Skip to main content
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Behav Res Ther. 2010 Feb 4;48(6):449–458. doi: 10.1016/j.brat.2010.01.006

Moderators of Continuation Phase Cognitive Therapy’s Effects on Relapse, Recurrence, Remission, and Recovery from Depression

Jeffrey R Vittengl 1, Lee Anna Clark 2, Robin B Jarrett 3
PMCID: PMC2871970  NIHMSID: NIHMS181340  PMID: 20163785

Abstract

About half of patients who respond to acute-phase cognitive therapy (CT) for major depressive disorder (MDD) will relapse/recur within 2 years; continuation-phase CT lowers this risk. We analyzed demographic, clinical, cognitive, social-interpersonal, and personality variables to clarify which patients continuation-phase CT helps to avoid relapse and recurrence and achieve remission and recovery. Participants had recurrent MDD, responded to acute-phase CT, were randomized to 8 months of continuation-phase CT (n = 41) or assessment control (n = 43), and were assessed 16 additional months (Jarrett, Kraft, Doyle et al., 2001). Consistent with an underlying risk-reduction model, continuation-phase CT was helpful for responders to acute-phase CT with greater risk and/or dysfunction as follows: Younger patients with earlier MDD onset who displayed greater dysfunctional attitudes and lower self-efficacy; personality traits suggesting low positive activation (e.g., reduced energy, enthusiasm, gregariousness); and transiently elevated depressive symptoms late in acute-phase CT and residual symptoms after acute-phase CT response. We emphasize the need for replication of these results before clinical application.

Keywords: depression, continuation-phase cognitive therapy, moderators, recurrence, recovery


Acute-phase cognitive therapy (CT) for major depressive disorder (MDD) reduces depressive symptoms more than non-active comparison conditions (e.g., placebo, no treatment) and as much as pharmacotherapy, interpersonal psychotherapy, and behavior therapy (Craighead et al., 2007; Nemeroff & Schatzberg, 2007). For example, roughly two-thirds of patients who complete acute-phase CT no longer meet criteria for a major depressive episode (Craighead et al., 2007). If acute-phase CT is discontinued after response, however, about half of patients will have a major depressive episode within 2 years (Dobson et al., 2008; Vittengl et al., 2007), a rate comparable to continued pharmacotherapy (Dobson et al., 2008; Hollon et al., 2006). The goal of post-acute-phase CT applied after response to an acute-phase treatment (see Vittengl et al., 2007 for types) is to decrease relapse and recurrence (defined as having a major depressive episode before and after recovery, respectively; Frank et al., 1991), and to increase remission and recovery (defined as 6 and 35 weeks, respectively, of few or no depressive symptoms; Jarrett et al., 2001). The purpose of the current analyses is to identify demographic, cognitive, social-interpersonal, and personality variables that moderate the effects of one form of post-acute-phase CT, continuation-phase CT (described below), in a randomized clinical trial (Jarrett et al., 2001). In particular, we aim to clarify which responders most need continuation-phase CT to achieve remission and recovery, and to avoid relapse and recurrence, after response to acute-phase CT, and which responders have positive outcomes without further immediate treatment. Identification of such moderators of intervention is critical to developing personalized preventive care (National Institute of Mental Health, 2008).

Prior research shows that post-acute-phase CT helps some but not all patients. Compared to inactive controls, post-acute-phase CT reduces but does not eliminate relapse (e.g., average 12% vs. 38% of patients relapsed during 9 months of treatment; Vittengl et al., 2007) and increases but does not assure recovery (84% vs. 62% of patients recovered within 2 years after ending acute-phase CT; Vittengl et al., 2009). These data also reveal that some responders to an acute-phase treatment stay well without post-acute-phase CT (e.g., 62% of patients did not relapse/recur within 9 months, and 62% recovered within 24 months, of ending acute-phase treatment; Vittengl et al., 2007, 2009). Understanding which patients benefit most from post-acute-phase CT would clarify the treatment’s theory and application, and if replicated inform public health policy.

We analyzed patient-level variables based on Jarrett’s risk-reduction model of continuation-phase CT (Jarrett, 1989; Jarrett et al., 2008b). In this biopsychosocial model, three overlapping domains of risk increase the likelihood of relapse and recurrence, and decrease patients’ chances of remission and recovery: Dysfunction in (a) genetic, biological, family, and developmental conditions; (b) personality, interpersonal, and social functioning; and (c) cognitive processing or content. After responding to acute-phase CT, recurrence or absence of recovery may result from dysfunction in these domains, especially when residual depressive symptoms, and such challenges as stressful life events, activate depressive cognition and ineffective behavior to overwhelm poorly learned or disused CT skills, and/or as the time away from active treatment increases. Continuation-phase CT aims to promote recovery and prevent recurrence by improving functioning in changeable domains (e.g., social-interpersonal, cognitive), reducing the consequences of less changeable domains (e.g., temperament dimensions), lowering residual symptoms, decreasing the probability of negative life events, and managing challenges better by understanding sources of risk and knowing when to activate new compensatory and coping skills. In the current analyses, we take initial steps in testing the intra-patient risks within the model, leaving the tests of their interactions with external life events for future studies.

Distinctions between acute-phase CT (Beck et al., 1979) and Jarrett’s continuation-phase CT (Jarrett, 1989; Jarrett et al., 2008b) are reflected in the phases’ primary goals and emphases. Although acute-phase CT, undoubtedly, includes relapse prevention given its aim to help the patient acquire CT skills, its primary goal is to reduce depressive symptoms, which is marked by a treatment response. Too often in clinical practice, it can take all of the 16-20 acute phase sessions to help patients acquire basic CT skills (e.g., facility with a thought record) and obtain a treatment response. The practical result is that there is insufficient time left to focus on relapse prevention, stress inoculation, and otherwise promoting a full recovery. In contrast, during continuation-phase CT responders focus on preventing relapse and recurrence, and on promoting remission and recovery. These aims are achieved as patients consistently maintain and generalize the skills that helped them previously to reduce symptoms. When patients’ CT skills were poorly learned in acute-phase CT or fall into disuse, and/or when stressful life events challenge their available repertoire of skills, and thus depressive symptoms occur, continuation-phase CT sessions may resemble acute-phase CT. In other words, skill acquisition and symptom reduction again become the focus. However, when patients evidence few symptoms and high mastery of skills, continuation-phase CT involves enhancing patients’ strengths and practicing, reinforcing, and extending CT skills to address individual patients’ risks in cognitive and interpersonal spheres. Both phases of CT rely heavily on a cognitive conceptualization (Beck, 1995).

Other researchers’ models of post-acute-phase CT share features with Jarrett’s model of continuation-phase CT and with one another. For example, Paykel et al.’s (1999) post-acute-phase CT model emphasizes reduction of residual symptoms, resolution of individual problems, and modification of underlying beliefs and schema through behavioral and cognitive techniques. Similarly, in Fava et al.’s (1998) conceptualization, post-acute-phase CT reduces residual symptoms through cognitive change and lifestyle modification to lower stress, and adds well-being therapy to reinforce behaviors promoting wellness and personal growth. Bockting et al. (2005) emphasize evaluating dysfunctional attitudes and fostering realistic attitudes, as well as interventions to enhance patients’ memory of specific positive experiences. Finally, Segal et al.’s (2002) mindfulness therapy teaches patients to disengage from (rather than change) dysfunctional cognitions activated by dysphoria, and instead to view negative thoughts and feelings as transient mental events. Treatments derived from these five models of post-acute-phase CT have been shown to decrease relapse or recurrence of major depression (Bockting et al., 2005; Fava et al., 2004; Jarrett et al., 2001; Ma & Teasdale, 2004; Teasdale et al., 2000; Paykel et al., 1999).

These theoretical models, including Jarrett’s continuation-phase CT, suggest that post-acute-phase CT may be more helpful for patients who are at greatest risk for relapse or recurrence and for failure to remit and recover. Conversely, other acute-phase treatment responders simply may not need immediate additional treatment and may experience positive outcomes for varying durations. Although a relatively large body of research identifies risk factors for relapse and recurrence of depression, very little research has identified the moderators of post-acute-phase CT ’s effects.

It is important to distinguish between risk factors and moderators of treatment effects—not all risk factors are moderators or vice versa. Risk factors are pretreatment or baseline variables that predict poor outcomes overall (i.e., main effects in statistical models), whereas moderators are pretreatment or baseline variables that predict outcomes differently in one treatment condition compared to another condition (i.e., interactions in statistical models; Kraemer, Wilson, Fairburn, & Agras, 2002). For example, high scores on test A may predict relapse equally well in both continuation-phase CT and control conditions (A is a risk factor), and high scores on test B may predict relapse in controls but not in continuation-phase CT patients (B is a moderator).

