Blatt Looking Back Towards the Future is It Time to Change the Dsm Approach to Psyquiatric Disorders the Case of Derpession

7/28/2019 Blatt Looking Back Towards the Future is It Time to Change the Dsm Approach to Psyquiatric Disorders the Case o

1/16

Psychiatry 70(2) Summer 2007 85

Looking Back Tow ards the Future: Is It Tim e toChange the DSM Approach to PsychiatricDisorders? The Case of DepressionPatrick Luyten and Sidney J. Blatt

With plans underw ay for the fifth edition of the Diagnostic and Statistical Manualof Mental Disorders (DSM), the debate between proponents of an atheoretical, de-scriptive approach of mental disorders versus an etiologically based classificationsystem has been revitalized. This paper critically reviews findings from three re-lated research areas that have begun to question the atheoretical, descriptive ap -proach to mental disorders of DSM-III and its successors: (a) research concerningthe underlying assumptions of DSM, (b) findings from treatm ent research, and (c)recent biopsychosocial research . Research on depression is used as a paradigm aticexample, but the extent to which these findings may generalize to other d isorders isalso discussed. Strengths and weaknesses of the current DSM approach versus amore etiologically based classification system are considered. This review showsthat a lthough an etiologically based classification system of mental d isorders seemsmore prom ising than a purely descriptive approach, the time seems not yet ripe forsuch a radical shift in psychiatric diagnosis. Further research oriented tow ards de-veloping a more etiologically based approach to diagnosis is urgently needed,taking into accoun t research, clinical, and policy implications that such a change inthe diagnosis of mental disorders would bring.DESCRIPTION: THE BOON ANDBANE OE CLASSIEICATION?

Historically, the current atheoretical,descriptive and categorical approach to men-tal disorders was introduced by DSM-III in1980 (APA, 1980) to halt a confusing pleth-ora of etiologically based classification sys-tems that often had little empirical suppo rt. Adescriptive approach was adopted with the

aim of fostering research on psychiatric disor-ders and facilitating the future developmentof a more em pirically and etiologically basedclassification system (APA, 1980). This de-scriptive approach was particularly clear inthe classification of depressive disorders,which eschewed traditional etiologicallybased classifications such as the distinctionbetween endogenous versus reactive depres-sion. Instead, with some minor exceptions(e.g., mood disorders due to a general medical

Patrick Luyten, PhD, is affiliated with the Department of Psychology at the University ofLeuven inLeuven, Belgium.Sidney]. Blatt, PhD, is affiliated with the D epartm ents of Psychiatry and Psychology at Yale Uni-


2/16

86 Is It Time to Change the DSM Approach?

condition), various types of depression werecategorized on symptom criteria alone.In retrospect, the adoption of a descrip-tive approach towards mental disorders madeperfect sense and clearly had a number of ad-vantages. It reduced diagnostic confusion byproviding a common language for the psychi-a tr ic community . In addi t ion, i t madebroad-ranging, systematic research on de-pression and other disorders possible. Hence,clearly, one of the main merits of DSM is itsdedication to systematic empirical research.Yet, several authors have suggested that thisresearch has begun to question a purely de-scriptive approach, and they argue that re-searchers should start to consider developinga more etiologically based approach towardsthe classification of depression and perhaps toother disorders as well (e.g., Clark, 2005;M cHugh, 200 5; Parker, 2005 ; Van Praag, deKloet, & van Os, 2004; Watson, 2005). Inwhat follows, we critically review three sets ofrelated findings concerning depression thathave emerged from the research literature inrecent years which have begun to question thecurrent descriptive approach of mood disor-ders, in add ition, as noted, we also discuss theexten t to which these findings may or may no tgeneralize to other disorders.

SHOULD WE CHANGE THEDESCRIPTIVE APPROACH TODEPRESSION?Problems with Key AssumptionsUnderlying the Current DSMApproach of DepressionIt is important to note that, as with anyclassification system, DSM-III and its succes-sors are based on a number of assumptions.Some of these assumptions are explicit in the

DSM; others, however, are more implicit. Inaddition, although some of these implicit and

assumptions and their rationales, followed bya discussion of relevant empirical findings.1. One of the basic assumptions ofDSM-III and its successors is thatclinical disorders are categoricallydistinct from subclinical disordersand norm ality (APA, 1994, p. xxi),and that, with some exceptions,disorders can and should be diag-nosed based on symptoms alone(APA, 1994, pp . xvii-xviii). Thereare a number of advantages associ-

ated with this assum ption. A cate-gorical approach facilitatesresearch by implying a clear demar-cation between cases andnon-cases. It is also congruent w iththe preferences of clinicians, insur-ance companies, and the public(APA, 1994; First, 2005). Finally, itwas also hoped that using manifestsymptoms, and not etiological fac-tors or latent characteristics, as thefoundation of a diagnostic systemwould lead to greater diagnosticreliability (Blatt &c Levy, 1998;Westen et al., 2002).2. Although the main purpose of theintroduction of a separate axis forpersonality disorders (Axis II) inDSM -III was to stimulate researchon personality disorders, many re-searchers subsequently made the(implicit) assumption that Axis Iand Axis II are independent (for anoverview, see Westen et al., 2002).Various rationales have been sug-gested for this assumption, such asthe fact that Axis I disorders likedepression have more ego-dystoniccharacteristics and are morestate-dependent, while personalitydisorders are more ego-syntonicand could be presumed to be more


3/16

Luyten and Blatt 87

origin. Whatever the assumptionsresearchers m ade, research on AxisI and A xis 11 disorders has been rel-atively isolated, except perhaps forresearch on comorbidity betweenAxis I and Axis 11 disorders (Clark,2005).

3. Finally, several autho rs (e.g., Fran-ces, First, & Pincus, 1995; Kupferet al., 2002) have pointed out thatmuch research on DSM has beeninspired by the (often implicit) as-sumption that each disorder has itsown relatively unique etiology andthat one therefore also can andshould develop a relatively specifictreatment for each disorder. Al-though this may not have been theoriginal intent of DSM-III and itssuccessors, Cuthbert (2005) hasnoted that many researchers seemto have taken this assumption forgranted. This has led to a wealth ofresearch on the etiology andpathogenesis of specific disorderswhile, until recently, relatively fewstudies have addressed the questionof whether several disorders mayshare important etiological factors.Part of the rationale for trying toidentify relatively specific biologicaland/or psychosocial vulnerabilitymarkers was hope that this wouldenable the development of specifictreatments for each disorder(Kupfer et al., 2002). Accordingly,most treatment studies and treat-ment guidelines have focused onthe efficacy and effectiveness of dis-order-specific treatments, and noton the effect of a particular treat-ment for different disorders(Westen et al., 2002) or particularaspects of treatment processes(Zuroff & Blatt, 2006). This ten-

