Research Article

DO DEPRESSIVE EPISODES LEAD TO ACCUMULATIONOF VULNERABILITY IN THE ELDERLY?

Albertine J. Oldehinkel, Ph.D.,1–3n

Marjan D. van den Berg, M.D., Ph.D.,1,2 Antoinette L. Bouhuys, Ph.D.,1,2

and Johan Ormel Ph.D.,2,3

The vulnerability-accumulation (or scarring) hypothesis postulates that theexperience of depression induces a lasting increase in vulnerability, and throughthis raises the risk of recurrence. We examined the validity of the vulnerability-accumulation model for depressive episodes in later life. The sample comprised26 elderly persons who had remitted from a depressive episode and 96 controlrespondents who were all selected from the participants of a large communitysurvey among persons aged 57 years or more. Several psychosocial vulnerabilityindicators were assessed premorbidly, during the depressive episode and afterremission. High levels of psychological distress, low life satisfaction, chronicsomatic diseases, high neuroticism, and low scores on extraversion, mastery, andself-efficacy appeared to be predictors of depression in this sample. During thedepressive episode, psychological distress was higher and life satisfaction,physical, role, and social functioning, as well as feelings of self-efficacy lowerthan before the episode. Physical and role functioning, cognitive function, andself-efficacy were lower after remission compared to premorbid levels, but(other) personality indices had not changed after remission compared topremorbid levels. Furthermore, we failed to find differences between first andrecurrent episodes. Support for the vulnerability-accumulation model waslimited at the most. Although psychosocial scarring may occur in the elderly, ourfindings tentatively suggest that this accumulation does not manifest itself inmajor vulnerability indicators such as neuroticism. Depression and Anxiety18:67–75, 2003. & 2003 Wiley-Liss, Inc.

Key words: depressive disorder psychology; aged; prospective studies; riskfactors; recurrence

INTRODUCTIONDepression is a common, often disabling illness incommunity-dwelling elderly [Beekman et al., 1999;Ormel et al., 1999; Penninx et al., 1999], with highrates of persistence and relapse [Cole et al., 1999;Denihan et al., 2000; Sharma et al., 1998]. A wide rangeof psychosocial vulnerability factors, among which aredisabilities and deviant personality traits, have beenfound to increase risk of onset and to be associated withchronicity of depressive symptoms [Oldehinkel et al.,2000, 2001; Ormel and Wohlfarth, 1991; Prince et al.,1997; Scott et al., 1995; Van den Berg et al., 2000].

The usefulness of psychosocial vulnerability mea-sures is limited if assessed during an episode ofdepression because depressed persons’ self-perception

DEPRESSION AND ANXIETY 18:67–75 (2003)

1Department of Psychiatry, University of Groningen, The

Netherlands2Graduate School of Behavioral and Cognitive Neurosciences,

University of Groningen, The Netherlands3Graduate School for Experimental Psychopathology, The

Netherlands

Contract grant sponsor: The Dutch Government; Contract grant

sponsor: University of Groningen, Faculty of Medical Sciences;

Contract grant sponsor: The Dutch Cancer Foundation (NKB/KWF);

Contract grant sponsor: Netherlands Organization for Scientific

Research (NWO); Contract grant number: NWO-MW 904-57-069.nCorrespondence to: Albertine J. Oldehinkel, Department of

Psychiatry, University of Groningen, P.O. Box 30.001, 9700 RB

Groningen, The Netherlands. E-mail: a.j.oldehinkel@med.rug.nl

Received for publication 18 October 2002; Accepted 25 May 2003

DOI: 10.1002/da.10116

Published online in Wiley InterScience (www.interscience.wiley.com).

&& 2003 WILEY-LISS, INC.

and recall may be biased negatively [Cohen et al., 1988;Margo et al., 1993; Monroe and Steiner, 1986;Morgado et al., 1991]. To date, increased vulnerabilityduring a depressive episode has commonly beeninterpreted as a temporary phenomenon [Dohr et al.,1989]. An exciting alternative interpretation is the scarhypothesis, postulating that the experience of depres-sion induces a lasting increase in vulnerability in thepsychological, social, and/or biological domain, at leastin some cases, and through this raises the risk ofrecurrence [Akiskal et al., 1983; Bouhuys and Sam,2000; Kessing et al., 1998; Lewinsohn et al., 1981; Postet al., 1986, 1992; Segal et al., 1996; Wilhelm et al.,1999]. Scarring would result in a spiral of vulnerabilityaccumulation, with increasing vulnerability leading tofurther episodes of depression producing even morevulnerability, and so on. The notion of vulnerabilityaccumulation would help to explain some puzzlingobservations, such as the prognostic value of thenumber of earlier episodes and the greater role ofsevere life events in association with first compared torecurrent depressive episodes [Brown et al., 1994;Kessing et al., 1998; Ormel et al., 2001; Post, 1992].

