Copyright 1992 by the American Psychological Association. Inc. 0021-843X/92/$3.00
Journal of Abnormal Psychology 1992, Vol. 101, No. 1,45-52
Psychiatric History and Stress: Predictors of Severity of Unipolar Depression Constance Hammen, Joanne Davila, Gary Brown, Aimee Ellicott, and Michael Gitlin
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
University of California, Los Angeles Unipolar depression is frequently a recurrent or chronic disorder. In studies on predicting its course, outcomes are typically linked to either psychiatric features or stressful life events. In order to integrate the 2 approaches, 51 unipolar patients were assessed periodically over at least 1 year for symptoms, stressful events, and chronic stressors. It was hypothesized that adverse family history and early age of onset impair role functioning and coping capabilities, thereby contributing to stressful circumstances that predict severity of depressive reactions. Results of causal modeling analyses supported a model in which background factors were associated with severity of depressive outcomes as mediated by their effects on stress variables. Such a model implicates the self-perpetuating nature of clinical depression, both for the individual and across generations.
(Bland, Newman, & Orn, 1986; Giles, Jarrett, Biggs, Guzick, & Ruch, 1989; Klein, Taylor, Dickstein, & Harding, 1988). Presence of concurrent dysthymic disorder with major depression has also been found to be predictive of increased likelihood of relapse or recurrence (e.g., Keller, 1988; Keller, Lavori, Endicott, Coryell, & Klerman, 1983). Similarly, Giles et al. (1989) reported that history of other affective reactions (such as intermittent depression or "labile personality") were associated with greater likelihood of recurrence in patients with major depression. In most of the work to date, investigators have studied relapse and recurrence as the variables to be predicted. Reports such as these give clues about correlates of the course of depressive disorder. However, they do not provide a conceptual basis for understanding why such historical factors predispose one to exacerbations and recurrences of unipolar depression. Even the specifically genetic-biological models do not rule out the potential effects of psychosocial influences, but few researchers have actually attempted to illuminate the processes that account for features of the course of disorder. According to an entirely different model, psychosocial factors influence the course of disorder; that is, stressors (or stressors interacting with a cognitive or psychological diathesis) affect the occurrence and the severity of depressive episodes. For instance, Paykel and Tanner (1976) found that patients who relapsed were more likely to report negative life events than were those who remained in remission. Lloyd, Zisook, Click, and Jaffe (1981) found that patients who had experienced negative life events responded more poorly to antidepressant treatment (although Monroe et al., 1983, failed to find such an association). In a nonpatient sample, Hammen et al. (1986) found that stressful events were predictive of relapse and recurrence of depression in persons with previous symptoms (but had less impact on subjects who had not suffered from depression). Billings and Moos (1985) assessed treated depressed clients for 1 year and found that posttreatment depression was associated with continuing high rates of stressful conditions. Several writers have called for further examination of the role that stress plays in relation to other predictors of relapse (e.g., Klein et al., 1988; Lewinsohn et al., 1989).
There are three empirical truths about unipolar depression that ought to guide efforts to understand and predict its course: (a) depression runs in families (Beardslee, Bemporad, Keller, & Klerman, 1983; Hammen, Gordon, etal., 1987; Rutter&Quinton, 1984; Weissman, et al., 1987); (b) the best predictor of future depression is previous depression (Belsher & Costello, 1988; Hammen, Mayol, deMayo, & Marks, 1986; Keller, 1988; Lewinsohn, Zeiss, & Duncan, 1989); and (c) for many clinically depressed persons, it is a recurrent if not chronic disorder (Keller, 1988; Sargeant, Bruce, Florio, & Weissman, 1990). The observed realities about unipolar depression imply not only a pernicious course but also a self-perpetuating one. Unfortunately, the major perspectives on the course of unipolar depression have generally proceeded along separate lines with little integrative effort. One approach is predominantly descriptive, in which previous history and features of the disorder are used to predict the subsequent course. One variant of this perspective is biological, and unipolar depression is viewed as a disease. Statistical loading for familial depression, early age of onset, and recurrence are regarded from this perspective as aspects of a possibly genetically transmitted disorder that develops according to largely endogenous processes. Recurrence and chronicity may be viewed as expected consequences of a disease process. Descriptive studies are rich in evidence of the role of background factors in the prediction of course. Loading for familial affective disorder is associated with onset of depression and is thought to predict a relatively pernicious course in comparison with the course in people who do not have a family history. Early age of onset has been suggested as a risk factor for a more negative course, including recurrence of episodes
The authors appreciate the assistance of interviewers Cheri Adrian, Dorli Burge, Ron Duran, Jean Kaufman, Aaron Oderberg, and the staff of the University of California, Los Angeles, Affective Disorders Clinic. Correspondence concerning this article should be addressed to Constance Hammen, Department of Psychology, University of California, 405 Hilgard Avenue, Los Angeles, California 90024. 45
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
46
HAMMEN, DAVILA, BROWN, ELLICOTT, GITLIN
Unfortunately, the descriptive research on background factors such as family psychopathology and age of onset has not been integrated into most psychosocial models of depression course. In the psychiatric studies of family history or age of onset and course of illness, investigators do not typically evaluate psychosocial events and their role in predicting symptoms. Consequently, our goal was to begin an integration of these disparate streams of research in order to take into account the three truths about unipolar depression that were noted earlier, including the practical goal of improving prediction of course of disorder and the conceptual goal of improving our theories of why a psychiatric history is predictive of recurrence of depression. In this study, we tested a model for predicting symptom severity over a longitudinal course, in which family history of psychopathologic disorder and early age of onset of depression relate to symptoms through their influence on episodic and chronic stressful events. The goal was not to pit biological and nonbiological models against each other but rather to test hypotheses about how certain psychiatric variables may influence the severity of unipolar depression in patients who are at risk for relapse. A history of depression is likely to be a strong predictor of subsequent depression because it may be a marker of several maladaptive factors, which reflect exposure to stress and impairment of coping capabilities and of adaptive functioning, that predispose a person to depression. For instance, clinical depression impairs role functioning in ways that may contribute to chronic stressful, unhappy situations in terms of occupational adjustment, financial stability, and supportive marital and family relations (e.g., Barnett & Gotlib, 1988; Hammen, Gordon et al., 1987). If the onset