been easier to obtain for researchon one specific DSM category (e.g.,major depression, generalized anxi-ety disorder) than for research oncommon etiological factors under-lying several disorders (Cuthbert,2005). Moreover, DSM categorieshave dominated both research andclinical practice. As First (2005, p.562) puts it: "Psychology, psychia-try, and social work textbooks areorganized using these diagnosticconceptualizations, practice guide-lines have been developed based onthese categories, and epidemiologi-cal data, service use and medicaleconomic data, outcome data, andso forth have been compiled basedon these categories. FDA -sanc-tioned drug indications for psychi-atric medications are for the mostpart expressed in terms of the DSMcategories." As a result of this "h e-gemony of the DSM categoricalsystem" (First, 20 05 , p. 562 ), it ishardly surprising that until recentlymost research concen trated on theetiology and treatment of specificdisorders, rather than on sharedetiological factors and the efficacyand effectiveness of treatments thatmay be effective for a range ofdisorders (Cuthbert, 2005; VanPraag et al., 2004).Empirical research, however, increas-ingly points to problems with each of these as-sumptions (e.g., Blatt & Levy, 1998; Luyten,Blatt, Van Houd enhove, 8c Corveleyn, 200 6;McHugh, 2005; Parker, 2005; Widiger &Samuel, 2005 ). Much of this research is in factbased on DSM categories. As Cuthbert (2005,p. 565) formulates it: "Although the currentsystem has been quite successful for communi-cating diagnostic information . . . experience


4/16

Is It Time to Change the DSM Approach?

Let us first consider em pirical da ta rele-vant to these underlying assumptions in thecurrent DSM approach to depression. Then,we will discuss findings relevant to otherdisorders.First, concerning the categorical ap-proach , the bulk of research evidence suggeststhat a dimensional approach, with depressionsituated on a continuum ranging from milddysphoria to full-blown clinical depression, ismore valid than the categorical approach cur-rently espoused by DSM (Blatt, 1974; Has-1am, 2003; Kendler & Gardner, 1998 ; Ruscio& Ruscio, 2000; Solomon et al., 2001). Thisdoes not necessarily imply that a dimensionalapproach should be adopted nor that no dis-crete depression categories (e.g., melancholicdepression) would exist (Parker, 2000). Itdoes imply, however, that the arbitrary con-sensus-based cut-off criteria used in DSM-IIIand its successors should be re-evaluated (seealso Brown & Barlow, 2005; First, 2005).This could be a gradua l process, with initiallylittle change to the current DSM system. Forinstance, instead of adop ting a categorical ap-proach with major depression as the main de-pression category, one could adopt a dimen-sional view of depressive disorder, rangingfrom norm al sadness to severe clinical depres-sion. Specifiers such as mild, moderate, andsevere with and without psychotic featurescould then be used to define meaningfulasopposed to consensus-basedcut-offs onthis dimension. The validity of these cut-offscould then be investigated by examining theirvalue for predicting course, etiopathogeneticfactors involved, and treatment response(Parker, 20 05; Widiger & Clark, 200 0).

Likewise, the reliance on "objective"symptoms in an attempt to improve the reli-ability of depression diagnosis may have re-sulted in poor vahdity (Blatt & Levy, 1998;Westen, Shedler, & Bradley, 2006; Widiger &Samuel, 2005). For instance, it is well knownthat patients with the same DSM diagnosis are

proach also does not m atch w ith they way cli-nicians make diagnoses in clinical practice,which may partly account for the fact tha t cli-nicians rarely follow diagnostic proceduresprescribed byDSM (Westen et al., 2006). Thislimits the clinical utility of DSM , an importan tcriterion to evaluate the value of anyclassification system (First et al., 20 04 ).Second, regarding the assumption oforthogonality between Axis I and Axis II,studies have clearly shown that depression isnot independent from pe rsonality. Evidence isaccruing tha t temperam ent (e.g., Clark, 200 5)and both broad (e.g., neuroticism) (Kendler,Kuhn, & Prescott, 2004; Ormel, Oldehinkel,& Brilman, 2001) and specific (e.g., interper-sonal dependency and perfectionism) (Blatt,2004; Cox, McWilhams, Enns, & Clara,2004; Zuroff et al., 2004) personality dimen-sions play a role in the etiopathogenesis of de-pression (Westen, Novotny, & Thomp-son-Brenner, 2004). These findings are alsocongruent with studies on gene-environmentcorrelations, which strongly suggest that indi-viduals vulnerable to depression in part createtheir own (stressful) environments (Moffit,Caspi, & R utter, 2005). They are also congru-ent with findings of high comorbidity betweendepression and Axis II disorders, particularlydependent, borderline, and obsessive-compul-sive personality disorder, making it highly un-likely that depression and personality disor-ders are independent (Clark, 20 05 ; Westen etal., 2004). Hence, toge ther, these findings sug-gest that it may be time to reconsider the dis-tinction between depression and personality(disorders). This may also have im portan t im-plications for treatment, as some depressedpatients could be more likely to benefit fromtreatments developed for personality disor-ders, such as Dialectical Behavior Therapy(Linehan, 1993), Mentalization-Based Treat-ment (Bateman & Fonagy, 2004) or Transfer-ence-Focused Psychotherapy (Levy et al.,2006) rather than from more narrow,


5/16

Luyten and Blatt 89

and anxiety disorders) is the rule rather thanthe exception, arguing against the assum ptionthat depression and other disorders are rela-tively distinct (Luyten, Blatt, & Corveleyn,2005; Nemeroff, 2002; Parker, 2005). Thishad led researchers to consider the validity ofmixed categories, such as a depressed-anx-ious disorder (e.g., Phillips et al., 20 03 ). Con-gruent with these suggestions, studies haveshown that both clinical and subclinical de-pressive disorders share many psychosocial(e.g., Ormel et al., 200 1) as well as biological(Claes, 2003; Heim, Plotsky, & Nemeroff,2005 ) etiological factors with other disorders,indicating that research may have been overlyconcerned with identifying the "un ique" etio-logical factors implied in depression (VanPraag et al., 200 4) instead of looking for com-mon mechanisms across different disorders(Nemeroff et al., 2003). The fact that variouspharmacological agents are often equally ef-fective in treating depression and anxietydisorders poin ts in the same direction (Parker,2005).