Several studies found differences between formerlydepressed persons and never-depressed controls on oneor more vulnerability factors [Billings and Moos, 1985;Perris et al., 1984; Reich et al., 1987]. The question iswhether these differences are a consequence ofvulnerability accumulation (scarring hypothesis) orwhether the formerly depressed persons alreadydif fered from the never-depressed group before theirfirst episode of depression (trait marker hypothesis).Prospective studies with assessments before and afterthe depressive episodes are required to distinguishbetween these two possibilities. Such studies arerelatively scarce and have yielded both results in favorof the vulnerability-accumulation hypotheses [Kendleret al., 1993; Rohde et al., 1994] and evidence against it[Rohde et al., 1990; Shea et al., 1996]. Compared topre-episode levels, Rohde and colleagues found a post-episode increase of psychosocial vulnerability inadolescents [Rohde et al., 1994] but not in personsaged 50 years or more [Rohde et al., 1990], suggestingthat vulnerability-accumulation may only occur inyoung persons.

In the study described in this paper, we examinedthe validity of the vulnerability-accumulation modelfor depressive episodes in later life, using a communitysample and a range of vulnerability indicators assessedpremorbidly, during the depressive episode andafter remission. Specific research questions were thefollowing.

1. Are premorbid vulnerability levels of depressedpersons higher than those of control respondents?

2. Are vulnerability levels of depressed personsmeasured during the depressive episode increasedcompared to premorbid levels?

3. Do increased levels of vulnerabilityFif anyFpersist after remission of the depressive episode?Otherwise stated, are postmorbid vulnerabilitylevels higher than premorbid levels?

4. Are vulnerability levels, assessed premorbidly orafter remission, higher for recurrent episodes thanfor first episodes?

SUBJECTS AND METHODSSUBJECTS

The study, including 26 elderly persons who hadremitted from a depressive episode and 96 controls,was nested in a large community survey among personsaged 57 years or more that was carried out in 1993[Kempen et al., 1996; Ormel et al., 1998]. Cases (surveyparticipants with a recent onset of a depressive episodeaccording to the below-described criteria) and controlswere selected during a 24-month period that started inApril 1996. After entry into the study, depressed caseswere telephoned bimonthly to chart the course of thedepression. The present study only includes those whoremitted within 2 years (the maximum duration of thefollow-up period). Measures of well being, personality,physical disorders, and functional disability wereassessed as part of the 1993 baseline survey, duringdepression, and after remission. The mean durationbetween the baseline measurement and the measure-ment during depression was 50.88 months (sd¼ 7.05),and between baseline and the measurement afterremission 68.57 months (sd¼ 10.35). Control groupdata involved only two measurements: baseline (in1993) and follow-up, on average 58.53 months(sd¼ 7.24) after baseline. Hence, the control groupwas measured later than the cases during depression(t¼ 4.81, Po.01) and earlier than the cases afterremission (t¼�5.62, Po.01). Informed consent wasobtained of all subjects after the nature of theprocedures had been fully explained. The selectionand follow-up procedures are described in more detailbelow.

SELECTION OF DEPRESSED CASES ANDCONTROLS

Of the 5,279 people who took the survey in 1993,approximately 3,700 were available for selection for afollow-study on depression. Non-availability was dueto no informed consent for further contact, death,severe impairments, or participation in another follow-up study.

