC1 secretion duringanxiety. But Cannon only considered one clear-cutobservation of HC1 secretion during anxiety (Le-Conte's observation) and that was an instance ofacute anxiety. In the psychosomatic disorders, how-ever, one deals with chronic emotional processesand there is strong evidence that increased HC1secretion is positively associated with chronic anx-iety. As far as HC1 secretion is concerned, one can-not simply extend Cannon's hypothesis to chronicanxiety. It has previously been suggested (27), onthe basis of evidence cited in the introduction, thatthis disagreement between Cannon's hypothesis andan anxiety hypothesis of peptic ulcer etiology mightbe resolved by consideration of the acute-chronicvariable. Reports of specific studies of this variableMAY-JUNE, 1950

I 6 5in monkeys and humans are now being prepared inwhich this point will be discussed in more detail.

The present proposal of an anxiety hypothesis ofpeptic ulcer etiology is similar in its formal aspectsto the hostility theory of hypertension (39). Hereone does not hesitate to speak of hostilities (i.e.hostility arising from varying sources) and of thephysiologic concomitants of hostility per se. (It iseven suggested (39) that anxieties per se mightbe important in this disorder.) In this case con-fusion of the role of hostility in the defense mecha-nisms and its role in the vegetative neuroses has notbeen troublesome. It appears to the writer that thelack of confusion in this instance might also be ajoint result of the history of psychodynamic theoryand the ease of extension of Cannon's hypothesis tothe particular chronic emotional process emphasized.It was not the tradition in psychodynamic theoryto place emphasis on hostility as a motive for de-fense mechanisms and there was no conflict betweenthe changes in blood pressure predicted by Cannon'shypothesis and those predicted by the hostility theoryof hypertension.

The increasing evidence that one of the autonomicconcomitants of chronic anxiety is increased HC1secretionconsidered together with the reports ofchronic anxiety in ulcer patients and the belief thatprotracted increased HC1 secretion is essential forpeptic ulcer etiologyshould make the role ofchronic anxiety in this disorder a matter for inten-sive, disinterested research.

In his critique, Szasz (42) considered the fact thatthe dogs subjected to the experimentally producedchronic fear did not show tissue pathology uponautopsy. The writer had suggested that this mightbe a result of the relatively short duration of theexperimental period. Szasz discounted the timefactor, however, and merely said that Wolf andWolff (47) had shown that tissue destruction occursrapidly. He failed to inform the readers that Wolfand Wolff's observations of tissue change were madeafter an erosion had already occurred in an area ofprotruding mucosa, that this area was stated bythem to be deficient in mucus which normally pro-tects the gastric mucosa from HC1, and that therapid tissue change followed continual administra-tion of gastric juice to this inadequately protectederosion. It does not seem reasonable to draw infer-ences concerning the physiologically intact stomachof the dogs from these particular observations ofWolf and Wolff, for nothing was known about themucous secretion in the dogs.

At the same time he was discounting the mean-ing of the dog study, Szasz cited some observations


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166concerning peptic ulcers in calves which he feltconfirmed an oral-dependency hypothesis of pepticulcer etiology. He referred to autopsy studies ofcalves, and said, . . . [The ] incidence of pepticulceration was as high as 98 per cent in calvesbe-tween the ages of twelve and fourteen weeks (42,p.303) .As Szasz says, this high incidenceof pepticulcer in calves is temporally related to prematureweaning of the calves and their initiation to a dietof dry fodder. If they are returned to a milk dietthe ulcers heal. While he acknowledges in a foot-note that mechanical irritation or trauma of thegastric mucosa by the dry fodder might play a rolein theetiology of these ulcersin calves, Szasz ratheramazingly says the following:

It is difficult to imagine how one could find amore striking confirmation, in the realm of animalexperiments, of Alexander's original psychoanalyticformulations concerningtheetiologyofpeptic ulcer(42, p. 303).He adds : Th edevelopment of this syndrome inyoung calves prematurely weaned, and the relief ofthese ulcers by permitting the calves to continueona milk diet, provides striking evidence for the cor-rectness of the psychoanalytic theory of ulcer for-

mation (42, p. 303).N owin one of the related references which Szaszcites (22),this very high incidence of peptic ulcerin calves is attributed to mechanical irritation (byth edryfodder) of themucosaof theabomasum,themost w ell-developed stomachof the cow atthis earlyage. Hutyra and Marek say that this mechanicalirritation arises from two special physiologic fea-tures of the youngcalf. One of these is the lackofdevelopment of the rumen which causes the dryfodder to be remasticated only slightly if at all andtobepassed rapidlyand directly intotheabomasum.The other feature is a strong constriction of theabomasum immediately anterior to the pylorus.This , they say, is a condition specific for the youngcalf. They state that with the development of therumen andperfection of rumination theulcers heal.The picture then seems to be as follows: A calfadapted tosucking milkisimmediatelyand abruptlydeprived of the milk andsucking and is placed ona dietof dry fodder. Becauseof the two physiologicdeficiencies described, the prepyloric mucosa issubjected to marked m echanical irritation.

Although the purely physiologic explanation forthe resulting ulcers seems adequate, Szasz choosesto emphasize the role of affective processes whichundoubtedly do occur upon premature weaningofthe calves.He saysin the same footnote referred toabove that he does not see how the affective com-

ULCER ETIOLOGYponents can be separated from the mechanical fac-tors.Th e writer proposes that the following simpleexperiment would enable one to do this.

One could obtain a sample of young calves withroughly equivalent nursing experience, and subjectthree-fourths of thecalves to abrupt weaning fromthe mothercow but permit one-fourth of the calvesto continue nursing for milk (Group 1). Theabruptly weaned calves could then be dividedrandomly into three sub-groups which would differfrom oneanother in their diet.Onegroup wouldbefed dry fodder (Group2), one group wouldbe fedmilk from a pail (Group 3), and the final groupwould be fed a nonmilk gruel mixture which re-quired no mastication for adequate digestion(Group 4) . After allowing all four groupsto eat inthis fashionfor thedesired period of time, examina-tion for peptic ulcer would be made.If the affective e lemen ts prod uce d by specificweaning from the mother are the essential factorsand the mechanical factors are unimportant , onewould predict a significantly greater incidence ofpeptic ulcers in Groups 2, 3, and 4 (the nonnursinggroups) compared with Group 1 (nursing group) ,but no significant differences betwe en Gro ups2, 3,an d 4. If themec hanic al factors arisin g from a dryfodder diet are the essential ones and the affectiveelements unimportant, one would predict a signifi-cantly greater incidence of peptic ulcers in Group2 (Dry Fodder Grou p) compared with Groups 1,3, and 4 (Liquid Diet Groups) , but no significantdifferences between Groups 1, 3, and 4. If weaningfrom milk, as distinct from w eaning from suckingor nursing, produced essential or contributory affec-tive elements, one would predictasignifiantly higherincidence of peptic ulcers in Group 4 (Nonmi lkLiquid Diet) than in Group 3 (Milk Diet) . Onecould continue such subgroup comparisions to testmore refined hypotheses.In the meantime, Szasz's rather startling em pha-sis on these findings of peptic ulcers in calves isirrelevant to the correctness or incorrectness ofeither an oral-dependency or an anxiety hypothesisof peptic ulcer etiology.

This study inhumansdid notinvestigatethevari-ables emphasized by Alexander and his co-workersan d sodoes not have any direct bearingon his hy-podiesis. But there are several possible avenues forthought and research in making a comparativeevaluation of an anxiety hypothesis of peptic ulcerand that of Alexander.First, exceptforAlexander's insistenceonunique-ness and specificity of the psychogenic aspects of