Findings Concerning Other DisordersAlthough the extent to which thesefindings generalize to disorders other th an de-pression is still largely unknow n, it can be as-sumed that there will be wide differences fordifferent disorders. Indications are clear, how -ever, that some of these findings may not be

isolated to the case of depression. First,taxometric studies suggest that, besides de-pression, several anxiety disorders, includingposttraumatic stress disorder (PTSD), but alsoborderline personality disorder, and even se-vere psychiatric disorders, such as psychoticand bipolar disorders (Haslam, 2003; Ruscio& Ruscio, 2000; Tsuang, Stone, Tarbox, &Faraone, 2003), are best understood as situ-ated on a continuum from normality tosubclinical pathology to manifest clinical dis-orders, contradicting a categorical approach.

meaningful quantitative points of demarca-tion along more continuous distributions"because currently "[t]he failure to conduct pi-lot studies of a criterion set is uncomfortablycomparable to releasing a psychological testfor publication in the absence of validationdata" (Widiger & Clark, 2000, p. 949), andjus t l ike any psychologica l tes t , thepsychometric properties of using these cut-offcriteria need to be investigated. Such cut-offcriteria would not be arbitrary, but ratherbased on empirical data, and could be differ-ent for different purposes (e.g., for researchversus insurance). These studies could alsoshed more light on the issue of comorbidity.For example, studies show that abo ut 7 5 % ofpatients with dysthymic disorder have a life-time history of major depression (Keller et al.,1995). Based on such findings, Widiger andClark (2000) argue that it seems unreasonableto assume that these individuals have tw o dis-tinct disorders. Rather, they seem to sufferfrom one disorder, with m ore chronic versusmore episodic manifestations, much likesomeone with diabetes may have episodicincreases in symptoms.Hence , concerns have been raised abouta descriptive, symptom-based approach ofmental disorders in general (Charney et al.,2002; Kupfer et al., 2002; McHugh, 2005),em phas iz ing the f ac t t ha t t he h ighcomorbidity between many disorders suggestsa regrouping of DSM categories based oncommon etiological and pathogenetic factors(see Widiger & Samuel, 2005 for an over-view). Or as Kupfer and colleagues (2002 , p.xviii) formulate it: "Epidemiologic and clini-cal studies have shown extremely high rates ofcomorbidities among the disorders, under-mining the hypothesis tha t the syndromes rep-resent distinct etiologies." For example, it hasbeen argued that research evidence suggeststhe existence of a category of obsessive-com-pulsive spectrum disorders (including obses-sive-compulsive disorder, Tourette Syndrome


6/16

90 Is It Time to Change the DSM Approach.'

etiological factors (Philips et al., 2003). In ad-dition, hierarchical models of mental disor-ders have been proposed, with disorders in apar t icu la r c lus te r p resumably shar ingetiopathogenetic factors (Watson, 2005).Hence, there is increasing evidence that thisshared vulnerability hypothesis (Widiger &Cla rk , 2000 ) cou ld i n fo rm a newclassification system and therefore deserves tobe further investigated.Second, concerning the relationship be-tween personality and Axis I disorders, per-sonality factors such as neuroticism and per-fectionism, for example, have been related toseveral other disorders besides depression,such as ea t ing d i sorders (Wes ten &Harnden-Fisher, 2001), opiate addiction(Blatt, Rounsaville, Eyre, & Wilber, 1984),cardiovascular and immunological disease(Blatt, Cornell, & Eshkol, 1993), bipolar dis-order (Lam, Wright, & Smith, 2004), psy-chotic disorders (Tsuang et al., 2003), andseveral anxiety disorders (e.g., Shafran &Mansell, 2001). In addition, there is increas-ing evidence for the role of temperamental d i-mensions, such as positive and negative affect,and disinhibition, in a variety of mental disor-ders (Weinstock & Whisman, 2006). As dis-cussed in more detail below , and as argued byothers (e.g., Claes, 2003; Cuthbert, 2005;Heim et al., 2005; Osuch et al., 2004), re-s ea rch i n t he neu rosc i ences andpsychobiological stress research, in particular,may be a central factor in reconsidering thedescriptive approach of DSM of depressionand psychiatric disorders in general. Again,however, much more research is needed.Moving away from studying the etiol-ogy of specific disorders to studying etiologi-cal pathways involved in different disorders,however, has important implications for fu-ture research. Cuthbert (2005, p. 566), for in-stance, notes that "a common approach tostudying the pathophysiology or genetics ofDSM disorders has been to select patients who

d e r s However, this strategy could be coun-terproductive" (Cuthbert, 2 005 , p. 567). In-stead, he argues, "given the increasing realiza-tion that most DSM diagnoses do notrepresent homogeneous categories, reliablegenetic associations or biomarkers are muchmore likely to be established w hen better defi-nitions and delineation of disorders areachieved."! The same is probably true forpsychosocial factors as well.Finally, there is a wide consensus thatmany DSM diagnoses have little predictivepower towards treatment response: "[L]ackof treatment specificity is the rule rather thanthe exception" (Kupfer et al., 2002, p . xviii),and thus seem not to be limited to the mooddisorders alone. This lack of treatment speci-ficity also limits the clinical utility of the cur-rent DSM system (First et al., 2004). Hence,future research, including research on an etio-logically based classification system, might in-crease the relevance of diagnoses for treat-ment response, an issue we will now discuss inmore detail.

TREATMENT RESEARCHThe introduction of DSM-III has notonly facilitated fundamental research on theetiology and pathogenesis of depression buthas also facilitated the identification of effec-tive treatments of this disabling disorder (e.g.,

Hollon et al., 2002). Because guidelines havealmost invariably adopted DSM categories,however, the current DSM app roach may alsobe hampering the further development ofmore effective treatments. Widiger and Sam-uel (2005, p. 494), for exam ple, conclude that"DSM -IV routinely fails in the goal of guidingthe clinician in the presence of one specific dis-ord er" precisely because of the excessive diag-nos t ic comorb id i t i es and unreso lvab leboundary disputes in the current DSMsystem.

As noted, one of the main problems


7/16

Luyten and Blatt 91

studies tend to focus on isolated DSM catego-ries, assuming that, as for any other disease, aspecific treatment for each psychiatric disor-der should he developed (Kupfer et al., 2002).Yet, studies increasingly suggest that thiss t r a t e g y m i g h t b e c o u n t e r p r o d u c t i v e(Cuthhert, 2005). For example, research hasconsistently shown that non-specific thera-peutic factors (such as the therapeutic rela-tionship) are often as important as, or evenm o r e i m p o r t a n t t h a n , s p e c i f i cpsychotherapeutic techniques or biologicalagents in predicting treatm ent outcome in de-pression (Blatt & Zuroff, 2005; Zuroff &Blatt, 2006). These findings suggest that m oreresearch efforts should be devoted toexamining these factors.In addition, the fact th at pa tients with aDSM diagnosis of depression are often hetero -geneous with respect to et iology andpathogenesis may have created considerabledifficulty in establishing the specificity oftreatments, confirming the famous "dodobird verdict," namely that all so-called bonafide treatments have similar efficacy for manydisorders (Blatt & Zuroff, 2005). This dodobird verdict, however, might be in part a resultof the fact tha t patients w ith the same DSM di-agnosis are heterogeneous in terms of etiologyand pathogenesis, which limits attempts tofind evidence for specificity of both biological(Parker , 2000; Zimmerman, Matt ia , &P o s t e r n a k , 2 0 0 2 ) a n d p s y c h o s o c i a ltreatments (Nemeroff et al., 200 3).Comparisons of etiologically differentsubgroups of patients, however, may facilitatethe emergence of differences in the effective-ness of specific treatments or specific dimen-sions in the treatment process. For example,several studies have shown that anachticallydepressed patients (i.e., patients w hose prob-lems are mainly focused around relational is-sues and conflicts) are particularly responsiveto the more supportive elements in psycho-therapy, whereas introjective depressed pa-