Possibly depressed survey participants were selectedby two complementary approaches: screening byquestionnaire and examining the records of generalpractitioners (GPs). The screening questionnaireincluded the 15-item version of the Geriatric Depres-sion Scale [GDS-15; Lesher and Berryhill, 1994;

Oldehinkel et al.68

Yesavage et al., 1982] that was extended with questionsabout the probable presence of one or more depressioncore symptoms (depressed mood, loss of pleasure, andloss of interest) and the duration of the symptoms.During the 24-month enrollment period, eligiblesurvey participants received this questionnaire abouttwice. In total, we sent out 7,566 questionnaires, ofwhich 85.4% returned fully completed. Subjects witha GDS-15 score of six or more and a depressionsymptom that had started or worsened in the preceding9 months were considered ‘‘screen-positive’’ (n¼ 269).In addition to the screening questionnaire, a researchphysician regularly visited GPC to retrieve, from themedical records, the names of eligible survey partici-pants whom the GP had diagnosed as having depressivesymptoms (ICPC codes P03 and P76; Lamberts andWood, 1987] during the past 3 months. This approachyielded 105 notifications of persons with a possibledepressive episode, of whom 22 had already beenrecruited via screening, leaving 83 additional persons.It should be noted that the selection procedureprobably traced only a relatively small part of allbaseline participants with an onset of depressionbetween 1996 and 1998, since late-life depression isoften not reported to or recognized by GPs and thescreening questionnaire covered, on average, only twoout of the 24 months of the recruitment period.

Persons selected by the screening questionnaire and/or their GP (n¼ 352) were interviewed shortly bytelephone (non-response 23.6%) to establish whetherthey had at least one depression core symptom that hademerged in the previous 9 months. Those who did(n¼ 188) were put through a face-to-face diagnosticinterview, the Present State Examination [PSE-10;Wing et al., 1998]. Nineteen cases were discardedbecause of incomplete or unreliable data. Respondentswere asked to indicate the 4-week period during the 3months preceding the interview at which they feltworst, and that period was assessed by the PSE-10.Only persons whose PSE covered the last month(n¼ 118) qualified for the follow-up part of the study,of whom 71 met the below-described diagnosticcriteria of DSM-IV major or minor depressive episode.Various factors may have introduced selection bias,such as the unavailability of some baseline participantsfor screening, and the nonresponse of some whoscreened positive and were eligible for further inter-viewing. Brilman and Ormel [2000] compared thesegroups of nonresponders to responders in terms ofbaseline characteristics. In general, nonresponderswere somewhat older and sicker, in particular physi-cally and cognitively.

Control subjects were randomly selected from thesurvey population within either the lowest (score 0 or1) or the highest (score 6 or more) quartile of thebaseline (T0) neuroticism score on the EysenckPersonality Questionnaire [Eysenck et al., 1985].Persons with a GDS-15 score of six or more wereexcluded because of the possible presence of depres-

sion. In total, we interviewed 97 control subjects, oneof whom was discarded on the basis of the GDS-15score, leaving 96 persons: 52 with low and 44 with highneuroticism scores. Stratified sampling on the basis ofbaseline neuroticism was irrelevant to the researchquestions dealt with in this paper. High and lowneuroticism subjects did not differ with respect to anyof the effects presented in this paper, except forneuroticism.

FOLLOW-UP

After the face-to-face interview, persons who met thecriteria of DSM-IV major or minor episode (n¼ 71)were interviewed by telephone every 2 months to chartthe course of the depression. The telephone interviewsinvolved the 15-item structured interview version ofthe Hamilton Depression Rating Scale (SI-HDRS),with a format allowing it to be administered face-to-face or by telephone with equivalent results [Pottset al., 1990]. If the score on the SI-HDRS was seven orless and the respondent reported to have felt this wayfor at least 6 weeks, an appointment was made foranother face-to-face interview. The maximum follow-up period was 2 years; after which all remainingrespondents were invited for a face-to-face interview,regardless of their SI-HDRS score. At the interview,diagnosis was assessed again with the PSE-10. Remis-sion was defined as not meeting the below-describedcriteria for DSM-IV major or minor episode anymore.

Of the 71 persons who qualified for the follow-uppart of the study, 29 dropped out prematurely (13refused further participation, 7 were mentally orphysically incapable, 5 died, and 4 dropped out forother reasons). The proportion of drop-outs (40.8%)was comparable to that of persons who were alsofollowed-up but did not meet the criteria for this study(n¼ 34, 44.1% drop-outs). Of the remaining 42persons, 26 remitted within 2 years. This 2-yearoutcome is largely consistent with other studies onthe prognosis of depression in elderly community andprimary samples, reviewed by Cole et al. [1999].

