a Expressed Emotion and Psychiatric Relapse A Meta-analysis, Ronald L. Butzlaff, AM; Jill M. Hooley, DPhil Background: Expressed emotion (EE) is a measure of the family environment that has been demonstrated, to be a reliable psychosocial predictor of relapse in schizophrenia, However, in recent years some promi- nent nonreplications of the EE-relapse relationship have been published. To more fully address the ques- tion of the predictive validity of EE, we conducted a meta-analysis of all available EE and outcome studies in schizophrenia, We also examined the predictive validity of the EE construct for mood disorders and ‘eating disorders, Methods: An extensive literature search revealed 27 studies of the EE-outcome relationship in schizophre- nla. Using meta-analytic procedures, we combined the Findings of these investigations to provide an estimate ‘of the elfect size associated with the EE-relapse relation- associated with EE for mood and eating Results: The results confirmed that EE fs a significant and robust predictor of relapse in schizophrenia. Addi- onal analyses demonstrated that the EE-relapse rela- onship was strongest for patients with more chronic schizophrenic illness. Interestingly, although the EE con- struct is most closely associated with research in schizo- phrenia, the mean effect sizes for EE for both mood dis orders and eating disorders were significantly higher than the mean effect size for schizophrenia, Coneluston: These findings highlight the importance of EE in the understanding and prevention of relapse in « broad range of psychopathological conditions, ship. We also used met ‘analysis to provide estimates of Arch Gen Psychiatry. 1998;55:547-552 From the Department of Psychology Harvard University, Cambridge, Mass. PRESSED EMOTION (EE) is a measure of the family environment that is based fon how the relatives of a psychiatric patient sponta- neously talk about the patient. Assessed during the Camberwell Family Interview (CED, relatives are classified as being, high in EE AT they make more than a specified threshold number of critical comments or show any signs of hostility for marked emotional overinvolvement In the last 15 years, the EE con- struct has been extensively studied More than 20 studies, conducted in many countries, have investigated the EE-relapse relationship in patients with schizophrenia. In addition, there is a growing literature concerning the role of EE in unipolar depression,”? bipolar dis- order," and eating disorders.” Expressed emotion has also been used in outcome studies of patients with dementia’ and diabetes mellitus.” The results of these investigations make 2 things clear. First, rather than being a construct of interest Anci GEN pSTCINTRIVOU SS, JUNE 1958 (©1908 American Med solely with respect to schizophrenia, EE fs a more general predictor of poor out- come across a range of conditions, Sec- ond, EE is a construct that is modifiable. Results from several rials of family- based treatment indicate that when family EE levels decrease, patients relapse rates also fall. From a elintcal perspective, these findings are clearly very encouraging Given this, it issuxprising that EE x mains a somewhat controversial con- struct. However, based on the results of a small number of nonreplications, some cli nicians and researchers have been quick to conclude that EE is not a reliable pre- dictor of relapse. This article represents an effort to examine this issue in a statis cally rigorous manner. Although age gate analyses of the EE literature do ex- fst" we chose to meta-analyze the studies because of the dangers of aggregating oF pooling raw data without blocking, espe- cially when using 2X2 tables.” Mor ver, because meta-analysis provides way tocombine similarstudies ina manner that Association, All rights reserved.MATERIALS AND METHODS LITERATURE SEARCH. ‘To be included, articles had to mest thefllowing citer (Dypaten diagnosis of schizophrenia or schzoafectve die order r mood or eating disorder, (2) EE assessed using the (CFtadniniaerd at the tine of the index hosptalzaton fone exception” was published before the CF became the stan dard method for assessing EE); (3) EE used to predict re- lap for9 to 12 month: sed (8) published dat alowed catimat ofthe elect size and significance level tbe calcu ined A total of 27 articles met these erteria We excluded 22 experimental articles forthe following reasons (1) the etwas not administered at intake; (2) the CF was used to measure EE in nonfaly members (g, nursing sa); {G) Ee was used to predict something other ham alt poy chiatric relapee (4) the sample subject didnot include both fow-and high-EE families or the tlape data were notre ted for both groups; and (5) the report described data that were ako published elsewhere. STATISTICAL ANALYSIS, ‘The studies data were cast into 2%2 tables of counts— high vs low EE by relapsed vs not relapsed status. We chose tose @as our measure of effect size because of the prob- Jems associated with other indices." In cases where at thors did not eport the number of subjects relapsing in the high- and low-EE groups.'