The current analyses contribute to the literature by identifying potential moderators of continuation-phase CT’s effects on relapse, recurrence, remission, and recovery. Further, our a priori definitions of remission and recovery (6 and 35 weeks of few or no depressive symptoms, respectively; Jarrett et al., 2001; Vittengl et al., 2009) intentionally are more rigorous than in most previous research (e.g., low symptoms at the end of acute-phase CT, DeRubeis et al., 2005; Dimidjian et al., 2006; absence of a major depressive episode during follow-up, Dobson et al., 2008; Hollon et al., 2005). Specifically, our definitions of remission and recovery capture outcomes that arguably are more important to patients and their families because they require a longer duration (Rush et al., 2006), and because few to no symptoms preclude significantly fluctuating and residual symptoms of depression that produce substantial psychosocial impairment (e.g., at work, in social relationships; Judd et al., 2000). Raising standards for defining positive outcomes will make research more clinically significant and have greater potential to improve public health in ways that matter significantly to patients and their families (Rush et al., 2006; Vittengl et al., 2009; Jarrett & Vittengl, in press).

Demographic, clinical, cognitive, social-interpersonal, and personality variables all have been identified as risks for relapse/recurrence in past research. For example, Burcusa and Iacono (2007) reviewed the literature to conclude that earlier age of onset of MDD, a history of more major depressive episodes, comorbid dysthmia, family history of depression, negative cognitive content, personality (e.g., high neuroticism), and poorer social support are frequently documented risks for recurrence. Fava et al. (2002) concluded that residual symptoms of depression also are strong predictors of relapse and recurrence of a major depressive episode after response to acute-phase treatment. Fava (2007) further conceptualized negative cognitive content and psychosocial dysfunction as broad markers of residual symptoms that predict failure to recover. Also related to residual symptoms, unstable remission involves elevated depressive symptoms late in acute-phase treatment and predicts relapse (Thase et al., 1992; Jarrett et al., 2001).

Among published clinical trials of post-acute-phase CT, presently the only partially replicated moderator of post-acute-phase CT ’s effects of which we are aware is the number of major depressive episodes. In particular, some forms of post-acute-phase CT may prevent relapse/recurrence for patients with at least 3 (Ma & Teasdale, 2004; Teasdale et al., 2000) or 5 (Bockting et al., 2005) prior major depressive episodes, but not for those with fewer episodes. Both research groups noted that patients with more major depressive episodes tended to have an earlier age of MDD onset, as would be expected (Ma & Teasdale, 2004; Teasdale et al., 2000; Bockting et al., 2005). In their general review of depression recurrence, Burcusa and Iacono (2007) discussed that earlier age of onset and more major depressive episodes are significantly correlated (but not synonymous), although it is unclear which variable is more fundamental or what underlying process (e.g., genetics and/or familial environment) may link them and account for recurrence. In the current dataset, Jarrett et al. (2001) reported that continuation-phase CT prevented relapse/recurrence during the 24 months after acute-phase CT for patients whose MDD began before age 18. Jarrett et al. (2001) also found that continuation-phase CT reduced relapse/recurrence for patients with unstable remission in acute-phase CT. Additional research suggests that post-acute-phase CT applied after partial remission of MDD with pharmacotherapy may prevent relapse partly via tempering dichotomous attributions for life events (e.g., attributing the cause of negative events entirely to oneself or entirely to other people; Teasdale et al., 2001).

The current analyses included patients with recurrent MDD who responded to 20 sessions of acute-phase CT, were randomized to 8 months of continuation-phase CT or assessment control, and were followed 16 additional months (Jarrett et al., 2001). Here we extend analyses of this dataset, and of continuation-phase CT in general, to test demographic (e.g., age, gender, ethnicity), clinical (e.g., residual symptoms, age of MDD onset, number of depressive episodes), social-interpersonal (e.g., social adjustment, interpersonal problems), cognitive (e.g., dysfunctional attitudes, self-efficacy), and personality (trait dimensions derived from basic research and DSM Axis II diagnoses) variables as potential moderators of continuation-phase CT’s effects. These variables are relevant to Jarrett’s continuation-phase CT model, fit established patterns of risk after remission of major depressive episodes, and were measured with well-established instruments. We tested the general hypothesis that patients with greater dysfunction before and after response to acute-phase CT would benefit more from continuation-phase CT than their counterparts with less dysfunction. We analyzed a wide range of variables to maximize generation of hypotheses about specific variables for validation in future studies before clinical application (Kraemer et al., 2002).

The current analyses add to the published literature in distinct ways. Although past research has addressed predictors of depressive relapse and recurrence (e.g., Burcusa & Iacono, 2007; Fava, 2007) and potential moderators of acute-phase CT’s effects (e.g., depression severity, presence of personality pathology, level of maladaptive cognition; Hollon et al., 2005), we examine a wide range of potential moderators of continuation-phase CT’s effects. Especially because depressed patients enter acute-phase CT, but treatment responders enter Jarrett’s continuation-phase CT, findings from the acute-phase may not generalize to continuation-phase CT. Additionally, we moved beyond a traditional focus on relapse, recurrence, and short-term cross-sectional estimates of positive outcomes to examine rigorously, longitudinally defined remission and recovery (few or no symptoms consistently for extended periods) as clinically significant outcomes (Rush et al., 2006; Vittengl et al., 2009; Jarrett & Vittengl, in press). From these analyses, we offer empirical guidance for future research that will test specific hypotheses about which patients most need continuation-phase CT, and perhaps other post acute phase CT treatments, to prevent negative and attain positive outcomes.

Method

Participants

Adult outpatients presenting with DSM-IV nonpsychotic, recurrent MDD with clear inter-episode recovery (≥2 months of at least nearly normal functioning; American Psychiatric Association, 1994) who scored ≥16 on the 17-item Hamilton Rating Scale for Depression (Hamilton, 1960) participated. Doctoral-level clinicians made diagnoses using the Structured Clinical Interview for DSM-III-R (outpatient version; Spitzer, Williams, Gibbon, & First, 1989), with additional questions to assess DSM-IV disorders and subtypes. Patients in the experiment (continuation-phase CT vs. control; N = 84) were M = 42.7 (SD = 10.4) years old with M = 15.4 (SD = 2.7) years of education; 72.6% were women; and 3.6% were African American, 3.6% Hispanic, 2.4% Native American, and 90.5% Caucasian. In addition to MDD, participants’ concurrent Axis I diagnoses at intake were social phobia (17.9%), specific phobias (10.7%), panic disorder without (9.5%) and with (1.2%) agoraphobia, posttraumatic stress disorder (8.3%), dysthymic disorder (4.8%), obsessive-compulsive disorder (1.2%), agoraphobia without a history of panic disorder (1.2%), and hypochondriasis (1.2%).

Procedure

Patients (N = 156) consented to a 12-14 week acute-phase CT protocol (Beck et al., 1979) including 20 individual sessions (50-60 minutes each). Acute phase CT aims to reduce depressive symptoms by eliciting thoughts associated with dysphoria, teaching patients to test the thoughts’ validity logically and empirically, and generating more realistic thoughts when negative thoughts are not supported. Responders to acute-phase CT (i.e., completed the protocol; no MDD and Hamilton Rating Scale for Depression ≤ 9 by an independent evaluator) who consented were randomized to continuation-phase CT (Jarrett, 1989; Jarrett et al., 2008b; n = 41) or assessment control (n = 43); 3 responders did not consent. The 8-month continuation-phase CT protocol included 10 individual sessions (60 minutes each, but 90 minutes allowed if necessary) provided by each patient’s acute-phase CT therapist. The 8-month control protocol included 10 evaluation visits scheduled as in continuation-phase CT. Evaluators of control patients had not provided acute-phase CT and did not use psychosocial interventions. Patients who relapsed were asked to complete all sessions and, if not receiving continuation-phase CT, were referred for treatment outside of the study. The follow-up protocol included 10 assessments scheduled over 16 months (ending 24 months post-acute-phase CT). Pharmacotherapy was not provided in this study.

Therapists

Five therapists with a PhD in clinical psychology or MD (i.e., trained as a psychiatrist), completed ≥ 1 year of CT training and demonstrated competence (scores ≥ 40 on the Cognitive Therapy Scale; Young & Beck, 1980) before treating study patients. Therapists received weekly group supervision (and additional supervision when requested) during both acute and continuation-phase CT from a PhD clinical psychologist with extensive experience supervising CT. To facilitate treatment competence and adherence, an offsite consultant (a PhD clinical psychologist with extensive experience evaluating CT) reviewed videotapes of the 4th and a randomly selected session of both acute and continuation-phase CT, scored therapists on the Cognitive Therapy Scale, and provided them written feedback. All therapists achieved mean Cognitive Therapy Scale scores > 40 during acute (grand M = 47.1, SE = 0.35) and continuation (grand M = 46.3, SE = 1.17) phase CT (Jarrett et al., 2001). Scores of 40 and above mark competence within both CT protocols.