of depressive symptoms occurs early in life, it is likely not only that the person has been exposed to adverse social conditions but also that the person has not acquired adequate coping mechanisms, and the symptoms may further impair the acquisition of adaptive skills. Thus early onset of depression may be associated with continuing elevated levels of chronic stress and episodic stressors, either because impaired functioning brings about the circumstances or because skills for coping with or adapting to the naturally occurring vicissitudes of life are inadequate. Moreover, we predicted that family history of psychopathologic disorder would be associated with early onset of depression. Whether the disorder is attributable to genetic or psychosocial causes or both, children of parents with psychiatric problems are themselves at elevated risk for disorder (Beardslee et al., 1983; Rutter & Quinton, 1984; Watt, Anthony, Wynne, & Rolf, 1984). There is ample evidence that depression runs in families, as noted earlier, and depression may indeed be a fairly frequent outcome of exposure to parental disability and adverse family circumstances (e.g., Hammen, Adrian, et al., 1987). Thus family history of depression or of any psychiatric disorder may likely be associated with early onset of depression, and disrupted family functioning may contribute to failure to acquire the kinds of adaptive capabilities that are necessary to avoid or resolve stressful circumstances. Although patients' family pedigrees are especially loaded statistically for parental affective disorder, we did not limit our analyses to only parental affective disorders; we also included family substance abuse disorder, and other major forms of psychopathology, because
we predicted that it is early disruption rather than a specific genetic mechanism that contributes to maladjustment and stressful conditions. Early disruption can be contributed by any family psychopathologic disorder, not just depression. For all of these reasons, we proposed that psychiatric history features that are markers of disrupted functioning (family psychopathology and personal early age of onset) would be associated with severity of recurrence and relapse of depression in patients, to the extent that they are predictive of elevated chronic and episodic stress levels that both precipitate depression and prolong its course. The outpatients in our sample were at risk for relapse, inasmuch as the majority of persons treated for major depressive episodes go on to have multiple episodes if not chronic symptoms (Keller, 1988; Sargeant et al., 1990). Over the longitudinal follow-up of up to 2 or 3 years in this study, nearly all patients did experience relapse or recurrences. Thus our goal was to predict the severity of the worst episode during the period of follow-up, on the basis of multiple background and stress variables. We used causal modeling analyses, testing hypothesized relations in a longitudinal design in which carefully diagnosed outpatients in medication treatment were followed for 1-3 years. Symptom status was regularly monitored, and systematic interviews were conducted to assess occurrence of stressful life events and chronic stressful conditions. The model predicted a causal path between depression severity and each of four factors: family history of psychopathologic disorders, age of onset, and episodic and chronic stressors. We hypothesized that the background factors would affect severity of depression through their impact on chronic and episodic stress; no specific predictions were made about the relative importance of paths between age of onset or family history of psychopathologic disorders and chronic or episodic stress.
Method Participants Participants included 38 patients with unipolar depression admitted to treatment in the University of California, Los Angeles, Affective Disorders Clinic with a diagnosis of major depressive episode, and a sample of 13 women with unipolar depression recruited from various agencies for a study of children of depressed mothers. Clinic patients participated at the point when they achieved remission (showing no more than one or two symptoms for at least 2 months) or "best clinical state," defined as a chronic baseline level of symptoms, unchanging for 6 months, that represents the patient's optimal emotional state. The sample of depressed mothers was recruited between 3 and 6 months after admission to treatment after remission of acute symptoms. The Clinic sample consisted of the first 38 unipolar depressed patients from the Clinic who had agreed to participate in the ongoing, longitudinal study of life stress and course of disorder and who had been in the study for at least 1 year (there had been an original pool of 45, but 7 dropped out before completing 1 year). Patients who met diagnostic criteria, who gave consent to be contacted, who actually remained in treatment in this Clinic, and who specifically consented to participate in the longitudinal study represented a minority of patients evaluated in the Clinic but appeared not to diner in any systematic fashion. Most of the subjects with unipolar depression were admitted to treatment between 1984 and 1987. The majority of eligible patients agreed to participate in this study when contacted. For instance, during this period, only 7 patients who met criteria and had given
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
PREDICTORS OF DEPRESSION consent to be contacted declined to participate. To give further details of representativeness, the records for all patients with unipolar depression admitted to the Clinic in a typical year, 1986, were inspected. Of the 40 unipolar patients who completed the evaluation, 23 gave consent to be contacted about research (either the others refused or the general consent form was not completed). Of the 23,13 did not continue treatment in the Clinic and were thus not eligible; many returned to treatment with referring psychiatrists in the community. The other 10 were contacted; 8 agreed to participate, and 2 declined. Of the 8 in our sample, 1 dropped out before the follow-up phase, and the other 7 completed the study. The initial pool of 23 who gave consent to be contacted and the 17 who refused or for whom information was not available indicated no significant differences in age, sex, marital status, race, or education. Overall, therefore, we believe that the participants in the study were representative of patients with unipolar depression who continued treatment in the Clinic. Overall, from the Affective Disorders Clinic there were 28 women and 10 men, with a mean age of 42.8 years (SD = 11.2). All participants were receiving medication treatment. The typical patient experienced recurrent episodes of major depression (M = 3.1 episodes, SD =1.5, and an additional 16 reported "too many to count" not included in the mean), and the majority fit the picture of "double depression" of recurrent major depression superimposed on chronic or intermittent dysthymic symptoms (Keller et al, 1983). Seven reported indeterminant childhood age of onset, and the remainder had an average age of onset of 25.7 (SD =13.1). The mean number of hospitalizations for depression was 1.0 (SD = 1.5). The sample of mothers with unipolar depression had a mean age of 37.4 years (SD=4.8). They experienced a mean of 8.0 major depressive episodes (SD = 4.7); 5 reported "too many to count." Their mean age of onset of diagnosable depression was 18.8 (SD = 8.3), and they experienced an average of 2.2 hospitalizations (SD = 2.3). All of the women in the sample of depressed mothers had at least one school-aged child, whereas only 36% of the Clinic sample had children. Most of the participants in both samples were currently single or divorced (88% of the Clinic sample and 69% of the mothers).