ferent treatment approaches for different pa-tients is provided by a re-analysis of data froma large randomized clinical trial comparingthe efficacy of 12-week psychotherapy (Cog-nitive Behavioral Analysis System of Psycho-therapy [CBASP]), antidepressant treatmentwith nefazodone, and a combination of thetwo in a sample of 681 patients suffering fromchronic forms of depression. This study ini-tially found that a combination of CBASP andmedication was associated with better out-come as compared to either monotherapy(Keller et al., 2000). In a re-analysis of thesedata, however, Nemeroff and colleagues(2003) found that in patients w ith a history ofearly childhood traum a, CBASP was superiorto antidepressant treatment, both in terms ofmean post-treatment depression severityscores and remission rates. In fact, in patientswith a history of early traum a (but not in pa-tients without such history), the combinationof CBASP with nefazodone was not superiorto treatm ent with CBASP alone. Because mostof these and similar studies are based on posthoc analyses of existing studies, more system-atic research is needed to replicate these find-ings. Nevertheless, if replicated, findings suchas these indicate that patients may show a dif-ferential response to different treatments as afunction of etiological and/or pathogeneticfactors, and not primarily as a function ofcurrently adopted DSM diagnoses (Blatt &cShahar, 2004; McHugh, 2005; Nemeroff etal., 2003).

BIOPSYCHOSOCIAL FINDINGSON DEPRESSIONA third and final reason why it may betime to abandon the descriptive approach ofDSM is that research evidence is increasinglychallenging the DSM assum ption that an etio-

logically based classification system of psychi-atric disorders is not yet feasible. At the time


8/16


possible. However, it is clear that progress hasbeen made in each of these areas, and develop-ments in the neurosciences in particular mayin the future be able to bridge the gap betweenvarious theoretical approaches towards psy-chiatric disorders, particularly as these devel-opm ents increasingly provide evidence for re-cursive interactions between biological,psychological, and social factors (Claes,2003; Gunnar, 2002; Heim et al. , 2005;Moffit et al., 20 05 ; Ursano, 200 4).Yet, the extent to which research find-ings are available, and thus integration be-tween psychosocial and biological ap-proaches is possible, varies widely fordifferent disorders. Concerning depression,although much work still lies ahead, severala t t em pts to in t eg ra te b io log ica l andpsychosocial approaches already exist (e.g.,Clark, 2005; Heim et al., 2005; Gold &Chrousos , 2002; Kendler , Gardner , &Prescott, 200 2; Luyten et a l., 2006). In all ofthese models, (recursive) interac tions betweengenetic and neurobiological processes, earlyand current life stress, and relatively stablepersonality dimensions or cognitive affectiveschemas of self and others play a pivotal ro le,suggesting considerable room for dialogueand integration between these approaches.In fact, together with research onPTSD, the study of depression may play aparadigm atic role in the further developmentof a valid classification system of psychiatricdisorders because of its focus on the interplaybetween environment and psychological andbiological factors (see also Ursano, 2004). Forexam ple, growing evidence from studies in ro -dents, non-human primates, and humans in-dicates the im portan t role of interactions be-tween early and curren t life stress and geneticfactors in Hypothalamic Pituitary Adrenal(HPA) axis dysfunction in depression and sev-eral psychiatric disorders that show highcomorbidity with depression, such as PTSDand borderline personality disorder, in vari-

al., 1993). These studies suggest th at early Ufestress may play a central role in explaininglater vulnerability (as well as resilience to-wards stress), leading to disturbances ins t r e s s - r e a c t i v i t y ( G u n n a r , 2 0 0 2 ; V a nHoudenhove et al., 2005), and in disturbancesin basic dispositions such as anxiety-prone-ness and the regulation of aggression that playa role in depression and other psychiatric(Osuch et al., 2004) and functional disorders(Van Houdenhove, Fgle, &c Luyten, 200 4).In addition, studies on depression sug-gest that genetic factors in psychiatric disor-ders most l ike ly cons is t of both"within-the-skin" and "outside-the-skin"effects (Kendler, 2001 ), with the former refer-ring to direct physiological effects of genes onneuroregulatory mechanisms implied inmoodregulation and/or stress responsivity (Claes &Nemeroff, 200 5), while the latter refer to theeffect of genes on the environment (and viceversa). Several studies, for exam ple, have pro -vided evidence for gene-environment interac-tions, in that a functional polymorphism ofthe 5-HTT gene is associated with depressiononly in the face of adverse life experiences(Caspi et al., 2003; Kaufman et al., 2004;Kencller et al., 2005; for a review, seeLevinson, 2006). Interestingly, the functionalpolymorphism of the 5-HTT gene has alsobeen associated with subclinical depression,again pointing to continuity between etiologi-cal factors implied in clinical and subchnicaldepression (Gonda et al., 2005) and the needfor a dimensional rather than categoricalview. These gene-environment interactionswork both ways, emphasizing the reciprocalnature of associations between biological andpsychosocial factors. Kaufman and colleagues(2004), for example, found that maltreatedchildren w ith the 5-HTT gene polymorphismhad elevated levels of depression com pared tonormal co ntrols, but only when they also hadlow levels of social support, providing strongevidence for the impact of environmental fac-