°we used a reliable formula for calculating an ellect size estimate.” Three other stud fies!” reported relapse rates of for one ofthe EE groups, We used a correction suggested by Overall” in calculating the effect size estimates for these studies, All elfect size estimates were transformed into Fisher z scores before any other calculations were done to ac- count for the nonnormal distribution of r.? We also cal- culated the associated standard normal deviate 2 score for cach study. This summary statistic is analogous toa or F {cstin stdies comparing differences between groups. Com- bining these = scores meta-analytically served as test sta Uistic forthe estimate of the overall significance ofthe com. bined average effect size estimate ofthe studies. Table 1 details the studies used in this meta-analysis, noting the corrections described abave.2!="=041 ‘Adistinetadvantage ofmets-analyticworksthatitallows uustouse contrat analyses to statistically test hypotheses us {ngallof hestudies as our sample population, Below we de- scribe the methods used to code or these contrast analyses, LENGTH OF ILLNESS. Iman eatlce review, one ofus J M.H.) suggested tha there might be «relationship between the duration of schizo- phrenic illness and the magnitude of the EE-relapse link, with longer durations of illness being associated with greater eflect sizes. We classified the EE reports according {fo the mean chronicity of the patient sample studied (table), ‘Our categorization criteria were as follows. ln the first group were studies in which the majority of patients (>50%) ‘were experiencing their first hospitalization, Our second. category included studies wth more heterogencoussampls, {in which the mean chronicity of the patient sample was ther very recent nor very chronic (eg, a sample that con- {ained 3036 recentonset patients but where the average num ber of prior hospitalizations was 28). The third category inclided studies with more chronic patients, where chronic was defined as more than 3 prior hospital admissions or 3 scan duration of illness ofa least 5 years GEOGRAPHIC LOCATION Recently, Bebington and Kuipers used visual inspec tion of @ graph to conclude that there was no variation in EE findings based on geographic location. We tested this hypothesis using an analysis ol variance (ANOVA) method!” involving the Q statistic, which is much the same as ax statistic but using meta-analytic data. Following Bebbing- ton and Kuipers, studies were grouped according to their ‘most obvious broad geographic location (ie, Northern Eu- rope, Southern Europe, North America, Australia, and Asia). EE AND OTHER PSYCHIATRIC CONDITIONS Expressed emotion was developed as a psychosocial predic. tor of relapse in schizophrenia. However, several research- cers have documented the link between EE and relapse in pa tients with mood disorders and eating disorders, such as, ssnorexis and obesity. We chose to meta-analyze these stud testo sablish thecllectsize of EE disorders ther than schis: phrenis, Because the number of studies in these geass l= ted, readers should view these findings as preliminary. EE AND MOOD DISORDERS Six studies have examined the relationship between EE and relapse in patients with major mood disorders (able 2) °°" Allfound a postive association between EE snd relapse. However, becaiseof the relatively small number bf stidiesthat havebeen conducted, thenumberof etical com- ‘mentsrequred toes lames ashigh-EEhasnot been firmly ‘tablished, Cuolfscores of 2ertisms’and criticisms" seer {ohave validity in unipolar patents. For patients with bipo- lar disorder acutolfscore of critical comments (e, the cut- olfscore used forschizophrenia) isthe mostapproprite* Our resultsarebased on cuolfscore of Zand for unipolar samples and 6 for bipolar samples. To facilitate future meta-analysis, ‘we encourage researchers to report relapse by varying levels, oferitical comments, inaddition to reporting the cutolfscore that proves most significantly predictive allows contrast analyses to be applied to the data, i al- lows us to consider several factors that might increase orattenuate the strength of the EE-relapse link. Finally, Ihecause we investigate the effect size of EE as a predic tor of