Procedures Overview. At admission to the Clinic, patients were evaluated by a psychiatrist and usually by a psychologist as well. Symptom status of patients was systematically evaluated by their psychiatrists during each medical visit, and these reports were routinely monitored by research staff. Patients entering the longitudinal study attended an initial, face-to-face interview and were then followed up by telephone interview every 3 months for a period of up to 2 years. Stressful life events were assessed initially and during the telephone follow-ups. The depressed mothers initially received their diagnoses at their agencies and then independently from the research project staff. They were followed up at 6-month intervals with systematic diagnostic and life stress evaluations for up to 3 years. Of the patients in both groups, only those who supplied data for at least 1 year were included. Symptom status. Symptom status was assessed for each patient during every visit to the Clinic. Frequency of visits was based on individual need, which differed among patients but ordinarily occurred at 2to 4-week intervals. At each visit, treating psychiatrists completed detailed symptom checklists and narrative reports of diagnostic status. The depressed mothers received systematic diagnostic evaluations by project staff that were based on the Schedule for Affective Disorders and Schizophrenia (SADS; Endicott & Spitzer, 1979) every 6 months. The symptom information for both samples was scored by research staff members on the following scale: 0 = no symptoms; 1 = mild (no more than two symptoms, or mild dysthymia); 2 = moderate (dysthymia, Research Diagnostic Criteria [RDC ] minor depression, or nearly
47
meets criteria for major depressive episode); 3 = marked (diagnosable major depressive episode); and 4 = severe (major depression requiring hospitalization or with suicide attempt). Interrater reliability of the scaling procedure for 220 clinician visit reports for 17 randomly selected Clinic patients was 100% within 1 scale point and 83% exact agreement. The symptom ratings and dates of occurrence of symptoms for all participants were plotted on a timeline without regard to the occurrence of life events; this procedure makes it possible to identify symptom changes, relapses, recurrences, and remission as well as to compute a total severity score by multiplying severity rating by duration (to be described). Identification of worst symptoms. The timelines of participants who had at least 1 year of follow-ups were inspected in order to determine the period of worst symptoms (if they were followed up for more than 1 year, the entire period was inspected). Among Clinic patients, the data included recurrence of major depression for 13 patients (onset of major depression after at least 8 weeks of mild or no symptoms), or relapse or exacerbation for 16 patients (ongoing symptoms that worsened to the point of major depressive episode [relapse] or did not quite meet diagnostic criteria for major depression [exacerbation]). Two patients remained symptom free, and levels of chronic symptoms remained unchanged in 7. Of the mothers, 4 experienced recurrence, 7 experienced relapse or exacerbation, 1 had no symptoms, and 1 had chronic, unchanging symptoms. We computed a total symptom score in the 3 months after the onset of the worst symptom period for each patient by multiplying each symptom rating by the number of days that the person remained at a particular emotional level, summed across a 3-month period. For patients who had no symptoms or chronic, unchanging symptoms, the middle 3-month period of the records was used. Stressful life events. Stressful life events were assessed as both episodic life events and chronic strain. Episodic life events were assessed through an interview modeled after the contextual threat procedures of Brown and Harris (1978). During the initial interview and each follow-up interview, participants were asked to describe in detail any event that had occurred since the previous interview or, in the case of the initial interview, during the previous 6 months. Paykel and Mangen's (1980) list of life events provided the guidelines for this assessment. Participants' descriptions of the event, the date of occurrence, the surrounding circumstances, experience with the event, coping resources, and consequences were prepared as a narrative report by the interviewer. Information regarding the participant's affective reaction to each event was specifically omitted. In accordance with Brown and Harris's (1978) procedures, each event was subsequently rated by a team of researchers (other than the interviewer) who were blind to the patient's psychiatric status as to the amount of "objective threat," ranging from 1 (no threat) to 5 (severe threat). In an initial reliability study based on two teams of raters of 50 events from 16 patients, Pearson r= .77 (p < .001). Events occurring within 6 months before the onset of worst symptom period were used for our analyses. Objective threat ratings were summed, which resulted in a total score for each participant's episodic life events. Chronic strains, defined as difficulties persisting for at least 6 months in different areas of participants' lives, were assessed at the initial research interview and every 6 months thereafter. Our concept of chronic strain stems from past assessments of chronic stressful conditions such as Brown and Harris's (1978) evaluation of ongoing difficulties and Pearlin, Menaghan, Lieberman, and Mullan's (1981) evaluation of life strains. Incorporating these two approaches, we organized interview probes around the following role content areas: marital/social, employment,finances,and relationships with family. Participants were asked to describe the state of each area over the preceding 6 months. Their descriptions were then scaled by the interviewer on a 5-point scale with behaviorally specific anchors: A rating of 1 was con-
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
48
HAMMEN, DAVILA, BROWN, ELLICOTT, GITLIN