Measures

Attributional Style Questionnaire

On the Attributional Style Questionnaire (Peterson et al., 1982), patients generate causes for hypothetical negative and positive situations and rate internal, global, and stable contributions to each cause. Negative and positive situations’ ratings are averaged (18 items each) to form failure and success composites (Peterson & Seligman, 1984); higher scores indicate stronger internal, global, and stable (i.e., hypothesized depressogenic) attributions. Correlations with self-report measures of depressive symptoms and self-concept support the measure’s validity (Tennen et al., 1987). Median alpha internal consistency was .88 for the failure composite and .84 for the success composite used in the current analyses (Jarrett et al., 2007).

Dysfunctional Attitudes Scale

The Dysfunctional Attitudes Scale (Form A; Weissman, 1979) includes 40 self-report items to measure attitudes hypothesized to relate to depression. Higher scores reflect stronger dysfunctional attitudes. The Dysfunctional Attitudes Scale’s validity has been demonstrated by correlations with depressive symptoms and negative cognitive content (e.g., Dobson & Breiter, 1983; Haeffel et al., 2005; Ilardi & Craighead, 1999). Median alpha internal consistency was .95 for the Dysfunctional Attitudes Scale total score used in the current analyses (Jarrett et al., 2007).

Self-Efficacy Scale

The Self-Efficacy Scale (Sherer et al., 1982) includes 23 self-report items measuring expected persistence and success in several domains. Higher scores mark greater self-efficacy. Correlations with interpersonal competency (Sherer et al., 1982) and self-esteem (Lansford et al., 2005) support the scale’s validity. Median alpha internal consistency was .92 for the Self-Efficacy Scale total score used in the current analyses (Jarrett et al., 2007).

Social Adjustment Scale—Self Report

The Social Adjustment Scale—Self Report (Weissman & Bothwell, 1976) includes 56 self-report items measuring functioning in important social domains (e.g., work, family, recreation). Patients complete sections reflecting their social roles (e.g., some omit marital and parenting). Higher scores reflect poorer adjustment. In support of its validity, the Social Adjustment Scale—Self Report correlates with clinical ratings of adjustment and is sensitive to change in psychopathology (Weissman & Bothwell, 1976; Weissmann et al., 1978). Median alpha internal consistency was .85 for the Social Adjustment Scale—Self Report total score used in the current analyses (Vittengl et al., 2004).

Inventory of Interpersonal Problems

The Inventory of Interpersonal Problems (Horowitz et al., 1988) measures the extent to which particular behaviors, thoughts, and feelings cause problems in personal relationships. The measure includes 127 self-report items, and higher values indicate greater problems. The scale correlates appropriately with measures of psychiatric symptoms, and decreases with psychotherapy (Horowitz et al.,1988). Median alpha internal consistency was .98 for the Inventory of Interpersonal Problems total score used in the current analyses (Vittengl et al., 2004).

Dyadic Adjustment Scale

The Dyadic Adjustment Scale (Spanier, 1976) measures satisfaction and positive adjustment in committed romantic dyads (e.g., marital). The scale includes 32 self-report items, and higher scores represent better relationship quality. Spanier (1976) provide data supporting both content and criterion-related validity. Median alpha internal consistency was .96 for the Dyadic Adjustment Scale total score used in the current analyses (Vittengl et al., 2004).

Working Alliance Inventory

The Working Alliance Inventory (Horvath & Greenberg, 1989) is a 36-item questionnaire completed by the therapist and the patient/client to rate the quality of the therapeutic relationship. Higher composite scores indicate a stronger alliance. Alpha internal consistency was .97 for the therapist form, and .96 or the patient form, at acute-phase CT session 18 in the current sample.

Schedule for Nonadaptive and Adaptive Personality

Personality was assessed with the Schedule for Nonadaptive and Adaptive Personality (Clark et al., in press), a 390-item, self-report instrument relevant to both normal and disordered personality. The inventory assesses the core of three higher order temperament dimensions (positive temperament, negative temperament, disinhibition) that reflect the instruments’ factor structure and 12 lower order trait dimensions (e.g., mistrust, impulsivity, detachment) derived from DSM Axis II disorders and other conceptualizations of nonadaptive personality. The scales have shown good internal consistency (Mdn alphas .80-.85 in student, adult, and patient samples), test-retest reliability (e.g., in normal adults, 1 week to 4 months mean r = .87), and discriminant validity (mean interscale r = ~ ∣.20∣; Clark et al., in press). Studies support the scales’ validity in relation to interview measures of personality disorder (Clark et al., in press), informant reports of personality (e.g., Ready & Clark, 2002), and external variables such as psychosocial functioning (e.g., Morey et al., 2007). The median alpha internal consistency was .82 for the 17 scales used in the current analyses (Clark et al., 2003).

Depressive symptoms

Two clinician-rated measures, the 17-item Hamilton Rating Scale for Depression and the Inventory for Depressive Symptomatology clinician version (Rush et al., 1986, 1996), and two self-report measures, the Beck Depression Inventory (Beck et al., 1961) and the Inventory for Depressive Symptomatology self-report version (Rush et al., 1986, 1996), demonstrated high convergence within and across time in the current sample, indicating that they measure the same symptom construct (Vittengl et al., 2005). Higher scores on each reflect more depressive symptoms. Median alpha internal consistency for the four measures’ standardized composite was .95 in this dataset (Vittengl et al., 2004) and indexed residual symptoms at randomization. Unstable response to acute-phase CT was defined as any Hamilton Rating Scale for Depression score ≥ 7 at the last 6 acute-phase CT sessions or at randomization (Jarrett et al., 2001).

Longitudinal Interval Follow-Up Evaluation

The Longitudinal Interval Follow-Up Evaluation (Keller et al., 1987), a semi-structured interview, measures DSM-IV Axis I psychopathology retrospectively. Independent evaluators completed the interview every 4 months post-acute-phase CT, at study exit, and when patients, therapists, or follow-up evaluators suspected major depressive relapse or recurrence. Independent evaluators were uninformed to group assignment at months 4, 8, 12, and 24, but not at months 16 and 20 because the primary aim of the parent study was to evaluate outcomes through 1 year from randomization and uninformed evaluations were costly. Independent evaluators did not provide acute or continuation-phase CT in this study and were highly experienced clinicians trained in the application of DSM-IV criteria, depressive symptom measures, and the Longitudinal Interval Follow-Up Evaluation. Weekly psychiatric status ratings of DSM-IV MDD (on a 1-6 scale) defined remission and recovery, respectively, as ≥ 6 and ≥ 35 continuous weeks of psychiatric status rating of 1 (no symptoms) or 2 (one or two mild symptoms); and relapse and recurrence as ≥ 2 weeks of psychiatric status rating of 5 (meets MDD criteria) or 6 (meets MDD criteria with severe impairment and/or psychosis) before and after, respectively, meeting criteria for recovery (Jarrett et al., 2001). Patients who relapsed before remission or recovery were coded as not achieving remission or recovery, respectively. Psychiatric status rating inter-rater reliability was .80 in the current dataset (Vittengl et al., 2009).

Analytic Strategy

To identify moderators, Kraemer et al. (2002) recommend that researchers compute statistical models including the main effect of treatment group, the main effect of the potential moderator, and the variables’ interaction. Moderators reflect baseline characteristics of participants, predict outcomes as interactions with treatment, and may operate with or without a main effect of treatment. We tested demographic, clinical, cognitive, social-interpersonal, and personality variables as predictors (main effects) and moderators (interactions with treatment group) of four outcome variables in Cox regression time-to-event analyses: Relapse over the 8-month experiment, relapse/recurrence over the 8-month experiment plus 16-month follow-up (24 months), remission over 24 months, and recovery over 24 months. These four outcome variables reflect the 8-month experimental design (relapse) plus extended follow-up (relapse/recurrence) as well as an emerging emphasis on patients attaining long-lasting positive outcomes (remission and recovery; e.g., Rush et al., 2006), which are only moderately correlated with avoidance of relapse and recurrence (Vittengl et al., 2009). We centered variables before regression analyses, and followed-up on interactions by computing simple slopes for each treatment group (Cohen, Cohen, West, & Aiken, 2003).