MEASURES

Diagnosis. Both during the depressive episode andafter remission, diagnostic assessment of the cases wasbased on the tenth version of the Present StateExamination [PSE-10; Wing et al., 1998], administeredby interviewers who were extensively trained byexperienced staff members and maintained their skillsin monthly booster sessions. The PSE-10, which is partof the Schedules for Clinical Assessment in Neurop-sychiatry [SCAN; World Health Organization, 1992],generates diagnoses according to the DSM-IV[American Psychiatric Association, 1994]. Diagnosiswas assessed for the month before the interview. Wedistinguished two categories of depression: DSM-IVmajor depressive episode and minor depressive episodeaccording to research criteria defined in the DSM-IV

Research Article: Vulnerability in Depressed Elderly 69

(two to four symptoms including depressed mood, lossof interest, or loss of pleasure). The depressivesymptoms did not meet criteria for a mixed episode,were not due to the direct physical effects of substanceuse or somatic illness, and were not better accountedfor by bereavement. Studies comparing major andsubsyndromal depression in the elderly suggestcommon vulnerability [Van den Berg et al., 2000]and common neurobiological substrates [Kumaret al., 1998]. The interview with the control res-pondents did not include the PSE-10, but we didassess the lifetime presence of depressive episodes(see below).

History of depression. Both in cases (at themeasurement during depression) and controls, infor-mation on the history of depression, among which thepresence of earlier depressive episodes, was gatheredwith an interview especially developed for this purpose.The depressive episode was labeled recurrent if therehad been at least one previous episode meeting thecriteria of at least minor depression.

Psychological distress and life satisfaction. At allmeasurement points, the level of psychological distresswas assessed with the 12-item version of the GeneralHealth Questionnaire [GHQ-12; Goldberg andWilliams, 1988] (range 0–36) and life satisfactionwith the Cantril Self-Anchoring Scale [Cantril, 1965],where respondents were asked to indicate their positionon a ladder with rungs ranging from 0 (worst possiblelife) to 10 (best possible life).

Physical health and functional disabilities. At allmeasurement points, the presence of chronic somaticdiseases in the year before the interview was assessed bymeans of a list of 18 diseases, concerning therespiratory, cardiac, gastrointestinal, endrocrinological,neurological, and dermatological systems, the kidneys,prostatic gland, locomotor apparatus, and neoplasms.Diseases were only included if the respondents usedmedication or were treated by a physician. Cognitivefunction was measured with the 12-item version of theMini Mental State Examination (MMSE-12; Kempenet al., 1995; range 0–12). The extend to which health,both physical and mental, interfered with physicalactivities, with usual daily role activity such as work andhousework, and with normal social activities wasmeasured with the Medical Outcome Study (MOS)Short-Form General Health Survey [Stewart et al.,1988]. All MOS-scores ranged from 0 (minimum levelof functioning) to 100 (maximum level of functioning).

Personality. A number of personality characteristicswere assessed at all measurement points. Neuroticism(range 0–12) and extraversion (range 0–12) weremeasured by subscales of the Revised Eysenck Person-ality Questionnaire [EPQ-R; Eysenck et al., 1985]. Theextent to which the respondents regarded their lives asbeing under their own control was assessed by a seven-item mastery scale (range 7–35) developed by Pearlinand Schooler [1978]. The 16-item Self-Efficacy Scaleof Sherer and Maddux [1982; Bosscher and Smit, 1998;

range 16–80) was used to measure feelings of compe-tence. Finally, interpersonal sensitivity was measuredby the 36-item Interpersonal Sensitivity Measure[IPSM; Boyce and Parker, 1989; range 36–144]. Insteadof during the baseline survey in 1993, the IPSM wasadministered in January 1995.