sidered exceptionally positive circumstances, and a rating of 5 indicated extremely adverse circumstances. For each point on each content scale, the rating was behaviorally specific, and so the ratings were based on objective circumstances, not on subjective impressions. An example of the scale (reversed in scoring direction) was given by Hammen, Adrian, et al. (1987). Overall interrater agreement for 2-person teams making ratings for 34 patients was .97. For specific areas of functioning, reliabilities ranged from .93 to .99, and additional information about validation of the scales was reported by Hammen, Adrian, et al. (1987). For the analyses used in this study, the chronic strain interview occurring closest to but before the onset of the worst symptom period was used in all cases except for those in which the chronic strain interview occurred only days after the worst symptom period began. Family psychopathology. Reports of family psychiatric history were obtained through the use of the Family History-Research Diagnostic Criteria (FH-RDC; Endicott, Andreasen, & Spitzer, 1975) at the initial diagnostic evaluation for admission to the Clinic study or the family study. The FH-RDC has been shown to have good reliability (Andreason, Endicott, Spitzer, & Winokur, 1977). Interviewers indicated the presence of significant symptoms of psychopathologic disorder and whether the family member met criteria for a diagnosis. Included were definite (treated) and probable (met criteria but not treated) diagnoses of affective disorder, substance use disorder, antisocial personality disorder, and schizophrenia. The majority of diagnoses involved depression; for instance, for 63% of patients, one or both parents had had diagnosable depression. Using the FH-RDC data, we scaled history of family psychopathologic disorder in terms of its likelihood of causing family disruption. Thus severe symptoms in parents were viewed as more disruptive than were psychopathologic disorder in grandparents or siblings. Hence the following scale was used: 4 = father or mother with major diagnosis; 3 = father or mother with some symptoms; 2 = sibling with major diagnosis; 1 = grandparent with major diagnosis. The effects of psychopathologic disorder in various family members were considered to be additive. Thus, for example, a patient with a depressed mother and an alcoholic sibling would receive a rating of 6 (4 + 2). Interrater reliability for a sample of 34 patients was .91. Age of onset. Age of onset was assessed through patients' self-reports at the initial clinical evaluation. We considered age of onset to be the age at which a patient experienced his or her first diagnosable episode or condition: 1 = first diagnosable depression after the age of 45; 2 = first diagnosable depression between the ages of 26 and 45; 3 = first diagnosable depression between the ages of 19 and 25; 4 = first diagnosable depression between the ages of 13 and 18; 5 = first diagnosable depression between the ages of13. Interrater reliability for a sample of 34 patients was .97.
Results Bentler's (1985) structural equation program, EQS, was used to test the model. The EQS program is an extension of singleequation regression analysis and is similar to the linear structural relations program (LISREL) of Joreskog and Sorbom (1981). The EQS technique generates an estimated covariance matrix for testing the model, enabling a series of hypothesized regression equations to be solved simultaneously. The estimated covariance matrix that is generated is compared with the actual
sample covariance matrix, and the two are compared with a chi-square statistic. A nonsignificant chi-square indicating that the two matrices are similar provides evidence of the accuracy of the model, reflecting the theory's ability to account for what is actually observed. The correlation matrix of symptom, stress, and psychiatric history variables, as well as means and standard deviations, is shown in Table 1. Both chronic stress and episodic stress, but neither psychiatric history variable, were significantly associated with the symptom measure. There were a moderate association between family history and age of onset and a marginal one between chronic and episodic stress. Finally, family history appears to be related to episodic stress (likely attributable in part to the occurrence of family-related events) and age of onset to chronic stress. Not shown in Table 1 are the associations between number of previous depressive episodes and the family history variable (r = .36, p < .05, one-tailed) and between number of earlier episodes and age of onset (r = —.62, p < .001). Thus course of disorder as typically measured in terms of earlier episodes was associated with background variables, as measured here. The full hypothesized structural model is shown in Figure 1; the general model predicted that chronic and episodic stress would influence depression severity and each of these in turn would be influenced by family history of psychopathologic disorder and age of onset. Thus background is predictive of depression level through its effects on stress. Paths eventually deleted are represented by dashed lines. Because there was no theoretical expectation that either of the psychiatric history variables (age of onset and family history of psychiatric disorder) would be differentially associated with either of the stress variables (chronic and episodic stress), all relevant paths between these variables were initially included in the model. In fitting the model, the multivariate Lagrange Multiplier (LM) and the Wald tests were used to evaluate the statistical necessity of model parameters (Bentler, 1989). A significant LM result indicates that the addition of a given parameter would incrementally improve the fit of the model, whereas a significant Wald result indicates that a parameter can be deleted without a significant degradation of the fit. In addition to the standard goodness-of-fit chi-square statistic, three comparative fit indexes were examined: the normed fit index (NFI; Bentler & Bonett, 1980), the nonnormed fit index (NNFI; Bentler & Bonett, 1980), and the comparative fit index (CFI; Bentler, 1990). All three indexes indicate the degree to which a model improves on the null model of complete independence; small values indicate no improvement, and large values reflect a fit approaching that of the saturated model. The NFI and CFI values can range from 0 to 1.0, whereas values of the NNFI can fall outside this range. Although the three indexes can be interpreted in a similar manner, they have slightly different properties. The NFI has the interpretive advantage of ranging from 0 to 1.0; however, it is affected by sample size and may not reach 1.0 in small samples, even when the model is correct (Bentler, 1990). The NNFI performs better than the NFI near 1.0, but its 0-1.0 range is lost, and it has a higher sampling variability than the NFI. The CFI has a slight downward bias in small samples but a smaller sampling variability than the NNFI (Bentler, 1990).
49
PREDICTORS OF DEPRESSION Table 1 Intercorrelations for Symptom, Stress, and Psychiatric History Variables 1
Variable
1. 2. 3. 4. 5.