9/16

Luyten and Blatt 93

that were aimed at identifying specific genesfor specific disorders (Cuthbert, 2005; Moffitet al., 2005). These findings also clearly sug-gest that there probably is no "true" geneticload for depression, but that genetic liabilityfor depression is different for different typesof individuals under different environmentalcircumstances (Kendler, 2001). In addition,they suggest the possible existence of othergene-environment interactions implied indepression and other disorders (Moffit et al.,2005).Finally, these studies also provide evi-dence for the mediating role of personality orcognitive affective schemas of self and other be-tween biological and psychosocial processes(e.g., Fonagy, Gergely, Jurist, & Target, 2004).For example, several studies have shown thatsecure attachment representations play a cru-cial role in the norm al development of the HPAaxis and thus resilience in the face of adversity,protecting against the adverse effects of earlyiife stress (Gunnar, 2002). Broad personalityfactors such as neuroticism, in turn, have beenassociated with the generation of life stress, in-creasing the probability for depression(Kendler, Kuhn, & Prescott, 2004), while morespecific personality dimensions such as de-pendency and perfectionism have been shownto influence the interpretation of life stress(Zuroff et al., 2004), which in turn influencesthe neurobiological effects of adversity (Luytenet al., 2006). Studies in this context suggest thatboth psychophysiological and biochemicalstress might be contingent on the "fit" betweenpersonality and the nature of the stressor(Allen, Horne, & Trinder, 1996; Ewart,Jorgensen, &C Kolodner, 1998; Gruen et al.,1997; Sauro et al., 2001). Gruen and col-leagues (1997), for instance, found that expo-sure to an induced failure-stressor was associ-ated with changes in plasma homovanillic acid(HVA), the primary dopamine metabolite inhumans, in highly perfectionistic, but not incontrol subjects.

as a disorder that shares etiological andpathogenetic factors with other disorders.Moreover, these findings suggest that a de-scriptive and a categorical approach may alsobe hampering further research from apsychosocial as well as from a biological pointof view on other disorders. For instance, bothOsuch et al. (2004) and Friedman and Harris(2004) discuss the fact that post-mortemstudies of the brain are extremely difficult be-cause of the high comorbidity of disorders inthe current DSM . Many brains in the depres-sion brain b ank, for example, probably comefrom individuals with PTSD. Another w ay toput this is tha t this problem is the result of thefact tha t brain banks have been established forspecific DSM diagnoses and have insuffi-ciently included information concerningcomorbidity and possible etiological factors(see also Bonne & Charney, 2004).Hence, as Charney and colleagues(2002) have argued that instead of focusingon (longitudinal) studies of disorders, the de-velopment of an etiologically based classifica-tion system should start with developm entallybased investigations of etiological andpathogenetic pathways from infancy to adult-hood and how these pathw ays give rise to sev-eral disorders. In addition, our increasingknowledge of the biological mechanisms in-volved in the successful treatm ent of psychiat-ric disorders (Ftkin, Pittenger, Polan, &Kandel, 2005) is also likely to transform ourconception of prevention and treatment ofthese disorders. As noted, identifying such de-velopmental processes will probably allowtailoring treatment to particular individuals,both from a neurobiological (Aitchison, Basu,McGuffin, & Craig, 2005) as well as from apsychotherapeutic perspective (Blatt &Zuroff, 200 5), and is likely to shed more lighton the etiological and pathogenetic factorsthat underlie psychopathology.

Several of these etiologically based the-oretical models that focus on temperament


10/16


model of depression and anxiety which hasdeveloped into a more comprehensive hierar-chical model (Clark, 2005; W atson, 200 5; foran alternative see Lara, Pinto, Akiskal, &Akiskal, in press), and theoretical models ex-amining gene-environment interactions (e.g.,Askland & Parsons, in press; Kendler,Prescott, Myers, & Neale, 2003; Krueger,Caspi, Moffitt, & Sliva, 1998). Yet, it is alsoclear that much more research in this area isneeded, particularly concerning the interrela-tionship between these various theoreticalmodels (Brown & Barlow, 2005; First, 2005 ).

CONCLUSIONS ANDFUTURE PERSPECTIVESIt is clear that we are on the brink of anew era in psychiatric diagnosis. Just as the in-troduction of DSM-III introduced a new erain psychiatry and psychology, findings re-viewed in this paper might lead to a radical

shift in the way we classify mental disorders(Brown & Barlow, 2005). Research findingsare increasingly challenging the way we con-ceptualize, classify, and treat psychiatric dis-orders, moving away from a descriptive to-wards an etiologically based approach. This istrue in research on depression, but also for anumber of other disorders (e.g., Charney etal., 20 02 ), although there are wide differencesbetween the various disorders. Thus, an im-po rtan t task for further research will be to dis-entangle the many etiological pathways frominfancy to adulthood in the genesis of psychi-atric disorders, and to investigate, rather thanaccept a priori, basic assumptions concerningthe nature of psychiatric disorders (Widiger &cClark, 2000).Yet, although some researchers have ar-gued that the available data suggest the adop -tion of a more etiologically based classifica-tion system in the next edition of DSM (e.g.,W atson, 2 005), we believe the time is not yet

noted, existing findings are still relativelypoorly integrated and it is highly unlikely tha ta consensus could soon be reached amongproponents of various theories (First, 2005).Moreover, much relevant research is simplylacking. As Brown and Barlow (200 5, p. 555)recently put it: "[Although] a clear consensushas emerged that we must move beyond de-scription and back to a consideration ofetiologic theory . . . this approach is so radi-cally different tha t we are unlikely to achieveconsensus in time for the publication of theDSM-V." In addition, the consequences ofsuch a radical shift on clinical practice, re-search, and public policy should first becarefully evaluated (First, 2005).

In the meantime, however, data re-viewed in this paper clearly suggest that re-search in this direction, comparing differentalternatives of classification systems, is ur-gently needed if we are to overcome limita-tions of our cu rrent classification system. Thismight entail the adoption of hybrid systems infuture editions of DSM, which combine di-mensional with categorical, and descriptivewith etiological considerations (Westen et al.,2006), or it might entail using a different c las-sification system for research and for clinicalpractice (Krueger et al., 2005). Hence, adaunting task lies ahead of us, which will ne-cessitate research and consensus on basic di-mensions and/or endophenotypes (First,2005) . This will also inevitably entail amultidisciplinary approach, spanning exper-tise from the fields of psychiatric genetics todevelopmental psychopathology, and fromce l l r e sea rch to ep idem io log ica l andsociocultural studies (Ursano, 2004). Ulti-mately, however, these studies may lead to amore comprehensive, etiologically based sys-tem of psychiatric disorders that could thenlead to more fully informed evidence-basedprevention and treatment strategies withgreater clinical utility (Watson, 2005).