outcome in mood disorders and eating disorders, this article provides the first estimates ofthe effect sizes of EE for nonschizophrenia-related conditions. ES} HOW WELL DOES EE PREDICT RELAPSE IN SCHIZOPHRENIA? The simple answer to this question is: quite well All but 3 of the studies described in Table 1 (89%) showed ass (©1908 American Med jamanetvrork.com/ on 12/13/2022 Association, All rights reserved.Blips nae data not avaabe. ee tndeates tos tansfrmaton, Frineates recent anset 2 med: ard 3, chron Scorected using the metod of Overal>™ nificant association between EE and patient relapse. If there were no relationship, we would expect 50% of the studies to have positive eflect sizes and 50% have negs- live effect sizes. The mean elect size for EE predicting relapse was r=0.30 (z= 11.30, P<.001). Weighting by degrees of freedom (which is preferable because it takes into account the number of subjects in each study) re- sulted in a weighted mean r=0.31. Thus, family levels Of EE ate significantly predictive of elevated rates of re lapse in schizophrenia patients. Moreover, our 95% con- fidence intervals (Cls) suggest there is only a 5% prob- ability that the effect size does not lie between 0.23 and 0.37. HOW IMPORTANT ARE THESE FINDINGS? I is not always easy to grasp the practical importance of ‘a mela-analytic effect size r=0.31, However, for a hypo- thetical sample of 200 patients (high EE =100; low EE = 100), an effect size r=0.30 translates into a high and low BE relapse rate of 65% and 35%, respectively.” In this model, EE s associated with approximately one third of the relapses that do occur and with wo thirds of the relapses that do not occur. Table 1. Summary Table of Included Stules: Table 2. Summary Table of Included Studies Expressed Emotion (EE) and Sehizoprenia® Expressed Emotion (EE) and Mood Disorders a. raapsedy “tata “ota te ont —— source ewe Winer 2p conse ‘tors Tom EE High co=2, 2° c0=9, 27° ‘enloandVecro” 538008 «3 FoaeyetaF(unpo) OS} 2a O37 0a Bure atal” ogg ze 05 NikowiestaP (pole 73D Osta Brando a= ais 1424038 it ta 1128 vans 08588 Brow sta ‘ud? 3850053 (olan Brown ea 5628503 taste aio 1622 014 se Bucierma ta a7 2 (unipalaripoa) and Osis wer tess al (oplay§ ND ott 058088 anvicandvueic# §— 211020723 ough anda (mpl) 20 1421 Oat Kamo ta mr iwi? ask Kegon ta? 11m the 0052 “2 ndetes to ransfomaton Lette ae set sig 027 ame ig ead Boat Chaos ata oi cl ae ie comme orp sans Makita ot a* “at aes om ‘The sample aso included 3 patents aagnased with schoatectve Nala" aa tattoo iors Hotes" Toi 928 ag? ony andVonphore= 1355 4169038 ea a ese WHAT ABOUT STUDIES THAT MIGHT feceianaa™ os feat ca? HAVE BEEN OVERLOOKED? Patra" ms 2-318 PhiipsandXiong 7 faz tz The issue of unpublished research is often called the “file- RostworowskaetaP® 111825081 drawer" problem, Itis addressed using a calculation sug- coe a gested by Rosenthal.” To lower the significance level of aes on thismetoanalsistojust barely ignifcan (P « 05) there Vane cad at eae would have to new, unpublished, oF undiscov- vata Meme 0m 3 cred studies averaging null results. When we consider Vaughan ta sou 2547 © 0a) that research that does not confirm the relationship be- tween EE and relapse often receives more attention than experimental replications, this seems unlikely Is HETEROGENEITY OF EFFECT SIZES ‘A PROBLEM? Combining the effect sizes of individual studies in a meta- analysis requires that the assumption of homogeneity of variance be tested and met, We used the X? statistic to test forthe heterogeneity of the effect sizes." The analy- ses resulted in a significant x'=54.01, d/=26, P=.001 We therefore conducted additional analyses to identify the variable(s) that accounted for the heterogeneity. These are described below. LENGTH OF ILLNESS The linear contrast ofthe relationship between effect siz for the EE-relapse association and the chronicity cat- gory ofthe patients resulted inacontrastz = 1.93, P =.03. As previously noted," EE appears to bea stronger predic- tor of relapse in patients with more longstanding ill- Grouping studies according to patient chronicity ac- counted for the heterogeneity of the elfect sizes for the recent-onset and the mixed chronicity groups. This sug- gests that illness chronicity was a hidden variable in the earlier combined analysis. Interestingly, however, the elect sizes of studies in the most chronic category still showed significant heterogeneity (x'=31.53, dj Anci GEN pSTCINTRVOU SS, JUNE 1958 (©1908 American Med Association, All rights reserved.P=.001). Further examination revealed that this was largely attributable to Parker et al."