Because the goal of our analyses is to generate hypotheses about personalizing preventive care rather than to test hypotheses about specific variables, we emphasize findings that are clinically meaningful (r ≥ .20) and likely to replicate (prep ≥ .90). Effect size r = .20 is roughly the average effect of continuation-phase CT versus non-active control on relapse/recurrence at the end of treatment (Vittengl et al., 2007). Kraemer et al. (2002) recommend that hypothesis-generating studies identify “strong” moderators, so in the context of continuation-phase CT, we highlight moderators as strong as the treatment itself. Effect size r = .20 also marks roughly 20% differences in event (e.g., relapse, recovery) probabilities between groups for dichotomous variables (e.g., employed vs. unemployed) and between +/- 1 SD contrasts for continuous variables (e.g., low vs. high social adjustment), and thus is likely important in most clinical situations. The statistic prep ≥ .90 indicates that there is at least a 90% chance of replicating the effect (r of the same sign) in a new sample from the same population (Killeen, 2005). Focusing on prep instead of p (e.g., p < .05 in null hypothesis significance testing) matches our goal to identify potential moderators that can be tested profitably in future clinical trials aimed at providing guidelines for matching patients to treatments (Kraemer et al., 2002). In this report, we label and interpret findings meeting both criteria, r ≥ .20 and prep ≥ .90, as “substantive.”

Relevant Results from Previous Analyses of the Current Dataset

It is important to consider the current findings in the context of previously reported results in this sample. Jarrett et al. (2001) reported that continuation-phase CT reduced relapse compared to assessment control (10% vs. 31%) over the 8-month experiment, and continuation-phase CT reduced cumulative relapse/recurrence compared to control over the full 2 years of follow-up after acute-phase CT among patients with early-onset MDD (16% vs. 67%) or unstable acute-phase remission (37% vs. 62%). Jarrett et al. (2008a) reported that continuation-phase CT reduced relapse (over 8 months) and relapse/recurrence (over 2 years) for acute-phase CT responders with higher-than-average residual symptoms (measured as a standardized composite of four measures at randomization: Hamilton Rating Scale for Depression, M = 3.6, SD = 2.8; Beck Depression Inventory, M = 3.8, SD = 4.3; Inventory for Depressive Symptomatology clinician report, M = 6.3, SD = 5.0; and Inventory for Depressive Symptomatology self-report, M = 7.6, SD = 6.4). Finally, Vittengl et al. (2009) found that relative to controls, a few more patients in continuation-phase CT remitted (88% vs. 97%) and significantly more recovered (62% vs. 84%) during 2 years after acute-phase CT.

Results

Table 1 lists variables tested as potential moderators of continuation-phase CT’s effects. Variables measured at intake to acute-phase CT included age, age of MDD onset, gender, years of education, length of depressive episode, number of depressive episodes, family history of depression, and number of comorbid axis I diagnoses. Variables assessed “late” were measured at the 18th acute-phase CT session (therapeutic alliance), during the last 6 acute-phase CT sessions and at randomization (un/stable symptom level), or after response to acute-phase CT at randomization to continuation-phase CT or assessment control (employment status, cognitive, social-interpersonal, personality, and residual symptom variables). Patients with higher residual symptoms have poorer outcomes in many studies (e.g., Fava et al., 2002), and relapsed and recurred less with continuation-phase CT (vs. control) in the current dataset (Jarrett et al., 2008a). Moreover, residual depressive symptoms and our outcome variables (depressive relapse, recurrence, remission, recovery) overlap conceptually. Consequently, we controlled residual symptoms (main effect and interaction with treatment group) in analyses of other “late” variables to find incremental predictors and moderators of continuation-phase CT’s effects.

Table 1.

Predictors and Moderators of Continuation Phase CT’s Effect on Relapse, Recurrence, Remission, and Recovery: Effect size r

Test Variable n M / % SD Relapse Relapse/Recurrence Remission Recovery
Predict Moderate Predict Moderate Predict Moderate Predict Moderate
Patient Characteristics
Age 84 42.7 10.4 -.05 .21* -.24* .28* .08 .00 .24* -.21*
Age of Onset 84 20.5 9.2 Addressed by Jarrett et al. (2001) .11 -.08 .22* -.16

Quality of Acute Phase CT Response
Residual Symptoms 84 11.7 6.9 Addressed by Jarrett et al. (2008a) -.17 .24* -.22* .24*
Stable Symptom Level 84 38% Addressed by Jarrett et al. (2001) .00 .00 .13 -.20*

Cognitive Content
ASQ-Failure Comp. 84 3.7 0.9 .23* .18 .01 -.13 -.11 .08 -.25* .01
Dysfunc. Attitudes 84 97.4 30.6 .16 -.12 .15 -.16 .03 .15 -.20* .24*
Self-Efficacy Scale 84 85.5 14.2 -.27* .08 -.14 .13 .00 -.13 .22* -.23*

Social-Interpersonal Functioning
Interpersonal Probs. 83 0.8 0.5 .20* -.03 .04 -.13 .14 .12 -.06 .08
(Low) Soc. Adjustment 84 1.6 0.3 .23* .14 .13 .03 .12 .08 -.16 .05
Dyadic Adjustment 47 102.0 23.0 .02 .02 .01 -.37* -.18 --- -.07 .12

Schedule for Nonadaptive and Adaptive Personality
Mistrust 77 4.4 4.0 .23* -.06 .11 -.12 .04 .11 -.18 .15
Manipulativeness 77 3.1 2.5 .00 .26* -.03 .03 .18 -.14 .11 -.25*
Aggression 77 3.3 2.8 .07 .13 .23* .13 .17 .06 -.09 .01
Eccentric Perceptions 77 2.0 2.1 -.04 .14 .13 .19 .13 -.20 -.09 -.14
Positive Temperament 77 17.4 6.0 -.11 .19 -.20 .15 -.13 -.13 .16 -.23*
Exhibitionism 77 6.2 3.4 -.25* .21* -.27* .17 .12 -.21* .19 -.26*
Entitlement 77 8.0 3.2 -.19 .18 -.13 .23* .07 -.19 .00 -.22*
Detachment 77 5.8 3.5 .13 -.16 .04 -.21* -.04 .13 -.16 .06

Note. Table contains effect size r estimated from Cox regression analyses. rs ≥ ∣.20∣ in bold type. CT = cognitive therapy. Nonspecific predictors are main effects of test variables; moderators are interactions of the test variables with treatment group (continuation-phase CT vs. assessment-only control). Analyses of cognitive content, social-interpersonal functioning, personality, and working alliance controlled residual depressive symptoms assessed at randomization and their interaction with treatment group. ASQ = Attributional Style Questionnaire. --- = variable excluded to allow the model to converge. Variables with all effect sizes < ∣.20∣ are not shown: gender; years of education; employment status; length of depressive episode; number of depressive episodes; family history of depression; total number of comorbid axis I diagnoses, Working Alliance--Therapist and Patient Reports; ASQ-Success Composite; and personality scales Negative Temperament, Self-harm, Dependency, Disinhibition, Impulsivity, Propriety, Workaholism, Low Self-esteem and Suicide Proneness (Self-harm subscales). Gender, family history, employment, and stable symptom level are dichotomous; all other test variables are continuous.

*

prep ≥ .90

Predictors and Moderators of Continuation Phase CT’s Effects on Four Outcomes

Relapse

We defined relapse as meeting criteria for MDD before recovery during the 8-month experiment after acute-phase CT. As shown in Table 1, higher failure attributions, lower self-efficacy, greater interpersonal problems, poorer social adjustment, higher mistrust, and lower exhibitionism (marking social inhibition) predicted relapse as main effects. In addition, patients’ age, manipulativeness, and exhibitionism interacted with treatment group. Younger age and lower exhibitionism predicted relapse in assessment control but not in continuation-phase CT (see Table 2). Simple slope analyses of manipulativeness did not yield substantive results.

Table 2.

Simple Slope Analyses for Moderators of Continuation Phase CT’s Effects: Effect size r

Test Variable Group
Assessment Control Continuation Phase CT
Moderators of Relapse
 Patient Age -.25* .09
 SNAP Manipulativeness -.18 .18
 SNAP Exhibitionism -.30* -.03
Moderators of Relapse/Recurrence
 Patient Age -.38* .02
 Dyadic Adjustment Scale .29* -.25
 SNAP Entitlement -.27* .07
 SNAP Detachment .21* -.10
Moderators of Remission
 Residual Symptoms -.25* .07
 SNAP Exhibitionism .18 -.12
Moderators of Recovery
 Patient Age .28* .03
 Residual Symptoms -.30* .02
 Stable Symptom Level .22* -.05
 Dysfunctional Attitudes Scale -.24* .05
 Self-Efficacy Scale .26* .00
 SNAP Manipulativeness .20* -.15
 SNAP Positive Temperament .24* -.05
 SNAP Exhibitionism .26* -.07
 SNAP Entitlement .17 -.15

Note. Table contains effect size r estimated from Cox regression analyses. rs ≥ ∣.20∣ in bold type. CT = cognitive therapy. SNAP = Schedule for Nonadaptive and Adaptive Personality.