11/16

Luyten and Blatt 95

REFERENCES

Aitchison, K. J., Basu, A., McGuffin, P., &Craig, I. (2005). Psychiatry and the "new genet-ics": Hunting for genes for behaviour and drugresponse. British Journal of Psychiatry, 186,91 -92 .Allen, N. B., H orn e, D. J., & Trinde r, J. (1996 ).Sociotropy, autonomy, and dysphoric emo-tional responses to specific classes of stress: Apsychophysiological evaluation. Journal of Ab-normal Psychology, 105, 2 5 - 3 3 .Am erican Psychiatric Association (1980). Diag-nostic and Statistical Manual of Mental Disor-ders, Third Edition. Washington, D C: AmericanPsychiatric Association.American Psychiatric Association (1994). Diag-nostic and Statistical Manual of Mental Disor-ders Fourth Edition. W a s h i n g t o n , D C :American Psychiatric Association.Askland, K., & Parsons, M . (in press). To wa rd abiaxial model of "bipolar" affective disorders:S pec t rum pheno types as t he p roduc t s o fneuroelectrical and neurochemical alterations.Journal of Affective Disorders.Bateman, A., & Fonagy, P. (2004). Psychother-apy for Borderline P ersonality Disorder.Mentalization-Based Treatment. Oxford: Ox-ford University Press.Beseler, C , Jaco bson , K. C , Kremen, W. S., Ly-ons, M. J., Clatt, S. J., Faraone, S. V., Cillespie,N . A., & T suang, M . T. (2006 ). Is there hetero-geneity among syndromes of substance use dis-order for illicit drugs. Addictive Behaviors, 31,929-947 .Beutler, L. E., & M alik, M . L. (Eds.). (2002).Re-thinking the DSM. A Psychological Perspective.W ashin gton , DC: Am erican PsychologicalAssociation.Blatt, S. J. (19 74). Levels of object represe nta-tion in anaclitic and introjective de pression. Psy-choanalytic Study ofthe Child, 29, 107-157.Blatt, S. J. (2004). Experiences of Depression:

clinical course in immunological and cardiovas-cular disease. Clinical Psychology Review , 13,421 -450 .B la t t , S. J . , & L evy , K . N . (1 99 8) . Apsychodynamic approach to the diagnosis ofpsychopathology. In J. W. Baron (Ed.), MakingDiagnosis Meaningful. Enhancing Evaluationand Treatment of Psychological Disorders (pp.73-109). Washington, DC: American Psycho-logical Association.Blatt, S. J., Rounsaville, B. J., Eyre, S., & W ilber,C. (1984). The psycho-dynamics of opiate ad-diction. Journal of Nervous and Mental Disease,172,342-352.Blatt, S. J., & Sh ahar, C. (200 4). Psychoanalysis:For what, with who, and how: A comparisonwith psychotherapy. Journal of the AmericanPsychoanalytic Association, 52, 3 93 -447 .Blatt, S. J., & Zuroff, D. C. (2005). Empiricalevaluation of the assumptions in identifying evi-dence-based treatments in mental health. Clini-cal Psychology Revietv, 25, 459-486 .Blatt, S. J., Zuroff, D. C , Bondi , C . M. ,Sanislow, C. A., & Pilkonis, P. A. (199 8). Whe nand how perfectionism impedes the brief treat-ment of depression: Further analyses of The N a-tional Institute of Mental Health Treatment ofDepression Collaborative Research Program.Journal of Consulting and Clinical Psychology,66, 4 2 3 - 4 2 8 .B o n n e , O . , & C h a r n e y , D . S . ( 2 0 0 4 ) .Neuropathology of stress: Prospects and cave-ats. Psychiatry, 67, 4 0 7 -4 11 .Brown, T. A., & Barlow, D. H. (2005). Dimen-sional versus categorical classification of men taldisorders in the Fifth Edition of the Diagnosticand Statistical Manual of Mental Disorders andbeyond: Comment on the special section. Jour-nal of Abnormal Psychology, 114, 551 -556 .Casp i, A., Sugden, K., Mo ffitt, T. E., Taylo r, A.,Craig, I. W., Harrington, H., McClay, J., Mill,


12/16


hen, J. , Goldman, D., Gur, J. D., Ling, K.-M.,Lopez, J. F., Mead or-Woodruff, J. H., M oldin,S. O ., Nestler, E. J., W atson, S. J., & Zalcm an, S.J. (2002). Neuroscience Research Agenda toguide development of a pathophysiologicallybased classification system. In D. J. Kupfer, M.B. First, & D. A. Regier (Eds.), A ResearchAgenda for DSM-V (pp. 31-83). Washington,DC: American Psychiatric Association.Claes, S. (2003). Corticotropin-releasing hor-mone (CRH) in psychiatry: From stress topsychopathology. Anna ls of Medicine, 35,1-12.Cla es, S. J. , & Nemeroff, C. B . (2005) .Corticotropin-Releasing Factor (CRF) and ma-jor depression: Towards an integration of psy-cho logy and neu rob io logy i n dep res s ionresearch . In J. Corveleyn , P. Luyten, &c S. J. B latt(Eds.), The Theory and Treatment of Depres-sion: Towards a Dynamic Interactionism Model(pp. 227-252). Leuven/Mahwah, NJ: LeuvenUniversity Press/Lawrence Erlbaum .Clark, L. A. (2005). Temp eram ent as a unifyingbasis for personality and psychopathology.Journal of Abnorm al P sychology, 114,5 0 5 -5 2 1 .Co x, B. J., McW illiams, L. A., Enns, M. W ., &Clara, I. P. (2004). Broad and specific personal-ity dimensions associated with major depressionin a nationally representative sample. Compre-hensive Psychiatry, 45, 2 4 6 - 2 5 3 .Cuthbert, B. N. (2005). Dimensional models ofpsychopathology: Research agenda and clinicalutility. Journal of Abnormal Psychology, 114,565-569.Etkin, A., Pittenger, C , Polan, H. J., & K andel,E. (2005). Toward a neurobiology of psycho-therapy: Basic science and clinical applications.Journal ofNeuropsychiatry and Clinical Neuro-science, 17, 145-158 .Ew art, C. K., Jorge nsen , R. S.,&C Kolodner, K. B.(1998). Sociotropic cognitions mode rates bloodpressure response to interpersonal stress inhigh-risk adolescent girls. International Journalof Psychophysiology, 28, 131-142 .