Symptoms Chronic stress Episodic stress Family history Age of onset
49*** .30** -.01 -.09
2
3
.19 .07 .28*
.36** .05
4
M
SD
— .26*
161.78 12.19 10.16 5.37 3.16
94.05 2.69 6.91 3.09 1.14
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
Note. N=5\. *p
Journal of Abnormal Psychology 1992, Vol. 101, No. 1,45-52
Psychiatric History and Stress: Predictors of Severity of Unipolar Depression Constance Hammen, Joanne Davila, Gary Brown, Aimee Ellicott, and Michael Gitlin
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
University of California, Los Angeles Unipolar depression is frequently a recurrent or chronic disorder. In studies on predicting its course, outcomes are typically linked to either psychiatric features or stressful life events. In order to integrate the 2 approaches, 51 unipolar patients were assessed periodically over at least 1 year for symptoms, stressful events, and chronic stressors. It was hypothesized that adverse family history and early age of onset impair role functioning and coping capabilities, thereby contributing to stressful circumstances that predict severity of depressive reactions. Results of causal modeling analyses supported a model in which background factors were associated with severity of depressive outcomes as mediated by their effects on stress variables. Such a model implicates the self-perpetuating nature of clinical depression, both for the individual and across generations.
(Bland, Newman, & Orn, 1986; Giles, Jarrett, Biggs, Guzick, & Ruch, 1989; Klein, Taylor, Dickstein, & Harding, 1988). Presence of concurrent dysthymic disorder with major depression has also been found to be predictive of increased likelihood of relapse or recurrence (e.g., Keller, 1988; Keller, Lavori, Endicott, Coryell, & Klerman, 1983). Similarly, Giles et al. (1989) reported that history of other affective reactions (such as intermittent depression or "labile personality") were associated with greater likelihood of recurrence in patients with major depression. In most of the work to date, investigators have studied relapse and recurrence as the variables to be predicted. Reports such as these give clues about correlates of the course of depressive disorder. However, they do not provide a conceptual basis for understanding why such historical factors predispose one to exacerbations and recurrences of unipolar depression. Even the specifically genetic-biological models do not rule out the potential effects of psychosocial influences, but few researchers have actually attempted to illuminate the processes that account for features of the course of disorder. According to an entirely different model, psychosocial factors influence the course of disorder; that is, stressors (or stressors interacting with a cognitive or psychological diathesis) affect the occurrence and the severity of depressive episodes. For instance, Paykel and Tanner (1976) found that patients who relapsed were more likely to report negative life events than were those who remained in remission. Lloyd, Zisook, Click, and Jaffe (1981) found that patients who had experienced negative life events responded more poorly to antidepressant treatment (although Monroe et al., 1983, failed to find such an association). In a nonpatient sample, Hammen et al. (1986) found that stressful events were predictive of relapse and recurrence of depression in persons with previous symptoms (but had less impact on subjects who had not suffered from depression). Billings and Moos (1985) assessed treated depressed clients for 1 year and found that posttreatment depression was associated with continuing high rates of stressful conditions. Several writers have called for further examination of the role that stress plays in relation to other predictors of relapse (e.g., Klein et al., 1988; Lewinsohn et al., 1989).
There are three empirical truths about unipolar depression that ought to guide efforts to understand and predict its course: (a) depression runs in families (Beardslee, Bemporad, Keller, & Klerman, 1983; Hammen, Gordon, etal., 1987; Rutter&Quinton, 1984; Weissman, et al., 1987); (b) the best predictor of future depression is previous depression (Belsher & Costello, 1988; Hammen, Mayol, deMayo, & Marks, 1986; Keller, 1988; Lewinsohn, Zeiss, & Duncan, 1989); and (c) for many clinically depressed persons, it is a recurrent if not chronic disorder (Keller, 1988; Sargeant, Bruce, Florio, & Weissman, 1990). The observed realities about unipolar depression imply not only a pernicious course but also a self-perpetuating one. Unfortunately, the major perspectives on the course of unipolar depression have generally proceeded along separate lines with little integrative effort. One approach is predominantly descriptive, in which previous history and features of the disorder are used to predict the subsequent course. One variant of this perspective is biological, and unipolar depression is viewed as a disease. Statistical loading for familial depression, early age of onset, and recurrence are regarded from this perspective as aspects of a possibly genetically transmitted disorder that develops according to largely endogenous processes. Recurrence and chronicity may be viewed as expected consequences of a disease process. Descriptive studies are rich in evidence of the role of background factors in the prediction of course. Loading for familial affective disorder is associated with onset of depression and is thought to predict a relatively pernicious course in comparison with the course in people who do not have a family history. Early age of onset has been suggested as a risk factor for a more negative course, including recurrence of episodes
The authors appreciate the assistance of interviewers Cheri Adrian, Dorli Burge, Ron Duran, Jean Kaufman, Aaron Oderberg, and the staff of the University of California, Los Angeles, Affective Disorders Clinic. Correspondence concerning this article should be addressed to Constance Hammen, Department of Psychology, University of California, 405 Hilgard Avenue, Los Angeles, California 90024. 45
This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
46
HAMMEN, DAVILA, BROWN, ELLICOTT, GITLIN
Unfortunately, the descriptive research on background factors such as family psychopathology and age of onset has not been integrated into most psychosocial models of depression course. In the psychiatric studies of family history or age of onset and course of illness, investigators do not typically evaluate psychosocial events and their role in predicting symptoms. Consequently, our goal was to begin an integration of these disparate streams of research in order to take into account the three truths about unipolar depression that were noted earlier, including the practical goal of improving prediction of course of disorder and the conceptual goal of improving our theories of why a psychiatric history is predictive of recurrence of depression. In this study, we tested a model for predicting symptom severity over a longitudinal course, in which family history of psychopathologic disorder and early age of onset of depression relate to symptoms through their influence on episodic and chronic stressful events. The goal was not to pit biological and nonbiological models against each other but rather to test hypotheses about how certain psychiatric variables may influence the severity of unipolar depression in patients who are at risk for relapse. A history of depression is likely to be a strong predictor of subsequent depression because it may be a marker of several maladaptive factors, which reflect exposure to stress and impairment of coping capabilities and of adaptive functioning, that predispose a person to depression. For instance, clinical depression impairs role functioning in ways that may contribute to chronic stressful, unhappy situations in terms of occupational adjustment, financial stability, and supportive marital and