ANALYSES

Differences between baseline vulnerability levels ofcases and controls were tested by means of t-tests.Within the group of cases, measurements at differenttime points were analyzed by means of (repeatedmeasures) analysis of variance. If the multivariate testindicated significant differences between the threemeasurement points (i.e., before, during, and after theepisode), we used simple contrasts to examine whethervulnerability during the episode was elevated comparedto baseline (premorbid) levels, as well as whetherpostmorbid vulnerability was higher than baselinevulnerability. The extent to which differences betweenpre- and post-morbid levels might be attributable toage-related decline rather than the depressive episodewas tested by the interaction of group (cases vs.controls) and time (pre- vs. post-morbid in cases andbaseline vs. follow-up in controls). A dif ference with atwo-sided Po.05 was considered statistically signifi-cant. We performed multiple statistical tests, the resultsof which may suffer from chance capitalization: witha¼ .05 one would expect some 5% of the associationsto be significant merely on the basis of chance. Itshould be noted that a statistically significant result inthis context does not have the same weight assignificant results in an experimental design.

RESULTS

ARE PREMORBID VULNERABILITY LEVELSOF DEPRESSED PATIENTS HIGHER THANTHOSE OF CONTROL RESPONDENTS?

Cases and controls did not differ significantlywith respect to the proportion of females (cases:61.5%; controls: 48.5%; w1

2¼ 2.02, P¼ .16), age atbaseline (cases: 67.18, sd¼ 7.26; controls: 66.81,sd¼ 6.93; t¼ 0.23, P¼ .82), proportion of personsliving alone at baseline (cases: 42.3%; controls:26.0%; w1

2¼ 2.60, P¼ .11), or education level (cases:38.5% at least secondary; controls 46.9%, w1

2¼ .59,P¼ .44). Mean values on (putative) psychosocialvulnerability indicator are listed in Table 1, whereasTable 2 presents results of t-tests comparing baselinevalues of cases and controls. At the baseline survey in1993, the (future) depressed cases showed higher levelsof psychological distress, lower levels of life satisfac-tion, and more vulnerability on all personality char-acteristics except interpersonal sensitivity.

Oldehinkel et al.70

ARE VULNERABILITY LEVELS OFDEPRESSED PATIENTS MEASURED DURINGTHE DEPRESSIVE EPISODE INCREASEDCOMPARED TO PREMORBID LEVELS?

Multivariate tests of differences between the mea-surements within cases were significant for psycholo-

gical distress; life satisfaction; physical, role, and socialfunctioning; and self-efficacy. Subsequent univariatetests of differences between measures at baseline andduring the depression revealed that levels of psycholo-gical distress were significantly elevated and lifesatisfaction reduced during the depressive episode

TABLE 1. Psychosocial vulnerability indicators for depressed cases (at baseline, during the depressive episode, and afterremission) and control respondents (at baseline and follow-up)

Depressed cases (n¼ 26) Controls (n¼ 96)

Variablea Baseline During depression After remission Baseline Follow-up

Psychological distress (GHQ-12) 14.79 (6.65) 18.88 (5.21) 12.79 (5.99) 9.77 (4.11) 8.79 (3.32)Life satisfaction (Cantril’s Ladder) 6.26 (1.40) 5.46 (1.67) 6.29 (1.37) 7.65 (1.12) 7.64 (1.06)

Number of chronic somatic diseases 1.71 (1.40) 2.04 (1.30) 2.00 (1.44) 0.95 (1.00) 1.04 (1.00)Cognitive function (MMSE-12) 11.33 (0.96) 11.08 (1.18) 10.79 (1.14) 11.37 (0.83) 11.31 (0.82)Physical functioning (MOS) 67.31 (28.08) 49.36 (31.79) 51.92 (33.77) 77.26 (23.71) 71.01 (25.04)Role functioning (MOS) 73.08 (40.57) 53.83 (39.81) 57.69 (44.03) 82.29 (36.98) 82.29 (29.00)Social functioning (MOS) 82.31 (18.18) 60.00 (28.84) 80.77 (22.26) 84.79 (26.56) 89.79 (17.65)

Neuroticism 6.75 (3.29) 7.54 (3.11) 6.42 (3.79) 3.88 (3.81) 2.97 (3.15)Extraversion 5.71 (3.24) 5.00 (2.87) 5.25 (3.03) 7.34 (3.25) 7.11 (3.29)Mastery 20.71 (3.90) 19.17 (4.06) 20.50 (4.04) 26.20 (4.81) 24.97 (4.98)Self-efficacy 58.46 (8.55) 52.46 (8.59) 53.00 (9.82) 63.09 (11.55) 62.43 (10.95)Interpersonal sensitivity 75.65 (16.40) 80.45 (15.02) 79.20 (14.01) 70.34 (12.94) 73.58 (13.13)

Values are expressed as mean (sd).aGHQ, General Health Questionnaire; MMSE, Mini Mental State Examination; MOS, Medical Outcome Study.