¥ This study ac- counted for 12.94 of the x" value of 31.53. Methodologt- cal problems associated with this study may explain its outlier status GEOGRAPHIC LOCATION Does the magnitude of the EE-relapse association vary according to the location of the research site? The test ‘of mean effect sizes across locations was not significant (Que 5.91, df=4). When categorized according to Beb- ington and Kuipers,"? geographic location is not re- lated to variations in effect size ‘One advantage of this analytic approach was that it followed the grouping method described by Bebington and Kuipers." Unfortunately, when we did this, the ANOVA assumption of homogeneity of variance was vio- lated (Qain=48.1, df=22, P =.001). Although ANOVA is relatively robust in this regard, we reanalyzed the data ‘employing more narrow geographic boundaries. We as- sumed that accounting for more ofthe variance using lo cation as a blocking variable would allow us to replicate the previously found nonsignificant effect of geographic region. However, this was not the case. Regrouping the studies as United Kingdom, Northern Europe, Southern Europe, Eastern Europe, North America, Australia, or Asia resulied in a significant variation in effect sizes between locations (Quovaa= 19-21, d/=6, P=.004), Further exami- nation revealed that the studies from Eastern Europe accounted for much of this heterogeneity (6.25 of the ‘Quon Statistic total). The second largest contributors 10 the total heterogeneity were the Australian studies,” accounting for 4.46 af the tolal Quganstalistic. These re ‘sults suggest that the effect sizes of EE in Eastern Europe are unusually high. In contrast, the effect size associated, ‘with 1 of the 2 EE studies conducted in Australia" is par- Uicularly low when compared with elect size estimates fom ‘other parts of the world. WHAT IS THE EFFECT SIZE FOR EE IN MOOD DISORDERS? With high EE defined as 2 or more critical comments, the mean and the weighted mean effect sizes were both 39. This effect size was associated with 2=5.21, P<001. There was no significant heterogeneity in the effect sizes, When eritical comments were set to 3 oF more for high BE, the mean and weighted mean effect sizes rose to 0.45 (2=6.12, P<.001), again with no significant het- cerogeneity in the data. is important to note that even when the EE cutoff forcritical comments was etat 2 or more, we found a meta- analytic effect size r =0.39. With a hypothetical group of 200 patients, this ranslates into expected relapse rates of| 69.5% for patients with high-EE relatives and 30.5% for patients with low-EE relatives.” The 95% Cls were also narrow (0.28-0.50). Our file drawer calculations show that there would need to he 54 unpublished studies to reduce the significance level to P=.05. When a critical com- ments cutoff of 3 of more Was used, the 95% Cls nar- rowed even further (0.40-0.50) with a flle-drawer stais- lic of 77. These Findings provide strong support for the role of EE in the course of mood disorders. WHAT IS THE EFFECT SIZE FOR EE IN EATING DISORDERS? Thrce studies have reported on the relationship be: tween EE and outcome in patients being tcated for eat- ing disorders. These studies differed from the sch phrenia studies in that outcome was measured by diet Compliance,” weight gain after treatment for obesity.” and premature termination of treatment in patients with anorexia.” The cutofls for determining high EE also var- fed across the 3 studies. For our analysis, where more than 1 atoll was provided we selected the eutoll score that would result nthe smallest effect size All ofthe studies found a positive association be- tween high EE and poor outcome. The weighted mean effect size was 0.51 (2=5.03, P<001), with 95% Cls of 0.36 10 0.70 and a file-drawer statis of 25. As was the case for mood disorders, there was no significant het- crogeneity ofthe effect sizes, Although only based on a few studies, ouranalyses suggest that EE is astrong pre dictor ofearly weatment outcome for patients with Weight or eating disorders, IS EE A STRONGER PREDICTOR OF OUTCOME IN NONSCHIZOPHRENIA-RELATED. CONDITIONS? The substantial and robust elfect sizes for EE in mood and eating disorders raise the question of whether EE is a significantly better predictor of outcome when pa- dents have disorders other than schizophrenia, We there- fore compared the effect sizes associated with EE in schizo- phrenia, mood disorders, and eating disorders. The analyses revealed that EE was a significantly better pre- dictor of outcome for mood disorders than it was for schizophrenia (t[31] =1.93, P =.03, using 3 critical com- ments as a cutolf for the depression studies). The same was also true for the comparison of the effect sizes of EE