family relations (e.g., Barnett & Gotlib, 1988; Hammen, Gordon et al., 1987). If the onset of depressive symptoms occurs early in life, it is likely not only that the person has been exposed to adverse social conditions but also that the person has not acquired adequate coping mechanisms, and the symptoms may further impair the acquisition of adaptive skills. Thus early onset of depression may be associated with continuing elevated levels of chronic stress and episodic stressors, either because impaired functioning brings about the circumstances or because skills for coping with or adapting to the naturally occurring vicissitudes of life are inadequate. Moreover, we predicted that family history of psychopathologic disorder would be associated with early onset of depression. Whether the disorder is attributable to genetic or psychosocial causes or both, children of parents with psychiatric problems are themselves at elevated risk for disorder (Beardslee et al., 1983; Rutter & Quinton, 1984; Watt, Anthony, Wynne, & Rolf, 1984). There is ample evidence that depression runs in families, as noted earlier, and depression may indeed be a fairly frequent outcome of exposure to parental disability and adverse family circumstances (e.g., Hammen, Adrian, et al., 1987). Thus family history of depression or of any psychiatric disorder may likely be associated with early onset of depression, and disrupted family functioning may contribute to failure to acquire the kinds of adaptive capabilities that are necessary to avoid or resolve stressful circumstances. Although patients' family pedigrees are especially loaded statistically for parental affective disorder, we did not limit our analyses to only parental affective disorders; we also included family substance abuse disorder, and other major forms of psychopathology, because
we predicted that it is early disruption rather than a specific genetic mechanism that contributes to maladjustment and stressful conditions. Early disruption can be contributed by any family psychopathologic disorder, not just depression. For all of these reasons, we proposed that psychiatric history features that are markers of disrupted functioning (family psychopathology and personal early age of onset) would be associated with severity of recurrence and relapse of depression in patients, to the extent that they are predictive of elevated chronic and episodic stress levels that both precipitate depression and prolong its course. The outpatients in our sample were at risk for relapse, inasmuch as the majority of persons treated for major depressive episodes go on to have multiple episodes if not chronic symptoms (Keller, 1988; Sargeant et al., 1990). Over the longitudinal follow-up of up to 2 or 3 years in this study, nearly all patients did experience relapse or recurrences. Thus our goal was to predict the severity of the worst episode during the period of follow-up, on the basis of multiple background and stress variables. We used causal modeling analyses, testing hypothesized relations in a longitudinal design in which carefully diagnosed outpatients in medication treatment were followed for 1-3 years. Symptom status was regularly monitored, and systematic interviews were conducted to assess occurrence of stressful life events and chronic stressful conditions. The model predicted a causal path between depression severity and each of four factors: family history of psychopathologic disorders, age of onset, and episodic and chronic stressors. We hypothesized that the background factors would affect severity of depression through their impact on chronic and episodic stress; no specific predictions were made about the relative importance of paths between age of onset or family history of psychopathologic disorders and chronic or episodic stress.
Method Participants Participants included 38 patients with unipolar depression admitted to treatment in the University of California, Los Angeles, Affective Disorders Clinic with a diagnosis of major depressive episode, and a sample of 13 women with unipolar depression recruited from various agencies for a study of children of depressed mothers. Clinic patients participated at the point when they achieved remission (showing no more than one or two symptoms for at least 2 months) or "best clinical state," defined as a chronic baseline level of symptoms, unchanging for 6 months, that represents the patient's optimal emotional state. The sample of depressed mothers was recruited between 3 and 6 months after admission to treatment after remission of acute symptoms. The Clinic sample consisted of the first 38 unipolar depressed patients from the Clinic who had agreed to participate in the ongoing, longitudinal study of life stress and course of disorder and who had been in the study for at least 1 year (there had been an original pool of 45, but 7 dropped out before completing 1 year). Patients who met diagnostic criteria, who gave consent to be contacted, who actually remained in treatment in this Clinic, and who specifically consented to participate in the longitudinal study represented a minority of patients evaluated in the Clinic but appeared not to diner in any systematic fashion. Most of the subjects with unipolar depression were admitted to treatment between 1984 and 1987. The majority of eligible patients agreed to participate in this study when contacted. For instance, during this period, only 7 patients who met criteria and had given
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PREDICTORS OF DEPRESSION consent to be contacted declined to participate. To give further details of representativeness, the records for all patients with unipolar depression admitted to the Clinic in a typical year, 1986, were inspected. Of the 40 unipolar patients who completed the evaluation, 23 gave consent to be contacted about research (either the others refused or the general consent form was not completed). Of the 23,13 did not continue treatment in the Clinic and were thus not eligible; many returned to treatment with referring psychiatrists in the community. The other 10 were contacted; 8 agreed to participate, and 2 declined. Of the 8 in our sample, 1 dropped out before the follow-up phase, and the other 7 completed the study. The initial pool of 23 who gave consent to be contacted and the 17 who refused or for whom information was not available indicated no significant differences in age, sex, marital status, race, or education. Overall, therefore, we believe that the participants in the study were representative of patients with unipolar depression who continued treatment in the Clinic. Overall, from the Affective Disorders Clinic there were 28 women and 10 men, with a mean age of 42.8 years (SD = 11.2). All participants were receiving medication treatment. The typical patient experienced recurrent episodes of major depression (M = 3.1 episodes, SD =1.5, and an additional 16 reported "too many to count" not included in the mean), and the majority fit the picture of "double depression" of recurrent major depression superimposed on chronic or intermittent dysthymic symptoms (Keller et al, 1983). Seven reported indeterminant childhood age of onset, and the remainder had an average age of onset of 25.7 (SD =13.1). The mean number of hospitalizations for depression was 1.0 (SD = 1.5). The sample of mothers with unipolar depression had a mean age of 37.4 years (SD=4.8). They experienced a mean of 8.0 major depressive episodes (SD = 4.7); 5 reported "too many to count." Their mean age of onset of diagnosable depression was 18.8 (SD = 8.3), and they experienced an average of 2.2 hospitalizations (SD = 2.3). All of the women in the sample of depressed mothers had at least one school-aged child, whereas only 36% of the Clinic sample had children. Most of the participants in both samples were currently single or divorced (88% of the Clinic sample and 69% of the mothers).