liams, J. B., Ustun, B., & Peele, R. (20 04). Clini-cal utility as a criterion for revising psychiatricdiagnoses. Am erican Journal of Psychiatry, 161,946-954 .Fonagy, P., Gergely, G., Jurist, E. L., & Target,M. (2004). Affect Regulation, Mentalization,and the Development of the Self. London/NewYork: Karnac.Frances, A. J., First, M. B., & Pincus, H. A.(1995). DSM-IV Guidebook. Washington, DC :American Psychiatric Press.Friedman, M. J. , & Harris, W. W. (2004). To-ward a national PTSD brain bank. Psychiatry,67, 384-390 .Gold, P. W., & Ch rouso s, G. P. (2002). Organ i-zation of the stress system and its dysregulationin melancholic and atypical depression: High vs.low CRH/NE states. Molecular Psychiatry, 7,254-275 .Go nda, X ., Juhasz , G., Laszik, A., Rihm er, Z., &Bagdy, G. (2005). Subthreshold depression islinked to the functional polymorphism of the5HT transporter gene. Journal of Affective Dis-orders, 87, 291-297 .Gru en, R. J., Silva, R., Ehrlich, J., Schweitzer, J.W., & Friedhoff, A. J. (1997). Vulnerability tos t r es s : S e l f -Cr i ti c i sm and s t r es s - i nd uce dchanges in biochemistry. Journal of Personality,65 , 33-47 .Gu nnar, M . R. (2002). Integrating neuroscienceand psychological approaches in the study ofearly experiences. Annals of the New YorkAcademy of Sciences, 1008, 238-247 .Haslam, N. (2003). Categorical versus dimen-s i o n a l m o d e l s o f m e n t a l d i s o r d e r : T h etaxometric evidence. Australian and New Zea-land Journal of Psychiatry, 37, 696-704 .Heim, C , Plotsky, P. M ., & Nemeroff, C. B.(2005). Importance of studying the contribu-t i o n s o f e a r l y a d v e r s e e x p e r i e n c e s t on e u r o b i o l o g i c a l f i n d i n g s i n d e p r e s s i o n .Neuropsychopharmacology, 29, 6 4 1 - 6 4 8 .Hollon, S. D., Munoz, R. F. , Barlow, D. H.,


13/16

Luyten and Blatt 97

ment for the prevention and treatm ent of depres-sion: Promoting innovation and increasingaccess. Biological Psychiatry, 52, 610-630 .Kaufman, J. , Yang, B.-Z., Douglas-Palumberi,H., H oush yar, S., Lipschitz, D., Krystal,J. H., &Gelernter, J. (2004). Social support and seroto-nin transporter gene moderate depression inmaltreated children. Proceedings of the Na-tional Academ y of Sciences of the USA , 1 01,17316-17321.Keller, M . B., Klein, D. N. , Hirschfeld, R . M . A.,Kocsis, J. H., Mc-Cullough, J. P., Miller, I. ,First, M. B., Holzer, C. P., Ill, Keitner, G. I.,Marin, D. B., & Shea, T. (1995). Results of theDSM-IV mood disorders trial . American Jour-nal of Psychiatry, 152, 843-849 .Keller, M . B., McCuUough, J. P., Klein, D. N ., etal. (2000). A comparison of nefazodone, thecognitive behavioral analysis system of psycho-therapy , and their combina tion for the treatme ntof chronic depression. Neto E ngland Journal ofMedicine, 342, 1462-1472.Kendler, K. S. (2001). Twin studies of psychiat-ric illness. An update. Archives of General Psy-chiatry, 58,1005-1014.K e n d l e r , K . S. ( 2 0 0 2 ) . H i e r a r c h y a n dheritability: The role of diagnosis and modelingin psychiatric genetics. American Journa l of Psy-chiatry, 2 5 9 , 5 1 5 - 5 1 8 .Kendler, K. S., & G ardne r, G. O. (1998). Bound-aries of major depression: An evaluation ofDSM -IV criteria. American Journal of Psychia-try, 155, 172-177 .Kend ler, K. S., Gard ner, G. O ., & Presco tt, G. A.(2002). Toward a comprehensive developmen-tal model for m ajor depression in wo men . Amer-ican Journal of Psychiatry, 159, 1133-1145 .Kendler, K. S., Kuhn, J., & Prescott, G. A.(2004). The interrelationship of neuroticism,sex, and stressful life events in the prediction ofepisodes of major depression. American Journalof Psychiatry, 161, 631-636 .Kendler, K. S., Kuhn, J. W., V ittum, J., Prescott,

Kendler, K. S., Prescott, G. A., Myers, J., &Neale, M. G. (2003). The structure of geneticand en vironmental risk factors for comm on psy-chiatric and substance use disorders in men andwomen. Archives of General Psychiatry, 60,929-937 .Kruege r, R. F., Gaspi, A., Moffit, T. E., & Silva,P. A. (1998). The structure an d stability of com-mon mental disorders (DSM-III-R): A longitu-d i n a l - e p i d e m i o l o g i c a l s t u d y . Journal ofAbnormal Psychology, 107, 216-227 .Krueger, R. F. , Watson, D., & Barlow, D. H.(2005). Introduction to the special section: To-ward a dimensional ly based taxonomy ofpsychopathology. Journal of Abnormal Psy-chology, 114, 491-A93.Kupfer, D. J., First, M. B., & Regier, D. A.(2002). A Research Agenda for DSM-V. Wash-ington, DG : Am erican Psychiatric A ssociation.Lam, D., Wright, K., & Smith, N. (2004). Dys-functional assumptions in bipolar disorder.Journal of Affective Disorders, 79, 193-199 .Lara, D. R., Pinto, O., Akiskal, K., & Akiskal,H . S. (2006). T ow ard an integrative model of thespectrum of mood, behavioral and personalitydisorde rs based on fear an d an ger traits : I. Glini-cal implications. Journal of Affective Disorders,94, 6 7 - 8 7 .Levy, K. N., Glarkin, J. F., Yeomans, F. E., Scott,L. N., Wasserman, R. H., &c Kernberg, O. F.(2006). The mechanisms of change in the treat-ment of borderline personality disorder withtransference-focused psychotherapy. Journal ofClinical Psychology, 62, 4 8 1 -5 0 1 .Levinson, D. F. (2006). The genetics of depres-sion: A review. Biological Psychiatry, 60, 84-92 .Linehan, M. M. (1993). Cognitive-BehavioralTreatrnent of Borderline Personality Disorder.New York: Guilford.Luyten, P., Blatt, S. J., & Gorveleyn, J. (2005).To wa rds integration in the theory and trea tmen tof depression? The time is now. In J. Gorveleyn,P. Luyten , & S. J. Blatt (Eds.), The Theory and


14/16


Corve leyn, J. (2006) . Dep ression research and PhiUips, K. A., First, M . B., & Pincus, H. A.treatm ent: Are we skating to where the puck is (Eds.). (2003). Advancing DSM. Dilemmas ingoing to be? Clinical PsycPjology Review, 26, Psychiatric Diagno sis. Wa shington, D C: Am eri-98 5- 99 9. can Psychiatric Association.M cH ugh , P. R. (2005). Striving for coherence: Rose, S. (2001). Moving on from old dichoto-Psychiatry's efforts over classification. Journal mies: Beyond nature-nurture towards lifelineof the American Medical Association, 293, perspective. British Journal of Psychiatry, 178252 6-25 28. (Suppl . 40), s3-s7.Moffitt, T. E., Caspi, A., & R utter, M. (2005). Ruscio, J., & R uscio, A. M . (2000 ). InformingStrategy for investigating interactions between the continuity controversy: A taxom etric analy-measured genes and measured environments, sis oi depression. Journal of Abn ormal Psychol-Archives of General Psychiatry, 62, 4 7 3 -4 8 1 . ogy, 109, 473-487 .National Institute of Mental Health. (2003).Breaking Ground, Breaking Through: The Stra-tegic Plan for Mood Disorders Research. Re-t r i e v e d S e p t e m b e r 3 , 2 0 0 4 , f r o mh t t p : / / w w w . n i m h . n i h . g o v / s t r a t e -gic/mooddisorders.pdf.