*

prep ≥ .90

Relapse/Recurrence

We defined recurrence as meeting criteria for MDD after recovery, and we analyzed relapse and recurrence cumulatively during the 24 months of follow-up after acute-phase CT. Younger age, higher aggression, and lower exhibitionism (marking social inhibition) predicted relapse/recurrence as main effects. Further, patients’ age, dyadic adjustment (for participants in long-term romantic relationships), entitlement, and detachment interacted with treatment group (see Table 1). Younger age, higher dyadic adjustment, lower entitlement (reflecting a negative self-view), and higher detachment (reflecting social and emotional distance) predicted relapse/recurrence in control but not in continuation-phase CT (see Table 2). Number of major depressive episodes did not predict relapse or recurrence.

Remission

We defined remission as at least 6 continuous weeks of few or no depressive symptoms during the 24 months of follow-up after acute-phase CT. No variables predicted remission as main effects, but residual symptoms and exhibitionism interacted with treatment group (see Table 1). Higher residual symptoms predicted less remission in control but not in continuation-phase CT. Simple slope analyses of exhibitionism did not yield substantive results (see Table 2).

Recovery

We defined recovery as at least 35 continuous weeks of few or no depressive symptoms during the 24 months of follow-up after acute-phase CT. Older age, later age of onset of depression, lower residual symptoms, lower failure attributions, lower dysfunctional attitudes, and greater self-efficacy predicted recovery as main effects. In addition, age, residual symptoms, stability of response to acute-phase CT, dysfunctional attitudes, self-efficacy, manipulativeness, positive temperament, exhibitionism, and entitlement interacted with treatment group (see Table 1). Older age, lower residual symptoms, stable response to acute-phase CT, lower dysfunctional attitudes, higher self-efficacy, higher manipulativeness (marking less selflessness and less hyperresponsibility), greater positive temperament, and greater exhibitionism (marking less social inhibition) predicted recovery in control but not in continuation-phase CT (see Table 2). Simple slope analyses of entitlement did not yield substantive results.

Overlap among Substantive Predictors and Moderators

Eighteen tested variables were substantive predictors and moderators of C-CT’s effects. Although these variables are often considered independently in clinical contexts, understanding their empirical overlap may inform theory of risk for relapse and recurrence, and failure to remit and recover. Table 3 shows correlations among these 18 variables. Correlations typically were small (median r = ∣.17∣), although several were strong (r ≥ ∣.50∣). Perhaps unsurprisingly, younger patients tended to have an earlier age of onset of MDD. Residual symptoms correlated strongly with greater dysfunctional attitudes and poorer social adjustment. Further, dysfunctional attitudes correlated strongly with greater interpersonal problems and poorer social adjustment; and poorer social adjustment additionally related to more interpersonal problems and poorer dyadic adjustment. Finally, lower self-efficacy correlated strongly with more interpersonal problems and mistrust, and mistrust additionally correlated with more interpersonal problems and detachment. Judged by the number of strong correlations (4 each), social adjustment and interpersonal problems were most central to this group of variables.

Table 3. Correlations among Substantive Predictors and Moderators.

Variable 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17
1. Age ---
2. Age of Onset .50 ---
3. Residual Symptoms .10 .15 ---
4. Stable Symptom Level -.15 -.07 -.46 ---
5. Failure Attributions .04 .15 .42 -.18 ---
6. Dysfunctional Attitudes .12 .04 .55 -.32 .44 ---
7. Self-Efficacy .08 -.10 -.36 .12 -.24 -.47 ---
8. Interpersonal Problems -.02 .30 .43 -.22 .45 .60 -.71 ---
9. (Low) Social Adjustment .07 .17 .61 -.22 .29 .55 -.49 .54 ---
10. Dyadic Adjustment -.12 -.20 -.31 .43 -.17 -.19 .13 -.24 -.61 ---
11. Mistrust -.16 -.01 .23 .03 .39 .36 -.50 .63 .41 -.11 ---
12. Manipulativeness .04 .11 .13 .12 .03 .13 -.30 .28 .28 .13 .30 ---
13. Aggression -.07 .05 .06 .19 .15 .15 -.27 .37 .29 -.01 .46 .24 ---
14. Eccentric Perceptions .02 .07 .29 -.19 .14 .07 -.14 .09 .13 -.13 .22 .14 .11 ---
15. Positive Temperament .09 .12 -.27 .03 -.08 -.29 .49 -.32 -.40 .24 -.30 -.11 -.13 .11 ---
16. Exhibitionism .11 -.02 -.14 .10 -.09 -.23 .25 -.23 -.18 .05 -.23 .10 -.11 .12 .35 ---
17. Entitlement .20 .00 .07 -.20 .02 -.12 .34 -.29 .01 -.06 -.11 .11 -.02 .16 .17 .27 ---
18. Detachment -.13 -.04 .14 -.17 .17 .17 -.40 .44 .31 -.11 .52 .26 .34 .11 -.32 -.29 -.12

Note. rs ≥ ∣.50∣ in bold type.

Discussion

Our analyses identified potential moderators of continuation-phase CT’s effects on relapse, recurrence, remission, and recovery among patients with recurrent MDD who responded to acute-phase CT. We note that the predictors and moderators of these four outcomes are distinct, supporting the idea that the constructs are also distinct. Consistent with Jarrett’s theoretical model (Jarrett, 1989; Jarrett et al., 2008b) and supporting our general hypothesis, we found variables that predicted relapse/recurrence or failure to remit/recover in the assessment control group but did not predict these outcomes for patients receiving continuation-phase CT. Our interpretation of this pattern is that continuation-phase CT “neutralized” some risks for poor outcomes after response to acute-phase CT. With replication of these moderators, our results may inform theory and application of continuation-phase CT by identifying acute-phase CT patients who likely require further treatment, such as continuation-phase CT, to avoid relapse or recurrence and to achieve recovery. Conversely, other acute-phase CT responders are less likely to need immediate continued care. Our research group is undertaking this replication and clinical translational research in a larger, ongoing two-site randomized controlled trial of continuation-phase CT compared to clinical management plus fluoxetine or matched pill placebo (Jarrett & Thase, in preparation). With the current hypothesis-generating goal in mind, below we summarize our findings as descriptions of patients more likely to avoid relapse/recurrence and to achieve remission and recovery if they receive continuation-phase CT.

Among patients who responded to acute-phase CT, patients more likely to need continuation-phase CT may stand out as having had a long course of illness beginning by late adolescence. Continuation phase CT appeared to neutralize the risk for relapse/recurrence attributable to younger age and age of onset. We also found that continuation-phase CT appeared to neutralize risk from residual symptoms for non-remission and non-recovery. The current findings for remission and recovery add to previous findings in this dataset that continuation-phase CT reduces residual symptoms’ prediction of relapse/recurrence (Jarrett et al., 2008a). We therefore controlled residual symptoms in evaluating other moderators of continuation-phase CT assessed late in acute-phase CT.

Beyond residual symptoms assessed at randomization, continuation-phase CT may be helpful for patients who display transiently elevated depressive symptoms late in acute-phase CT (i.e., show incomplete or partial acute-phase remission), report greater depressive cognitive content, and have low positive activation (e.g., low energy, enthusiasm, initiation and enjoyment of social contact; Clark et al., 1994). Other researchers have concluded that personality traits reflecting behavioral passivity present risk for poor outcomes after acute-phase CT (Gollan, Gortner, & Dobson, 2006), and our research suggests that continuation-phase CT reduces this risk. More research is needed to determine the extent to which these variables represent distinct constructs or are largely overlapping.

Among moderators assessed late in acute-phase CT, continuation-phase CT neutralized risk for relapse attributable to low exhibitionism (marking social inhibition); risk for relapse/recurrence attributable to low entitlement (marking low self-esteem) and high social and emotional detachment; and risk for non-recovery attributable to unstable remission to acute-phase CT, dysfunctional attitudes, low self-efficacy, low manipulativeness (marking selflessness and hyperresponsibility) low positive temperament, and low exhibitionism (marking social inhibition). Unexpectedly, higher dyadic adjustment predicted more relapse/recurrence in assessment control (but not in continuation-phase CT). Why relatively better dyadic adjustment was a risk among our control patients is unclear, but we note that mean dyadic adjustment for the full sample (102) and for control patients who relapsed/recurred (107) was below average for married couples (M = 115, SD = 18; Spanier, 1976). The unclear risk for relapse/recurrence in this range of dyadic adjustment was “neutralized” by continuation-phase CT.