TABLE 2. Levels of psychosocial vulnerability indicators for depression: comparisons between cases and controls;between measurements within cases; and between recurrent and first episodes

Comparisons within cases (n¼ 26)

Cases (n¼ 26)vs. controls

(n¼ 96), baselineMultivariate

testUnivariate

testsb

Recurrent (n¼ 12)vs. first (n¼ 14)

episodes, after remission

Variablesa t P f2, 24 P Dep vs. Base Rem vs. Base t P

Psychological distress (GHQ-12) 3.74 o.01 29.66 o.01 nn �0.10 .92Life satisfaction (Cantril’s Ladder) �4.94 o.01 7.86 o.01 nn �1.05 .31

Number of chronic somatic diseases 2.85 o.01 0.71 .50 0.00 1.00Cognitive function (MMSE-12) �0.91 .85 2.43 .11 1.36 .10Physical functioning (MOS) �1.83 .07 6.45 o.01 nn nn 0.89 .38Role functioning (MOS) �1.10 .27 5.10 o.01 nn nn �0.37 .71Social functioning (MOS) �0.45 .65 8.75 o.01 nn �2.52 .02

Neuroticism 4.06 o.01 2.38 .12 �0.11 .92Extraversion �2.83 o.01 1.68 .12 0.94 .36Mastery �5.39 o.01 2.17 .14 0.20 .85Self-efficacy �2.16 .04 6.03 o.01 nn nn 1.31 .20Interpersonal sensitivity 1.43 .16 2.03 .16 �0.58 .57

Numbers in bold indicate Po .05.nPo.05.nnPo.01.aGHQ, General Health Questionnaire; MMSE, Mini Mental State Examination; MOS, Medical Outcome Study.bOnly tested when the multivariate F-value was significant. Base¼ baseline, Dep¼ during the depressive episode, Rem¼ after remission.

Research Article: Vulnerability in Depressed Elderly 71

compared to baseline levels. Furthermore, the depres-sion was associated with a significant increase infunctional limitations, with respect to physical, role,and social functioning, and reduced feelings of self-efficacy.

DO INCREASED LEVELS OFVULNERABILITY PERSIST AFTERREMISSION OF THE DEPRESSIVEEPISODE?

The amount of psychological distress as well as thescore on Cantril’s Ladder returned to baseline levelsafter remission, validating our criterion of remission.Postmorbid social functioning was comparable tosocial functioning at baseline, but physical functioning,role functioning, and feelings of competence (self-efficacy) remained significantly reduced.

The effect of role functioning could partly beexplained by physical functioning and self-efficacy, inthat the effect was no longer significant (P¼ .22 andP¼ .27, respectively) if adjusted for the difference inthese two variables. Otherwise, all ef fects remainedsignificant if adjusted for the dif ference in any of theother variables.

To investigate to what extent the results might beattributable to age-related decline rather than thedepressive episode, we tested whether differencesbetween pre- and post-morbid levels were larger thanthose between baseline and follow-up measures inthe control group. The interaction of time andcaseness was significant for self-efficacy (F1,120¼6.27, P¼ .01) and cognitive function (F1,120¼ 5.34,P¼ .02), and showed a trend (Po.10) for physicalfunctioning (F1,120¼ 3.02, P¼ .09) and role function-ing (F1,120¼ 3.34, P¼ .07), indicating that differencesbetween pre- and post-morbid vulnerability withincases could not be attributed to normal age-relateddecline. Other variables neither showed a significantinteraction effect nor a trend (F-values ranging from0.01 to 1.18, corresponding P-values from .97 to .28).

ARE VULNERABILITY LEVELS HIGHER FORRECURRENT EPISODES THAN FOR FIRSTEPISODES?

About half (46%) of the episodes of depression wererecurrent. First and recurrent episodes did not dif ferwith respect to any of the baseline vulnerabilityindicators. With respect to levels assessed after remis-sion, the only significant dif ference concerned socialfunctioning, which was higher for those remitted fromfirst episodes (t¼ 2.52, P¼ .02).