Procedures Overview. At admission to the Clinic, patients were evaluated by a psychiatrist and usually by a psychologist as well. Symptom status of patients was systematically evaluated by their psychiatrists during each medical visit, and these reports were routinely monitored by research staff. Patients entering the longitudinal study attended an initial, face-to-face interview and were then followed up by telephone interview every 3 months for a period of up to 2 years. Stressful life events were assessed initially and during the telephone follow-ups. The depressed mothers initially received their diagnoses at their agencies and then independently from the research project staff. They were followed up at 6-month intervals with systematic diagnostic and life stress evaluations for up to 3 years. Of the patients in both groups, only those who supplied data for at least 1 year were included. Symptom status. Symptom status was assessed for each patient during every visit to the Clinic. Frequency of visits was based on individual need, which differed among patients but ordinarily occurred at 2to 4-week intervals. At each visit, treating psychiatrists completed detailed symptom checklists and narrative reports of diagnostic status. The depressed mothers received systematic diagnostic evaluations by project staff that were based on the Schedule for Affective Disorders and Schizophrenia (SADS; Endicott & Spitzer, 1979) every 6 months. The symptom information for both samples was scored by research staff members on the following scale: 0 = no symptoms; 1 = mild (no more than two symptoms, or mild dysthymia); 2 = moderate (dysthymia, Research Diagnostic Criteria [RDC ] minor depression, or nearly
47
meets criteria for major depressive episode); 3 = marked (diagnosable major depressive episode); and 4 = severe (major depression requiring hospitalization or with suicide attempt). Interrater reliability of the scaling procedure for 220 clinician visit reports for 17 randomly selected Clinic patients was 100% within 1 scale point and 83% exact agreement. The symptom ratings and dates of occurrence of symptoms for all participants were plotted on a timeline without regard to the occurrence of life events; this procedure makes it possible to identify symptom changes, relapses, recurrences, and remission as well as to compute a total severity score by multiplying severity rating by duration (to be described). Identification of worst symptoms. The timelines of participants who had at least 1 year of follow-ups were inspected in order to determine the period of worst symptoms (if they were followed up for more than 1 year, the entire period was inspected). Among Clinic patients, the data included recurrence of major depression for 13 patients (onset of major depression after at least 8 weeks of mild or no symptoms), or relapse or exacerbation for 16 patients (ongoing symptoms that worsened to the point of major depressive episode [relapse] or did not quite meet diagnostic criteria for major depression [exacerbation]). Two patients remained symptom free, and levels of chronic symptoms remained unchanged in 7. Of the mothers, 4 experienced recurrence, 7 experienced relapse or exacerbation, 1 had no symptoms, and 1 had chronic, unchanging symptoms. We computed a total symptom score in the 3 months after the onset of the worst symptom period for each patient by multiplying each symptom rating by the number of days that the person remained at a particular emotional level, summed across a 3-month period. For patients who had no symptoms or chronic, unchanging symptoms, the middle 3-month period of the records was used. Stressful life events. Stressful life events were assessed as both episodic life events and chronic strain. Episodic life events were assessed through an interview modeled after the contextual threat procedures of Brown and Harris (1978). During the initial interview and each follow-up interview, participants were asked to describe in detail any event that had occurred since the previous interview or, in the case of the initial interview, during the previous 6 months. Paykel and Mangen's (1980) list of life events provided the guidelines for this assessment. Participants' descriptions of the event, the date of occurrence, the surrounding circumstances, experience with the event, coping resources, and consequences were prepared as a narrative report by the interviewer. Information regarding the participant's affective reaction to each event was specifically omitted. In accordance with Brown and Harris's (1978) procedures, each event was subsequently rated by a team of researchers (other than the interviewer) who were blind to the patient's psychiatric status as to the amount of "objective threat," ranging from 1 (no threat) to 5 (severe threat). In an initial reliability study based on two teams of raters of 50 events from 16 patients, Pearson r= .77 (p < .001). Events occurring within 6 months before the onset of worst symptom period were used for our analyses. Objective threat ratings were summed, which resulted in a total score for each participant's episodic life events. Chronic strains, defined as difficulties persisting for at least 6 months in different areas of participants' lives, were assessed at the initial research interview and every 6 months thereafter. Our concept of chronic strain stems from past assessments of chronic stressful conditions such as Brown and Harris's (1978) evaluation of ongoing difficulties and Pearlin, Menaghan, Lieberman, and Mullan's (1981) evaluation of life strains. Incorporating these two approaches, we organized interview probes around the following role content areas: marital/social, employment,finances,and relationships with family. Participants were asked to describe the state of each area over the preceding 6 months. Their descriptions were then scaled by the interviewer on a 5-point scale with behaviorally specific anchors: A rating of 1 was con-
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HAMMEN, DAVILA, BROWN, ELLICOTT, GITLIN