Several limitations of our analyses may be important for future research that builds on our findings. The current results with Jarrett’s continuation-phase CT (Jarrett, 1989; Jarrett et al., 2008b) applied to acute-phase CT responders and thus may not generalize to other acute- and continuation-phase treatments or to acute-phase treatment non-responders. For example, we did not replicate findings that other models of post-acute-phase CT prevent relapse/recurrence for patients with at least 3 (Ma & Teasdale, 2004) or 5 (Bockting et al., 2005) prior major depressive episodes (but not for those with fewer prior episodes). We did find that the related variable of earlier age of onset of MDD predicted less recovery overall, and more relapse/recurrence in only the control group. Pending replication, these findings raise the hypothesis that unlike other forms of post-acute-phase CT, continuation-phase CT may prevent relapse and recurrence in patients with 2 or more episodes and the risk factors mentioned above. To improve understanding of risk factors and moderators, future research might test this hypothesis against alternative hypotheses about differences in patient samples among studies.

We analyzed many potential moderator variables (i.e., 12 demographic/clinical, 4 cognitive, 3 social-interpersonal, and 17 personality variables) of four outcomes (relapse, relapse/recurrence, remission, and recovery) to maximize identification of potential moderators for confirmation in future research (Kraemer et al., 2002). Because we used a hypothesis-generating analytic strategy (i.e., computed and focused on r and prep instead of p), the issue of Type I error does not apply in the conventional sense. Nonetheless, replication is essential to rule out sampling error in novel findings before clinical application. Because the observed effects were modest in size (effect size r was in the .2-.4 range), future research aimed at replication of these putative moderators with traditional hypothesis testing may require large samples for adequate statistical power (e.g., roughly 200 patients to achieve power = .80, given rho = .20 and alpha = .05, two-tailed; Cohen, 1988). Furthermore, additional unmeasured variables (e.g., therapists’ characteristics, patients’ genetic markers or developmental histories) may also moderate continuation-phase CT’s effects. Finally, observed predictors and moderators typically were not highly interrelated but exceptions (e.g., the negative relation between self-efficacy and mistrust) are consistent with hypothesized overlap among vulnerabilities to depression (e.g., between depressive cognition and personality pathology; Ilardi & Craighead, 1999; Otto et al., 2007).

Our patients had carefully diagnosed recurrent MDD with clear inter-episode recovery and received acute-phase CT and continuation-phase CT from closely supervised expert therapists. Moreover, our definitions of remission and recovery intentionally mark and attempt to motivate a higher standard of patient success than definitions in most of the depression treatment literature (Vittengl et al., 2009). We cannot rule out the possibility of bias at months 16 and 20 when evaluators were not blind to patients’ treatment with continuation-phase CT or assessment-only control. In sum, moderators of continuation-phase CT’s effects may vary by the subpopulation of MDD patients studied, therapist qualifications and supervision, and definitions and measurement of patients’ outcomes during follow-up.

The current analyses are the most comprehensive examination of moderators of continuation-phase CT’s effects of which we are aware. Our results both replicate previous findings of risks for poor outcomes after response to acute-phase treatment (e.g., early age of MDD onset, poor social-interpersonal and cognitive functioning, residual symptoms, personality pathology; Burcusa & Iacono, 2006; Fava et al., 2007) and also add to the literature by identifying demographic, clinical, cognitive, and personality variables that may moderate continuation-phase CT’s effects on relapse, recurrence, remission, and recovery. Our moderator results with the SNAP, a trait dimensional assessment derived largely from DSM personality disorder criteria, extend previous findings regarding personality disorder as a risk for poorer post-acute-phase treatment outcomes (e.g., Ilardi, Craighead, & Evans, 1997; Mulder et al., 2006). Continuation phase CT, and other preventive and related models, arose in recognition that, despite acute-phase treatments’ reduction of depressive symptoms, MDD often is a chronic or recurrent illness and effective treatment can require extended intervention. Our reports have summarized continuation-phase CT’s benefits–but also identified limitations–in reducing relapse/recurrence and producing recovery. We offer these findings to stimulate efforts to test hypotheses about when to treat patients with continuation-phase CT to maximize benefits, and to personalize preventive care and reduce the burden of illness for patients with MDD.

Acknowledgments

The clinical trial was conducted at The University of Texas Southwestern Medical Center at Dallas, Department of Psychiatry, in the Psychosocial Research and Depression Clinic directed by Dr. Jarrett and was supported in part by grants MH-38238 and MH-01571 from the National Institute of Mental Health (NIMH), Bethesda, MD (Dr. Jarrett). The NIMH had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication. Gratitude is expressed to the patients and to our colleagues named in Jarrett et al. (2001) who contributed to this research.

Footnotes

All authors report that they have no financial interests related to the research reported here.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Contributor Information

Jeffrey R. Vittengl, Department of Psychology, Truman State University

Lee Anna Clark, Department of Psychology, University of Iowa.

Robin B. Jarrett, Department of Psychiatry, The University of Texas Southwestern Medical Center at Dallas