DISCUSSIONThe aim of this study was to examine the validity

of the vulnerability-accumulation model for depres-sive episodes in later life. We examined which

vulnerability factors showed higher premorbid levelsin depressed persons compared to controls, whichwere increased during the depression comparedto premorbidly assessed levels and which remainedelevated after remission. Furthermore, we investigateddifferences between first and recurrent depressiveepisodes.

Consistent with other studies [Clark et al., 1994;Duggan et al., 1995; Hirschfeld et al., 1989; Lynesset al., 1998; Prince et al., 1997], high levels ofpsychological distress, low life satisfaction, chronicsomatic diseases, and personality traits characterizedby high neuroticism-scores and low scores on extra-version, mastery, and self-efficacy appeared to bepredictors (trait markers) of depression in this sample.

During the depressive episode, psychological distresshad increased and life satisfaction decreased, asexpected, and we found lower levels of physical, role,and social functioning. This association betweendepression and disabilities has been found in manyother studies, both in non-elderly [Broadhead et al.,1990; Ormel et al., 1993, 1994, 1999; VonKorff et al.,1992; Wells et al., 1989; Wohlfarth et al., 1993] andelderly samples [Beekman et al., 1995; Bruce et al.,1994; Penninx et al., 1998; Prince et al., 1997, 1998].Furthermore, reported feelings of self-efficacy werelower during the depressive episode than before,implying that this measure may be especially sensitiveto mood-induced bias in the elderly.

Subsequently, we investigated whether increasedlevels of vulnerability (scars) persisted after remissionof the depressive episode. Physical and role function-ing, cognitive function, and reported feelings ofcompetence were lower after remission compared topremorbid levels; hence our findings provide limitedsupport for the scarring hypothesis. However, the factthat most personality indices had not changed afterremission compared to premorbid levels, as well as ourfailure to find differences between first and recurrentepisodes, clearly militates against the model. Especiallythe lack of change in neuroticism and interpersonalsensitivity is noteworthy, since these personalityfeatures are well-established vulnerability factors fordepression and have been found to be susceptible toscarring effects in some other studies [Kendler et al.,1993; Rohde et al., 1994]. Perhaps our sample size wastoo limited or our measures of neuroticism andinterpersonal sensitivity not sensitive enough for thepresumably subtle changes in vulnerability to becomeapparent. Another explanation may be that vulner-ability accumulation is more likely to occur in youngerpersons than in elderly ones: Rohde and colleagues[1990, 1994] found more psychosocial scars in adoles-cents than in elderly persons. It is also possible thatneuroticism is not affected by depression after all. Notonly has lack of change between pre- and post-morbidassessments of neuroticism been reported by others aswell [Duggan et al., 1991; Shea et al., 1996], supportfor lack of accumulation also comes from Kendler and

Oldehinkel et al.72

Gardner [2001], who found that monozygotic twinsdiscordant for major depression did not differ inneuroticism.

Physical and role functioning were lower post- thanpre-morbid, but it may be premature to attributethe increase in vulnerability to the depressive episode.One reason for caution is that the decline in physicaland role functioning could well be a cause, rather thana consequence, of the depression. Depressive symp-toms have been found to be associated with anincreased risk of subsequent disabilities in elderly[Bruce et al., 1994; Penninx et al., 1998], but theopposite, i.e., disabilities preceding the depression, hasfrequently been reported as well [Beekman et al., 1995;Kennedy et al., 1990; Oldehinkel et al., 2001; Princeet al., 1997, 1998]. Stressful events and difficulties,which are often health-related in the elderly, are majorrisk factors for late-life depression [Brilman and Ormel,2001]. Hence, at least part of the sample may havebecome depressed because of the decline in abilitiesand functioning, rather than the opposite. Whereas thedepressive symptoms may fade away once a person hasadapted to the altered state, the physical and roledisabilities are likely to be permanent and the level offunctioning will often not return to its original(premorbid) level in the elderly. As opposed to physicaland role functioning, social functioning seemed tochange synchronously with the depressive symptoms.Synchrony of change between depression and socialdisability has been reported by others as well [Hayset al., 1995; Ormel et al., 1993, 1994; VonKorff et al.,1992].