sidered exceptionally positive circumstances, and a rating of 5 indicated extremely adverse circumstances. For each point on each content scale, the rating was behaviorally specific, and so the ratings were based on objective circumstances, not on subjective impressions. An example of the scale (reversed in scoring direction) was given by Hammen, Adrian, et al. (1987). Overall interrater agreement for 2-person teams making ratings for 34 patients was .97. For specific areas of functioning, reliabilities ranged from .93 to .99, and additional information about validation of the scales was reported by Hammen, Adrian, et al. (1987). For the analyses used in this study, the chronic strain interview occurring closest to but before the onset of the worst symptom period was used in all cases except for those in which the chronic strain interview occurred only days after the worst symptom period began. Family psychopathology. Reports of family psychiatric history were obtained through the use of the Family History-Research Diagnostic Criteria (FH-RDC; Endicott, Andreasen, & Spitzer, 1975) at the initial diagnostic evaluation for admission to the Clinic study or the family study. The FH-RDC has been shown to have good reliability (Andreason, Endicott, Spitzer, & Winokur, 1977). Interviewers indicated the presence of significant symptoms of psychopathologic disorder and whether the family member met criteria for a diagnosis. Included were definite (treated) and probable (met criteria but not treated) diagnoses of affective disorder, substance use disorder, antisocial personality disorder, and schizophrenia. The majority of diagnoses involved depression; for instance, for 63% of patients, one or both parents had had diagnosable depression. Using the FH-RDC data, we scaled history of family psychopathologic disorder in terms of its likelihood of causing family disruption. Thus severe symptoms in parents were viewed as more disruptive than were psychopathologic disorder in grandparents or siblings. Hence the following scale was used: 4 = father or mother with major diagnosis; 3 = father or mother with some symptoms; 2 = sibling with major diagnosis; 1 = grandparent with major diagnosis. The effects of psychopathologic disorder in various family members were considered to be additive. Thus, for example, a patient with a depressed mother and an alcoholic sibling would receive a rating of 6 (4 + 2). Interrater reliability for a sample of 34 patients was .91. Age of onset. Age of onset was assessed through patients' self-reports at the initial clinical evaluation. We considered age of onset to be the age at which a patient experienced his or her first diagnosable episode or condition: 1 = first diagnosable depression after the age of 45; 2 = first diagnosable depression between the ages of 26 and 45; 3 = first diagnosable depression between the ages of 19 and 25; 4 = first diagnosable depression between the ages of 13 and 18; 5 = first diagnosable depression between the ages of13. Interrater reliability for a sample of 34 patients was .97.
Results Bentler's (1985) structural equation program, EQS, was used to test the model. The EQS program is an extension of singleequation regression analysis and is similar to the linear structural relations program (LISREL) of Joreskog and Sorbom (1981). The EQS technique generates an estimated covariance matrix for testing the model, enabling a series of hypothesized regression equations to be solved simultaneously. The estimated covariance matrix that is generated is compared with the actual
sample covariance matrix, and the two are compared with a chi-square statistic. A nonsignificant chi-square indicating that the two matrices are similar provides evidence of the accuracy of the model, reflecting the theory's ability to account for what is actually observed. The correlation matrix of symptom, stress, and psychiatric history variables, as well as means and standard deviations, is shown in Table 1. Both chronic stress and episodic stress, but neither psychiatric history variable, were significantly associated with the symptom measure. There were a moderate association between family history and age of onset and a marginal one between chronic and episodic stress. Finally, family history appears to be related to episodic stress (likely attributable in part to the occurrence of family-related events) and age of onset to chronic stress. Not shown in Table 1 are the associations between number of previous depressive episodes and the family history variable (r = .36, p < .05, one-tailed) and between number of earlier episodes and age of onset (r = —.62, p < .001). Thus course of disorder as typically measured in terms of earlier episodes was associated with background variables, as measured here. The full hypothesized structural model is shown in Figure 1; the general model predicted that chronic and episodic stress would influence depression severity and each of these in turn would be influenced by family history of psychopathologic disorder and age of onset. Thus background is predictive of depression level through its effects on stress. Paths eventually deleted are represented by dashed lines. Because there was no theoretical expectation that either of the psychiatric history variables (age of onset and family history of psychiatric disorder) would be differentially associated with either of the stress variables (chronic and episodic stress), all relevant paths between these variables were initially included in the model. In fitting the model, the multivariate Lagrange Multiplier (LM) and the Wald tests were used to evaluate the statistical necessity of model parameters (Bentler, 1989). A significant LM result indicates that the addition of a given parameter would incrementally improve the fit of the model, whereas a significant Wald result indicates that a parameter can be deleted without a significant degradation of the fit. In addition to the standard goodness-of-fit chi-square statistic, three comparative fit indexes were examined: the normed fit index (NFI; Bentler & Bonett, 1980), the nonnormed fit index (NNFI; Bentler & Bonett, 1980), and the comparative fit index (CFI; Bentler, 1990). All three indexes indicate the degree to which a model improves on the null model of complete independence; small values indicate no improvement, and large values reflect a fit approaching that of the saturated model. The NFI and CFI values can range from 0 to 1.0, whereas values of the NNFI can fall outside this range. Although the three indexes can be interpreted in a similar manner, they have slightly different properties. The NFI has the interpretive advantage of ranging from 0 to 1.0; however, it is affected by sample size and may not reach 1.0 in small samples, even when the model is correct (Bentler, 1990). The NNFI performs better than the NFI near 1.0, but its 0-1.0 range is lost, and it has a higher sampling variability than the NFI. The CFI has a slight downward bias in small samples but a smaller sampling variability than the NNFI (Bentler, 1990).
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PREDICTORS OF DEPRESSION Table 1 Intercorrelations for Symptom, Stress, and Psychiatric History Variables 1
Variable
1. 2. 3. 4. 5.
Symptoms Chronic stress Episodic stress Family history Age of onset
49*** .30** -.01 -.09
2
3
.19 .07 .28*
.36** .05
4
M
SD
— .26*
161.78 12.19 10.16 5.37 3.16
94.05 2.69 6.91 3.09 1.14
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Note. N=5\. *p