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MAHLpeptic ulcer (2), the two viewpoints are not in-herently diametrically opposed. It is possible that thephysiologic aspects of chronic anxiety and of un-conscious eating desires, associated with wishes tobe loved, both include increased HCl secretion andthat both thus contribute to ulcer development. Butit remains to be demonstrated that regressively-aroused oral wishes are accompanied by increasedHCl secretion.Secondly, it is possible that the anxiety which isproduced by and which motivates the repression ofthe oral drives, together with anxiety arising fromother sources, rather than the arousal of oral wishes,is the essential response that is accompanied by in-creased HCl secretion. There is not yet available thecontrolled evidence needed for attributing primaryimportance in these cases to the orality factors.Thirdly, one might ask if the increased HCl se-cretion associated with chronic anxiety is not theresult of the arousal of unconscious oral cravingsin the face of the anxiety-producing stimulationrather than to the arousal of anxiety itself For ex-ample, in the present study might not the observablesurface anxiety have been simply a manifestationof, or have been accompanied by, unconscious long-ings to be loved (by the faculty and admissions offi-cers as parental surrogates, for example) which inthese subjects were equivalent to unconscious oralcravings? The present study, of course, did not in-clude measures of such unconscious processes andso it is inconclusive in this respect. Analytic theorywould predict such unconscious wishes only in

167and to the degree of conscious anxiety aroused bythe stated stress situation.This third point is basically the one raised bySzasz (42) in his reinterpretation of the results ofthe previous study with dogs (27). Szasz concludedthat the increased HCl secretion of these dogs wasa function of regression of their behavior and notof chronic fear. While he did not state clearly howbehavioral regression could account for the in-creased HCl secretion, it is strongly implied that hebelieves it does so because it involves a mass auto-nomic regression in the sense of the mass vegeta-tive retrea t postulated by Alexander and thearousal of oral cravings. In fact this is the necessary,logical conclusion he must reach in reinterpretingthe study in terms of Alexander's oral-dependencyhypothesis. The review of this dog study in the in-troduction presented evidence that there was nomassive disintegration or behavioral regression inthese dogs; the behavior observations showed thatthese dogs were reacting to the fear-inducing pro-cedure exactly as one would predict frightened dogswould react. It was also shown in the introductionthat the concept of vegetative retreat parallelingthe supposed general behavioral regression couldnot explain the concomitant increased HCl secretionand incre sed heart rate. If there had been a mass vegetative retreat there would necessarily havebeen found increased HCl secretion and decre sedheart rate. Furthermore, that there was no regres-sive-arousal of intense oral cravings in these dogsis strongly suggested by the complete dis ppe r nce

those subjects who were at least partially fixated a.t_ of self-licking by the dogs during the discretethe oral stage. In the present study, 5 of the 8 sub-jects showed increases in gastric acidity in the ex-perimental condition, and all 5 fell within the Hig h Anxiety category. One could say that sincethe group was not intentionally selected for pregeni-tal fixations it seems improbable that 5 of the 6 High A nxiety subjects would be sofixated Possi-bly some would argue, though, that a large propor-tion of subjects volunteering for an experiment in-volving intubation would do so because they wereso fixa ted, or tha t a large majority of people whoare the age of these subjects were probably subjectedto oral trauma as infants because self-regulation offeeding schedules was not the vogue when theywere infants. The writer was not impressed by thepresence of oral derivatives in these subjects, butthese are not significant observations in view of themethod of the study. In this study one is limited tothe conclusion that the increase in HCl secretionwas very closely related to a stated stress situationMAY-JUNE 1950

conditioned fear stimulation by the buzzer (27,Table 2). Except for the limited number of trialsper day when the dogs were also shocked (andwhen E never saw self-licking occur), their anx-iety behavior was most intense when the buzzerwas being sounded. If there were any regressively-aroused oral cravings in these animals and if theregressive-arousal is in any way connected with theintensity of the fear, it is surprising tha t self-lick-ing completely disappeared at the time one wouldexpect it to be most frequent. This is further sub-stantiated by observations that the same fear-pro-ducing procedure resulted in a significant decreasein daily food consumption in the two dogs used inthe study (Nip, Tuck) whose daily food consump-tion was measured under both control and experi-mental conditions (28). Control observations onother dogs ruled out variations in environmentaltemperature as a contributing factor. This samefear-producing procedure also results in a signifi-


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icant decrease in daily food intake in albino rats