In addition to the lasting reduction in physical androle functioning, we also found a persistent decline incognitive function and self-efficacy. Although it shouldbe noted that the reduction in cognitive function wasquite small (only half a point on the twelve-itemMMSE-12 and not significant at the within-casesanalyses), it was significantly larger than in the controlgroup. The fact that the interaction of time andcaseness was significant for cognitive function, despitethe non-significant test for dif ferences within cases, isprobably due to increased power because of therelatively large control group. The association betweendepression and cognitive decline is well known, but ithas not been established yet whether depression is(only) a risk factor for dementia or also a prodrome ofor early reaction to perceived cognitive decline [ Jorm,2000]. If depression and cognitive function mutuallyaffected each other, vulnerability accumulationthrough cognitive decline would be conceivable indepressed elderly.

It may seem plausible that the reduced feelings ofcompetence (self-efficacy) were a consequence of thedecline in cognitive, physical, or role functioning.However, the effect of self-ef ficacy could not beexplained by the difference in these factors. It isinteresting to note that Rohde et al. [1990], in the onlyother, to our knowledge, prospective community study

on vulnerability accumulation in elderly persons, foundno evidence in favor of vulnerability accumulation,except, tentatively, that feelings of social competencewere lower after the depressive episode. Kendler andGardner [2001], in their before-mentioned study ofmonozygotic twins discordant for depression, foundthat these twins did not differ in neuroticism but didshow differences in measures of self-efficacy. Hence,perhaps the experience of a depressive episode actuallytends to lower feelings of competence in (some) elderlypersons. Self-efficacy, that is, the conviction that onecan successfully execute behavior required to produceoutcomes desired, can be reduced by failure experi-ences [Bandura, 1977], and a depressive episode may beconsidered a failure (not being able to cope with thesituation properly).

Strong features of the present study are its prospec-tive design, the use of rigorous diagnostic criteria, andthe fact that the respondents were selected from acommunity survey, which makes them more represen-tative than a treatment sample. There are alsolimitations. First, only 26 of the depressed patientsremitted within 2 years. Our failure to find significanteffects for many of the vulnerability markers couldtherefore be due to inadequate statistical power,especially in comparisons between first and recurrentepisodes. Second, no diagnostic interview was adminis-tered at baseline; hence part of the respondents mayhave been depressed at that time. Considering the factthat the scores on the General Health Questionnaireand Cantril’s Ladder did not differ significantlybetween baseline and after remission, we do not believethat this has been the case. Third, the time betweenbaseline and follow-up in control respondents wasshorter than the time between baseline and remissionin cases, which means that we cannot exclude that thevulnerability accumulation in cases was, to some extent,caused by age-related decline rather than the depressiveepisode. This is not very likely, however, since thedifference in duration was only 10 months. Further-more, in case of age-related changes, we would at leastexpect to find a trend in the same direction in controls,which we did not. Finally, despite our prospective studydesign, we cannot exclude the possibility of reversecausality: it is still conceivable that the decline infunctioning caused the depression, rather than theopposite.

In conclusion, although vulnerability accumulationmay occur in the elderly, our findings tentativelysuggest that this accumulation does not manifest itselfin major vulnerability indicators such as neuroticism.Feelings of competence, however, may decrease as aconsequence of depression. More research, preferablywith accurate dating of both changes in vulnerabilitymeasures and changes in depressive symptoms, isneeded to find out whether the changes in functioning(cognitive, physical, and role) are caused by thedepression itself or rather by factors associated withthe depression, such as health-related stressful events.

Research Article: Vulnerability in Depressed Elderly 73

ACKNOWLEDGMENTSThis research is part of the Groningen LongitudinalAging Study (GLAS). GLAS is conducted by theNorthern Centre for Healthcare Research (NHC) andvarious Departments of the University of Groningen inThe Netherlands. The central office of GLAS islocated at the NCH, P.O. Box 196, 9700 ADGroningen, The Netherlands (online at http://www.med.rug.nl/nch/). The data were collected incollaboration with Els Brilman. Furthermore, we thankGerda Bloem, Erwin Geerts, Roelie Nijzing, andMieke van Schepen for their assistance during thedata collection, and the following mental healthclinics for their willingness to recruit patients forthis study: RIAGG Groningen, RIAGG Assen,Psychiatrische Universiteitskliniek Groningen, Ambu-latorium Drachten, Medisch Centrum Leeuwarden,RIAGG Winschoten, and CGG Zuid.

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