inschizophrenia vs eating disorders (t[28] =2.03, P=.03). The elfect sizes for EE in mood disorders and eating dis orders did not differ significantly, however. These find- ings suggest that although EE is reliable predictor of poor outcome for schizophrenia, mood disorders, and eat- Ing disorders, EE isa significantly better predictor for the latter 2 disorders than itis for schizophrenia. Given the overwhelming amount of research that examines EE in families of patients with schizophrenia, this difference in effect sizes isan interesting and potentially important finding Less} —_ The results of this meta-analysis confirm that EE is ar liable predictor of relapse in patients with schizophre nia. Although several nonreplications exist, these do not require that the predictive validity of the construct be called into question, The association between geographiclocation and the magnitude of the EE-relapse link is less clear. Although (©1908 American Med jamanetvrork.com/ on 12/13/2022 Association, All rights reserved.‘Downloaded From: ‘our primary analysis revealed no significant relation- ship between study site and effeet size, additional analy sis indicated that this might not invariably be the case. Specifically, the effect size for EE appears to be unust= ally high in studies coming from Eastern Europe, and un- usually low in one Australian investigation.”” More re~ search from Eastern Europe would obviously be valuable, as would further examination of the EE-relapse link in ‘Australian samples, Although EE predicts relapse regardless ofthe chro- nicity of the patients being studied, the magnitude of the EE-relapse association increases when research samples contain more chronically ill patients. One explanation for this is that EE is a more reliable measure of the fam ily environment when patients have been illlonger." An- other possibility is that patients may become more sen- sitive to EE as the illness continues, perhaps through a process that resembles kindling or sensitization." This, ‘of eourse, assumes that EE does indeed play some causal role in the relapse process. However, there is some evi- dence that this isthe ease" Schizophrenia isa disorder in which biological fae~ tors play a very central role. The role that psychosocial factors play might thus be somewhat restricted. That psy- chosoctal factors are important is indicated by the sig- nificant EE-relapse relationship and by the success of fam~ ily-based interventions designed to reduce patient relapse rates." However, EE may play an even more impor- tant role in the eourse of mood and eating disorders than schizophrenia. Examining the effect of family-based in- terventions on relapse rates and outcome for mood= disordered and eating-disordered patients is also likely to be a worthwhile avenue of empirical inquiry. Finally, it warrants mention that more studies of the EE-relapse link in schizophrenia will not influence the effect sizes reported here in any appreciable way. Al- most 40 years after the initial observation of Brown et al. the elevated risk for relapse associated with high EE family environments appears well established. The time has now come for creative and sophisticated research that will tell us why EE is associated with relapse in such a ‘wide range of psychopathologieal conditions “Accepted for publication February 12, 1998. We thank Robert Rosenthal, PAD, for statistical con- sultation and Lisa Vagge for assistance with the literature search Reprints: Jill M. Hooley, DPhil, Department of Psy~ ‘chology, Harvard University, 33 Kirkland St, Cambridge, ‘MA 02138 (e-mail: jmh@wjh harvard edu) Es} Vaugh OE, aft. Th measurement xressdemosonin fis of payee ptm Bed Sac Cin Pye 0761515716, Hoole JM, Rosen Ras JE. xpesed anton: tna cain ‘al onc a i, The Bebra gh Rk Paradigm i Ps hapa Ne Yak KY Spinge 128 88-20 4. Keangh Dl Race emepmentsnexpetedamatin an cope Br Psyeniay- 092160 601-520. Hoole JM, Ol J Test D Lavo exes emetion ard relapse in Seprsced pons Br Pye. 186 4862-67 aig CE, ef JP. The infunc ot aly and soc tri te couse of (©1908 American Medical Ass https:/fjamanetwork.cony on 12/13/2022. 20 2 2 Es En 8 6 a. 28 0 2. a 2 2 yc: compari ot chopra depressed sue fans a Payoh 107612825197 Milt, Bofstan MU, Machen WH, Syd KS, Mn J Fay tasand th couse of ip atecive dare Arch Ger aye. BBS 528 ‘Sum eer, sel GPA Dare Anon nanos pal ered tai, an oping out ot esman. Br Psy 15 4 26827. inane P, ec usso J MagataArto A Malu RD, Epes omc- fan in pase carer of pens wh Aimar’ sae. pl So Se sano3215250, ower HY Klausner, lino, Resnik PCampbl xsd eno Tn and gees col nsuir-dependen able mais. 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