References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4. Washington, DC: Author; 1994. [Google Scholar]
  2. Beck JS. Basics and Beyond. New York: Guilford Press; 1995. Cognitive Therapy. [Google Scholar]
  3. Beck AT, Rush AJ, Shaw BF, Emery G. Cognitive Therapy of Depression. New York: Guilford Press; 1979. [Google Scholar]
  4. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Archives of General Psychiatry. 1961;4:561–571. doi: 10.1001/archpsyc.1961.01710120031004. [DOI] [PubMed] [Google Scholar]
  5. Bockting CLH, Schene AH, Spinhoven P, Koeter MWJ, Wouters LF, Huyser J, Kamphuis JH. Preventing relapse/recurrence in recurrent depression with cognitive therapy: A randomized controlled trial. Journal of Consulting and Clinical Psychology. 2005;73:647–657. doi: 10.1037/0022-006X.73.4.647. [DOI] [PubMed] [Google Scholar]
  6. Burcusa SL, Iacono WG. Risk for recurrence in depression. Clinical Psychology Review. 2007;27:959–985. doi: 10.1016/j.cpr.2007.02.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Clark LA, Vittengl JR, Kraft D, Jarrett RB. Separate personality traits from states to predict future depression. Journal of Personality Disorders. 2003;17:152–172. doi: 10.1521/pedi.17.2.152.23990. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Clark LA, Simms LJ, Wu KD, Casillas A. Schedule for Nonadapative and Adaptive Personality—2nd Edition (SNAP-2): Manual for Administration, Scoring, and Interpretation. Minneapolis, MN: University of Minnesota Press; in press. [Google Scholar]
  9. Clark LA, Watson D, Mineka S. Temperament, personality, and the mood and anxiety disorders. Journal of Abnormal Psychology. 1994;103:103–116. [PubMed] [Google Scholar]
  10. Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2. Hillsdale, NJ: Erlbaum; 1988. [Google Scholar]
  11. Cohen J, Cohen P, West SG, Aiken LS. Applied multiple regression/correlation analysis for the behavioral sciences. 3. Mahwah, NJ: Erlbaum; 2003. [Google Scholar]
  12. Craighead WE, Sheets ES, Brosse AL, Ilardi SS. Psychosocial treatments for major depressive disorder. In: Nathan PE, Gorman JM, editors. A Guide to Treatments that Work. 3. New York: Oxford Press; 2007. pp. 289–308. [Google Scholar]
  13. DeRubeis RJ, Hollon SD, Amsterdam JD, Shelton RC, Young PR, Salomon RM, O’Reardon JP, Lovett ML, Gladis MM, Brown LL, Gallop R. Cognitive therapy vs medications in the treatment of moderate to severe depression. Archives of General Psychiatry. 2005;62:409–416. doi: 10.1001/archpsyc.62.4.409. [DOI] [PubMed] [Google Scholar]
  14. Dimidjian S, Hollon SD, Dobson KS, Schmaling KB, Kohlenberg RJ, Addis ME, Gallop R, McGlinchey JB, Markley DK, Gollan JK, Atkins DC, Dunner DL, Jacobson NS. Randomized trial of behavioral activation, cognitive therapy, and antidepressant medication in the acute treatment of adults with major depression. Journal of Consulting and Clinical Psychology. 2006;74:658–670. doi: 10.1037/0022-006X.74.4.658. [DOI] [PubMed] [Google Scholar]
  15. Dobson KS, Breiter HJ. Cognitive assessment of depression: reliability and validity of three measures. Journal of Abnormal Psychology. 1983;92:107–109. doi: 10.1037//0021-843x.92.1.107. [DOI] [PubMed] [Google Scholar]
  16. Dobson KS, Hollon SD, Dimidjian S, Schmaling KB, Kohlenberg RJ, Gallop RJ, Rizvi SL, Gollan JK, Dunner DL, Jacobson NS. Randomized trial of behavioral activation, cognitive therapy, and antidepressant medication in the prevention of relapse and recurrence in major depression. Journal of Consulting and Clinical Psychology. 2008;76:468–477. doi: 10.1037/0022-006X.76.3.468. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Fava GA, Fabbri S, Sonino N. Residual symptoms in depression: An emerging therapeutic target. Progress in Neuro-Psychopharmacology & Biological Psychiatry. 2002;26:1019–1027. doi: 10.1016/s0278-5846(02)00226-9. [DOI] [PubMed] [Google Scholar]
  18. Fava GA, Rafanelli C, Grandi S, Conti S, Belluardo P. Prevention of recurrent depression with cognitive behavioral therapy: Preliminary findings. Archives of General Psychiatry. 1998;55:816–820. doi: 10.1001/archpsyc.55.9.816. [DOI] [PubMed] [Google Scholar]
  19. Fava GA, Ruini C, Belaise C. The concept of recovery in major depression. Psychological Medicine. 2007;37:307–317. doi: 10.1017/S0033291706008981. [DOI] [PubMed] [Google Scholar]
  20. Fava GA, Ruini C, Rafanelli C, Finos L, Conti S, Grandi S. Six-year outcome of cognitive behavior therapy for prevention of recurrent depression. American Journal of Psychiatry. 2004;161:1872–1876. doi: 10.1176/ajp.161.10.1872. [DOI] [PubMed] [Google Scholar]
  21. Frank E, Prien RF, Jarrett RB, Keller MB, Kupfer DJ, Lavori PW, Rush AJ, Weissman MM. Conceptualization and rationale for consensus definitions of terms in major depressive disorder: remission, recovery, relapse, and recurrence. Archives of General Psychiatry. 1991;48:851–855. doi: 10.1001/archpsyc.1991.01810330075011. [DOI] [PubMed] [Google Scholar]
  22. Gollan JK, Gortner ET, Dobson KS. Predictors of depressive relapse during a two year prospective follow-up after cognitive and behavioral therapies. Behavioural and Cognitive Psychotherapy. 2006;34:397–412. [Google Scholar]
  23. Haeffel GJ, Abramson LY, Voelz ZR, Metalsky GI, Halberstadt L, Dykman BM, Donovan P, Hogan ME, Hankin BL, Alloy LB. Negative cognitive styles, dysfunctional attitudes, and the remitted depression paradigm: A search for the elusive cognitive vulnerability to depression factor among remitted depressives. Emotion. 2005;5:343–348. doi: 10.1037/1528-3542.5.3.343. [DOI] [PubMed] [Google Scholar]
  24. Hamilton M. A rating scale for depression. Journal of Neurology, Neurosurgery, and Psychiatry. 1960;23:56–61. doi: 10.1136/jnnp.23.1.56. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Hollon SD, DeRubeis RJ, Shelton RC, Amsterdam JD, Salomon RM, O’Reardon JP, Lovett ML, Young PR, Haman KL, Freeman BB, Gallop R. Prevention of relapse following cognitive therapy vs medications in moderate to severe depression. Archives of General Psychiatry. 2005;62:417–422. doi: 10.1001/archpsyc.62.4.417. [DOI] [PubMed] [Google Scholar]
  26. Hollon SD, Stewart MO, Strunk D. Enduring effects for cognitive behavior therapy in the treatment of depression and anxiety. Annual Review of Psychology. 2006;57:285–315. doi: 10.1146/annurev.psych.57.102904.190044. [DOI] [PubMed] [Google Scholar]
  27. Hollon SD, Jarrett RB, Nierenberg AA, Thase ME, Trivedi M, Rush AJ. Psychotherapy and medication in the treatment of adult and geriatric depression: Which monotherapy or combined treatment? Journal of Clinical Psychiatry. 2005;66:455–468. doi: 10.4088/jcp.v66n0408. [DOI] [PubMed] [Google Scholar]
  28. Horowitz LM, Rosenberg SE, Baer BA, Ureño G, Villaseñor VS. Inventory of interpersonal problems: psychometric properties and clinical applications. Journal of Consulting and Clinical Psychology. 1988;56:885–892. doi: 10.1037//0022-006x.56.6.885. [DOI] [PubMed] [Google Scholar]
  29. Horvarth AO, Greenberg LS. Development and validation of the Working Alliance Inventory. Journal of Counseling Psychology. 1989;36:223–233. [Google Scholar]
  30. Ilardi SS, Craighead WE. The relationship between personality pathology and dysfunctional cognitions in previously depressed adults. Journal of Abnormal Psychology. 1999;108:51–57. doi: 10.1037//0021-843x.108.1.51. [DOI] [PubMed] [Google Scholar]
  31. Ilardi SS, Craighead WE, Evans DD. Modeling relapse in unipolar depression: The effects of dysfunctional cognitions and personality disorders. Journal of Consulting and Clinical Psychology. 1997;65:381–391. doi: 10.1037//0022-006x.65.3.381. [DOI] [PubMed] [Google Scholar]
  32. Jarrett RB. Cognitive Therapy for Recurrent Unipolar Depressive Disorder: The Continuation/maintenance Phase. 1989. Unpublished manuscript. [Google Scholar]
  33. Jarrett RB, Thase ME. Comparative Efficacy and Durability of Continuation Phase Cognitive Therapy for Preventing Recurrent Depression: Design of a Double Blinded Fluoxetine and Pill Placebo- Controlled Randomized Trial with 2 Year Follow-up. under review. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Jarrett RB, Kraft D, Doyle J, Foster BM, Eaves GG, Silver PC. Preventing recurrent depression using cognitive therapy with and without a continuation phase. Archives of General Psychiatry. 2001;58:381–388. doi: 10.1001/archpsyc.58.4.381. [DOI] [PMC free article] [PubMed] [Google Scholar]
  35. Jarrett RB, Vittengl JR. Efficacy of cognitive-behavioral therapy for depression. In: Fisher PL, Wells A, editors. Treating depression: Principles and practice of CBT, MCT, and third wave therapies. New York: Wiley; pp. xx–xx. in press. [Google Scholar]
  36. Jarrett RB, Vittengl JR, Clark LA. How much cognitive therapy, for which patients, will prevent depressive relapse? Journal of Affective Disorders. 2008a;111:185–192. doi: 10.1016/j.jad.2008.02.011. [DOI] [PMC free article] [PubMed] [Google Scholar]