In brief the present human study shows that in-creased HC1 secretion occurs in response to an ex-ternal stress situation and is very closely related tothe degree of conscious chronic anxiety as judged bythe writer. The results of the dog study stronglysupport the belief that chronic anxiety is positivelyassociated with increased HC1 secretion in thsence of regressively-aroused oral wishes (unlessit is suggested that increased oral wishes in dogswould not lead to increased oral activity such as

self-licking and eating ). The extent to which onecan generalize from the latter observations to thehuman, where the early conditions of learning inassociation with nutritive processes is much morecomplex than in dogs, is of course unknown. Butthis is not something to be settled mainly by apriori reasoning; it is a matter for investigation.The third point is related to the general questionof how the chronic anxiety-HCl-secretion relation-ship varies with respect to the location of the emo-tion on a conscious-unconscious continuum. In theabsence of any positive or negative experimentaldata and theoretical contraindications, the writer is

assuming that this relationship is always positivewith respect to this continuum. No assumption ismade as to whether or not the intensity of bothprocesses varies with respect to the continuum. Justexactly how these relationships do vary and howthey are altered by other concurrent unconsciousemotional processes, are specific aspects of a majorarea for future investigation.Although methodologically imposing, these areall important questions that still require empiricalanswers considering the exploratory nature of thisfield. They will be most rigorously answered whenthe type of reliability and validity controls noted

in the introduction are used in the study of auto-nomic changes related to both conscious and un-conscious emotional processes, as well as when theyare used in the more general personality investiga-tions of ulcer patients. Upon such study it mighteven happen that such categories of emotional proc-esses as anxiety, hostility, and oral-dependency willbe abandoned completely. Such would be the case,This food decrement is not due to the association of fear-pain stimuli with food or the acts of eating. The dogs werenever shocked or stimulated by the buzzer during theirdaily hour of free-feeding. The daily food intake of the ratsis the same whether their daily free-feeding takes place in

the experimental cages while the fear-pain stimuli arerandomly administered or in special feeding cages wherethese stimuli have never been and are never administeredduring the time of free-feeding.

ULCER ETIOLOGYfor example, if it is found that each of these proc-esses cannot be judged individually or each dis-tinguished from the other, with any degree of re-liability.

Summary1. It is impossible to make a critical evaluation ofan oral-dependency and an anxiety hypothesis ofpeptic ulcer etiology solely on the basis of availableanamnestic or psychoanalytic studies of personalityprocesses in peptic ulcer patients. A method whichwould enable one to do so is briefly described.2. Both the oral-dependency and the anxiety hy-pothesis assume that increased HC1 secretion isassociated with the em otional processes emphasized.There are no published experimental data, positiveor negative, concerning HC1 secretion during thearousal of unconscious wishes to be loved, to eat,or to be fed. There is evidence that chronic overtanxiety behavior in dogs and conscious chronicanxiety in humans are positively associated withincreased HC1 secretion. Some of the results arecontradictory, however, and further studies, es-pecially at the human level, are needed. Suchstudies also aid in resolving the contradictory pre-

dictions of HC1 secretion made by Cannon's emer-gency theory of emotions and by an anxiety hypoth-esis of peptic ulcer etiology.3.A study of the gastric acidity of male studentsduring the undergraduate examination period andduring control periods is reported. The gastricacidity of these students was significantly higherduring the examination period than during the con-trol periods. The rise in gastric acidity was veryclosely related to the degree of conscious anxietymanifested by these subjects. These results agreewith an anxiety hypothesis of peptic ulcer etiology;they do not bear directly upon an oral-dependency

hypothesis.4. A recent critique of an anxiety hypothesis ofpeptic ulcer etiology and of a previous experimentof the writer is considered. It is shown that thiscritique did not adequately describe the experi-mental procedure or the results of the study it dis-counted. The theoretical objections raised in thiscritique are shown to be a function of confusion ofthe differential role of anxiety in the conversionneuroses and in the vegetative neuroses. The reluc-tance to consider the autonomic concomitants ofanxiety is regarded as a joint result of the historyof psychodynamic theory and the unqualified ex-tensions of Cannon's emergency theory of emotionsto chronic emotional processes.5. Possible fruitful lines of research for a com-VOL. XII , NO. 3


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MAHLparative evaluationof the oral-dependency and anx-iety hypotheses of peptic ulcer etiology are discussed.

24.Bibliography

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MAY-JUNE, 1950

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Anxiety, Hci Secretion and Peptic ulcer

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