Sauro, M. D., Jorgensen, R. S., Larson, C. A.,Frankowski, j . J . , Ewart, C. K., & Wh ite, J.(2001 ) . S oc io t rop i c cogn i t i on mo dera t esstress-induced cardiovascular responsiveness incollege wo men . Journal of Behavioral Medicine,24, 423-439 .Nemeroff, C. B. (2002). Editorial. Com orbidity Shafran, R., & M ansell, W . (2001). Perfection-of mood an d anxiety disorders: The rule, not the ism and psychopa thology: A review of researchexception? American Journal of Psychiatry, 3ind treatment. Clinical Psychology Review 21159, 3-4 . 879-906.Nemeroff, C. B., Heim, C. M., Thase, M. E.,Klein, D. N., Rush, J. A., Schatzberg, A. F.,Ninan, P. T., McCullough, J. P., Jr, Weiss, P. M .,Dunner, D. L., Rothbaum, B. O., Kornstein, S.,Keitner, G ., & Keller, M . B. (200 3). Differentialr e s p o n s e s t o p s y c h o t h e r a p y v e r s u spharm acoth erap y in patients with chronic formsof major depression and childhood tra um a. Pro-ceedings of the National Academy of Sciences ofthe USA, 100, 14239-14296.Ormel, J., Oldehinkel, A. J., & Brilman, E. I.(2001). The interplay and etiological continuityof neuroticism, difficulties, and life events in theetiology of major and subsyndromal, first andrecu rrent depressive episodes in later life. Ameri-can Journal of Psychiatry, 158, 885-891 .Osuch, E., Ursano, R., Li, H., Webster, M.,Hou gh, C , Fullerton, C , & Leskin, G. (2004).B r a i n e n v i r o n m e n t i n t e r a c t i o n s : S t r e s s ,Posttraum atic Stress Disorder, and the need for apostmortem brain collection. Psychiatry, 67,353-383 .

Solomon, A., Ha aga, D. A. F. , & Arnow , B. A.(2001). Is clinical depression distinct fromsubthreshold depressive symptoms? A review ofthe continuity issue in depression research./owr-nal of Nervous and Men tal Disease, 189,498-506 .Tsuang, M. T., Stone, W. S., Tarbox, S. I., &Faraone, S. V. (2003). Insights from neurosci-ence for the concept of schizotaxia and the diag-nosis of schizophrenia. In K. A. Phillips, M. B.First, &c H. A. Pincus (Eds.), Advancing DSM.Dilemmas In Psychiatric Diagnosis (pp.105-127). Washington, DC: American Psychi-atric Association.Ursano, R. J. (2004). Editor's note. Psychiatry,67, 309.Van Houdenhove, B., & Egle, U. T. (2004).Fibromyalgia: A stress disorder? Piecing thebiopsychosocial puzzle together. Psychotherapyand Psychosomatics, 73, 2 6 7 - 2 7 5 .Van Houdenhove, B., Egle, U., & Luyten, P.


15/16

Luyten and Blatt 99

Watson, D. (2005). Rethinking the mood andanxiety disorders: A quantitative hierarchicalmodel for DSM-V. Journal of Abnormal Psy-chology, 114, 522-536 .Weinstock, L. M., & Whisman, M. A. (2006).Neuroticism as a comm on feature of the depres-sive and anxiety disorders: A test of the revisedintegrative hierarchical model in a national sam-ple. Journal of Abno rmal Psychology, 115,68 -7 4 .Westen, D., & Harnden-Fischer, J. (2001). Per-sonality profiles in eating disorders: Rethinkingthe distinction betw een axis I and axis II. Ameri-can Journal of Psychiatry, 158, 54 7 -562 .Westen , D. , Heim, A. K. , Morr i son , K. ,Patterson, M ., &C Cam pbell, L. (2002 ). Simplify-ing diagnosis using a prototype-matching ap-proach: Implications for the next edition of theDS M . In L. Beutler &C M. Malik (Eds.), Rethink-ing the DSM: A Psychological Perspective (pp.2 2 1 - 2 5 0 ) . W a s h i n g t o n , D C : A m e r i c a nPsychological Association.W es t en , D . , Novo tny , C . M. , & Thomp-son-B renner, H. (2004). The empirical status ofempirical ly supported psychotherapies: As-sum ptions, findings, and rep orting in controlledclinical trials. Psychological Bulletin, 130,631-663.Westen, D., Shedler, J., &c Bradley, R. (20 06). Aprototype approach to personality disorder di-agnosis. American Journal of Psychiatry, 163,8 4 6-8 56 .Widiger, T. A., & Clark, A. (2000). TowardD S M - V a n d t h e c l a s s i f i c a t i o n of

psychopathology. Psychological Bulletin, 126,94 6-963 .Widiger, T. A., Sc Samuel, D. B. (2005). Diag-nostic categories or dimensions? A question forthe Diagnostic and Statistical M anua l of M entalDisorders-Fifth Edition. Journal of AbnormalPsychology, 114, 4 94 -504 .Widiger, T. A., & Simonsen, E. (Eds.) (2005a).Special section: A research agenda for the devel-opment of a dime nsional classification system ofPersonality disorders. Part I. Journal of Person-ality Disorders, 19(1).Widiger, T. A., & Simonsen, E. (Eds.) (2005b).Special section: A research a genda for the devel-opment of a dimen sional classification system ofPersonality disorders. Part 11. Journal of Person-ality Disorders, 19(3).Zimm erman, M ., Mattia, J. I., & Posternak, M .A. (2002). Are subjects in pharmacologicaltreatment trials of depression representative ofpatients in routine clinical practice? AmericanJournal of Psychiatry, 159, 4 6 9 - 4 7 3 .Zuroff, D. C , & Blatt, S. J. (2006). The thera-peutic relationship in the brief treatment of de-pression: Con tributions to clinical im provem entand enhanced adaptive capacities. Journal ofConsu lting and Clinical Psychology, 74,130-140.Zuroff, D. C , M ongrain, M. , &C Santor, D.(2004). Conceptuahzing and measuring person-ality vulnerability to depression: Comment onCoyne and W hiffen( 1995). ^ / / / Zfw, 130 , 4 8 9-511 .


16/16

Documents

Blatt Looking Back Towards the Future is It Time to Change the Dsm Approach to Psyquiatric Disorders the Case of Derpession