  37. Jarrett RB, Vittengl JR, Clark LA. Preventing recurrent depression. In: Whisman MA, editor. Adapting Cognitive Therapy for Depression: Managing Complexity and Comorbidity. New York: Guilford Press; 2008b. pp. 132–156. [Google Scholar]
  38. Jarrett RB, Vittengl JR, Doyle K, Clark LA. Changes in cognitive content during and following cognitive therapy for recurrent depression: Substantial and enduring, but not predictive of change in depressive symptoms. Journal of Consulting and Clinical Psychology. 2007;75:432–466. doi: 10.1037/0022-006X.75.3.432. [DOI] [PMC free article] [PubMed] [Google Scholar]
  39. Judd LL, Akiskal HS, Zeller PJ, Paulus M, Leon AC, Maser JD, Endicott J, Coryell W, Kunovac JL, Mueller TI, Rice JP, Keller MB. Psychosocial disability during the long-term course of unipolar major depressive disorder. Archives of General Psychiatry. 2000;57:375–380. doi: 10.1001/archpsyc.57.4.375. [DOI] [PubMed] [Google Scholar]
  40. Keller MB, Lavori PW, Friedman B, Nielsen E, Endicott J, McDonald-Scott P, Andreasen NC. The Longitudinal Interval Follow-up Evaluation. A comprehensive method for assessing outcome in prospective longitudinal studies. Archives of General Psychiatry. 1987;44:540–548. doi: 10.1001/archpsyc.1987.01800180050009. [DOI] [PubMed] [Google Scholar]
  41. Killeen PR. An alternative to null-hypothesis significance tests. Psychological Science. 2005;16:345–353. doi: 10.1111/j.0956-7976.2005.01538.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  42. Kraemer HC, Wilson GT, Fairburn CG, Agras WS. Mediators and moderators of treatment effects in randomized clinical trials. Archives of General Psychiatry. 2002;59:877–884. doi: 10.1001/archpsyc.59.10.877. [DOI] [PubMed] [Google Scholar]
  43. Lansford JE, Antonucci TC, Akiyama H, Takahashi K. A Quantitative and Qualitative Approach to Social Relationships and Well-Being in the United States and Japan. Journal of Comparative Family Studies. 2005;36:1–22. [Google Scholar]
  44. Ma SH, Teasdale JD. Mindfulness-based cognitive therapy for depression: Replication and exploration of differential relapse prevention effects. Journal of Consulting and Clinical Psychology. 2004;72:31–40. doi: 10.1037/0022-006X.72.1.31. [DOI] [PubMed] [Google Scholar]
  45. Morey LC, Hopwood CJ, Gunderson JG, Skodol AE, Shea MT, Yen S, Stout RL, Zanarini MC, Grilo CM, Sanislow CA, McGlashan TH. Comparison of alternative models for personality disorders. Psychological Medicine. 2007;37:983–994. doi: 10.1017/S0033291706009482. [DOI] [PubMed] [Google Scholar]
  46. Mulder RT, Joyce PR, Frampton CMA, Luty SE, Sullivan PF. Six months of treatment for depression: Outcome and predictors of the course of illness. American Journal of Psychiatry. 2006;163:95–100. doi: 10.1176/appi.ajp.163.1.95. [DOI] [PubMed] [Google Scholar]
  47. National Institute of Mental Health. Strategic Plan. Bethesda, MD: Author; 2008. [Google Scholar]
  48. Nemeroff CB, Schatzberg AF. Pharmacological treatments for unipolar depression. In: Nathan PE, Gorman JM, editors. A Guide to Treatments that Work. 3. New York: Oxford; 2007. pp. 271–287. [Google Scholar]
  49. Otto MW, Teachman BA, Cohen LS, Soares CN, Vitonis AF, Harlow BL. Dysfunctional attitudes and episodes of major depression: Predictive validity and temporal stability in never-depressed, depressed, and recovered women. Journal of Abnormal Psychology. 2007;116:475–483. doi: 10.1037/0021-843X.116.3.475. [DOI] [PubMed] [Google Scholar]
  50. Paykel ES, Scott J, Teasdale JD, Johnson AL, Garland A, Moore R, Jenaway A, Cornwall PL, Hayhurst H, Abbott R, Pope M. Prevention of relapse in residual depression by cognitive therapy: A controlled trial. Archives of General Psychiatry. 1999;56:829–835. doi: 10.1001/archpsyc.56.9.829. [DOI] [PubMed] [Google Scholar]
  51. Peterson C, Seligman ME. Causal explanations as a risk factor for depression: theory and evidence. Psychological Review. 1984;91:347–374. [PubMed] [Google Scholar]
  52. Peterson C, Semmel A, von Baeyer C, Abramson LT, Metalsky GI, Seligman MEP. The Attributional Style Questionnaire. Cognitive Therapy and Research. 1982;6:287–300. [Google Scholar]
  53. Ready RE, Clark LA. Correspondence of psychiatric patient and informant ratings of personality traits, temperament, and interpersonal problems. Psychological Assessment. 2002;14:39–49. [PubMed] [Google Scholar]
  54. Rush AJ, Giles DE, Schlesser MA, Fulton CL, Weissenburger JE, Burns CT. The Inventory for Depressive Symptomatology (IDS): Preliminary findings. Psychiatry Research. 1986;18:65–87. doi: 10.1016/0165-1781(86)90060-0. [DOI] [PubMed] [Google Scholar]
  55. Rush AJ, Gullion CM, Basco MR, Jarrett RB, Trivedi MH. The Inventory of Depressive Symptomatology (IDS): Psychometric Properties. Psychological Medicine. 1996;26:477–486. doi: 10.1017/s0033291700035558. [DOI] [PubMed] [Google Scholar]
  56. Rush AJ, Kraemer HC, Sackeim HA, Fava M, Trivedi MH, Frank E, et al. Report by the ACNP Task Force on response and remission in major depressive disorder. Neuropsychopharmacology. 2006;31:1841–1853. doi: 10.1038/sj.npp.1301131. [DOI] [PubMed] [Google Scholar]
  57. Segal ZV, Williams JMG, Teasdale JD. Mindfulness-based Cognitive Therapy for Depression A New Approach for Preventing Relapse. New York: Guilford; 2002. [Google Scholar]
  58. Sherer M, Maddux JE, Mercadante B, Prentice-Dunn S, Jacobs B, Rogers RW. The self-efficacy scale: Construction and validation. Psychological Reports. 1982;51:663–671. [Google Scholar]
  59. Spanier GB. Measuring dyadic adjustment: New scales for assessing the quality of marriage and similar dyads. Journal of Marriage and the Family. 1976;38:15–28. [Google Scholar]
  60. Spitzer RL, Williams JBW, Gibbon M, First MB. Structured Clinical Interview for DSM-III-R-Outpatient Version (with Psychotic Screen) New York: New York State Psychiatric Institute; 1989. [Google Scholar]
  61. Teasdale JD, Scott J, Moore RG, Hayhurst H, Pope M, Paykel ES. How does cognitive therapy prevent relapse in residual depression? Evidence from a controlled trial. Journal of Consulting and Clinical Psychology. 2001;69:347–357. doi: 10.1037//0022-006x.69.3.347. [DOI] [PubMed] [Google Scholar]
  62. Teasdale JD, Segal ZV, Williams JMG, Ridgeway VA, Soulsby JM, Lau MA. Prevention of relapse/recurrence in major depression by mindfulness-based cognitive therapy. Journal of Consulting and Clinical Psychology. 2000;68:615–623. doi: 10.1037//0022-006x.68.4.615. [DOI] [PubMed] [Google Scholar]
  63. Tennen H, Herzberger S, Nelson HF. Depressive attributional style: The role of self-esteem. Journal of Personality. 1987;55:631–660. doi: 10.1111/j.1467-6494.1987.tb00456.x. [DOI] [PubMed] [Google Scholar]
  64. Thase ME, Simons AD, McGeary J, Cahalane JF, Hughes C, Harden T, Friedman E. Relapse after cognitive behavior therapy of depression: potential implications for longer courses of treatment. The American Journal of Psychiatry. 1992;149:1046–1052. doi: 10.1176/ajp.149.8.1046. [DOI] [PubMed] [Google Scholar]
  65. Vittengl JR, Clark LA, Dunn TW, Jarrett RB. Reducing relapse and recurrence in unipolar depression: A comparative meta-analysis of cognitive-behavioral therapy’s effects. Journal of Consulting and Clinical Psychology. 2007;75:475–488. doi: 10.1037/0022-006X.75.3.475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  66. Vittengl JR, Clark LA, Jarrett RB. Improvement in social-interpersonal functioning after cognitive therapy for recurrent depression. Psychological Medicine. 2004;34:643–658. doi: 10.1017/S0033291703001478. [DOI] [PMC free article] [PubMed] [Google Scholar]
  67. Vittengl JR, Clark LA, Jarrett RB. Continuation-phase cognitive therapy’s effects on remission and recovery from depression. Journal of Consulting and Clinical Psychology. 2009;77:367–371. doi: 10.1037/a0015238. [DOI] [PMC free article] [PubMed] [Google Scholar]
  68. Vittengl JR, Clark LA, Kraft D, Jarrett RB. Multiple measures, methods, and moments: A factor-analytic investigation of change in depressive symptoms during acute phase cognitive therapy. Psychological Medicine. 2005;35:693–704. doi: 10.1017/s0033291704004143. [DOI] [PMC free article] [PubMed] [Google Scholar]
  69. Weissman AN. Dissertation Abstracts International. Vol. 40. 1979. The Dysfunctional Attitudes Scale: A validation study. (Doctoral dissertation, University of Pennsylvania) pp. 1389B–1390B. [Google Scholar]
  70. Weissman MM, Bothwell S. Assessment of social-adjustment by patient self-report. Archives of General Psychiatry. 1976;33:1111–1115. doi: 10.1001/archpsyc.1976.01770090101010. [DOI] [PubMed] [Google Scholar]
  71. Weissman MM, Prusoff BA, Thompson WD, Harding PS, Myers JK. Social adjustment by self-report in a community sample and in psychiatric outpatients. Journal of Nervous and Mental Disease. 1978;166:317–326. doi: 10.1097/00005053-197805000-00002. [DOI] [PubMed] [Google Scholar]
  72. Young J, Beck AT. Cognitive Therapy Scale: Rating Manual. Philadelphia, PA: Center for Cognitive Therapy; 1980. [Google Scholar]

RESOURCES