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Prevention of Depression and Bipolar Disorder 

Prevention of Depression and Bipolar Disorder
Prevention of Depression and Bipolar Disorder
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date: 08 December 2021

The prevention of an individual's first episode of depression is worthy of greater study among investigators concerned with mood disorders. Not only is the first episode devastating for individuals and those around them but it is a major burden within our health system and society (Murray & Lopez, 1997). Once the first episode of major depressive disorder (MDD) occurs, the sequelae are substantial. Following an episode of MDD, the probability of subsequent episodes is significantly increased, even to the point that many now consider MDD to be a chronic disease. As noted in Chapter 1, the sequelae to MDD are numerous and include poorer social relationships, increased substance abuse, increased use of medical services, interference with long-term cognitive functioning, significant comorbidity with major health problems, and younger ages of death (even when deaths by suicide are taken into account). Most investigators of mood disorders believe that the first episode lays down neural pathways that are difficult to overcome and, without modification via medications or psychosocial interventions or their combination, are likely to be lasting pathways that impact individuals' lives.

Even though prevention of MDD is an important topic, empirical work in this area is difficult and has been slow to progress. Some recent work has been conducted on the prevention of second and subsequent episodes (Craighead, Hart, Craighead, & Ilardi, 2002), but the work designed to prevent the first episode of MDD has been meager. Before addressing the empirical work on prevention of MDD, it is important to note again the conceptual and historical context in which general prevention research has been defined.


A Brief History of Prevention in Mental Health

During the last decade, three reports have established a historical context and defined the mental health prevention classification system:

  • 1. Reducing Risk for Mental Disorders: Frontiers for Prevention Intervention Research, Institute of Medicine (1994)

  • 2. Priorities for Prevention Research at NIMH: A Report by the National Advisory Mental Health Council Workgroup on Mental Disorders Prevention Research, National Institutes of Health, National Institute of Mental Health (1998)

  • 3. Mental Health: A Report of the Surgeon General, U.S. Department of Health and Human Services (US-DHHS), Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health (1999)

In 1998, the National Institute of Mental Health (NIMH) established an ad hoc committee to review the progress of mental health prevention research. The committee's report, Priorities For Prevention Research at NIMH: A Report by the National Advisory Mental Health Council Workgroup on Mental Disorders Prevention Research, traced the history of prevention in mental health and proposed the following generational taxonomy:

The first generation of efforts to prevent mental disorder began in the 1930s when, as an outgrowth of the turn-of-the-century mental hygiene movement, the focus gradually expanded beyond ameliorating the plight of those in asylums to include the prevention of many forms of social and emotional maladjustment. The new goal was to assure the well-being and “positive mental health” of the general population through primary-prevention interventions aimed at creating health-promoting environments for all. These efforts were based on humanitarian concern, but had few, if any, research underpinnings.

The second generation of interventions to prevent mental disorder, which began in the late 1960s, reflected the impact of a growing health and mental health research knowledge base. Some scientists retained their broad-based emphasis on primary prevention, while others began to target specific “at-risk” groups for study and intervention. During the 1960s there had been a burgeoning of research on the causes, mechanisms, and effects of stress on bodily and mental functioning. “At-risk” persons were defined as those who would predictably experience periods of substantial life stress, such as domestic violence, divorce, bereavement, or unemployment as precursors of mental distress or disorder. Changing behavior for health also became an active area of study and prevention during the same period. Those studies placed a strong emphasis on preventing lung cancer and heart disease through programs to prevent or reduce smoking, obesity, high cholesterol intake, and sedentary life styles.

NIMH, 1998

This NIMH committee observed that over the next decade mental health prevention interventions continued to proliferate. After reviewing progress in this field, however, the 1978 President's Commission on Mental Health determined that previous investigation had been “unfocused and uncoordinated.” As a remedy the commission recommended the establishment of a Center for Prevention at NIMH to coordinate and enhance research in mental health primary prevention research. The NIMH report determined that “during the last 20 years The NIMH Center for Prevention Research and its programmatic successors have stimulated considerable progress in building the scientific foundation of an interdisciplinary field of prevention research in areas of epidemiology, human develop-ment, and intervention research methodology” (NIMH, 1998). The committee concluded that sufficient progress had been made in establishing the scientific basis for mental health prevention science to declare that we were then in a third generation of prevention activity. Thus, prevention research could build on prior accomplishments of prior preventive interventions and integrate these with advances in the biomedical, behavioral, and cognitive sciences.

Despite the described significance and need for prevention research and this sanguine view of the 1998 NIMH committee, the amount of work studying the prevention of an initial episode of depression has remained meager. In contrast, considerable progress has been made in the development of a nomenclature for prevention research. In order for the field to progress, it was necessary to develop a clear terminology for investigators to follow.

Early Classification Systems

The Commission on Chronic Illness (1957) developed the original public health classification system of disease prevention. Three types of preventive interventions were identified: primary, secondary, and tertiary. During the last 40 years the definitions of these types of prevention have expanded to include an array of nuanced but related meanings.

Gordon's Definitions

In 1983 and in 1987, Robert Gordon proposed an alternative classification of prevention that was based on the empirical relationships found in practically oriented disease prevention and health promotion programs. These included programs which he labeled universal, selective, and indicated prevention.

Although Gordon's classification system was to be distinct from that of the Commission on Chronic Health, the use of these two classification systems slowly deteriorated into a confusing, merging and mixing of definitions, e.g., “universal primary prevention.” This confusion was particularly problematic when this terminology was applied to the classification of the prevention of psychiatric disorders, because the classical public health prevention classification system and Gordon's reclassification were both designed for use in the description of the prevention of biological disorders, not of interventions to prevent psychiatric and psychological disorders. The 1994 Institute of Medicine (IOM) report, Reducing Risk for Mental Disorders: Frontiers for Prevention Intervention Research, presented a cogent discussion of the inherent pitfalls in applying general prevention classifications to problems in mental health:

One of the main problems has been the notion of “caseness” that is used in public health. It is often more difficult to document that a “case” of mental disorder exists than it is to document a physical health problem. Agreement regarding the occurrence of a case of mental disorder varies with time and with the instruments and diagnostic systems employed and with the theoretical perspective of the evaluators. Also symptoms and dysfunctions may exist even though criteria for a DSM-III-R diagnosis are not present. Finally, the outcomes in very young children (birth to age 5) are often not diagnosable as “psychiatric caseness” but rather as impairments in cognition and psychosocial development.

IOM, 1994

Recent Attempts to Define Prevention

The IOM report chose to resolve the confusion in terminology by using the term prevention to refer only to interventions that occur before the initial onset of a disorder. In this system, prevention included all three elements of Gordon's system (1983, 1987). Efforts to identify cases and provide care for known disorders were called treatment, and efforts to provide rehabilitation and reduce relapse and reoccurrence of a disorder were called maintenance/interventions. Further distinctions were made within the prevention category. We have employed these definitions throughout this chapter. The definitions are described in the following paragraphs.

Universal mental health prevention interven-tions are defined as efforts that are beneficial to a whole population or group. They are targeted to the general public or a whole population group that has not been designated or identified as being at risk for the disorder being prevented. The goal at this level of prevention is the reduction of the occurrence of new cases of the disorder.

Selective mental health prevention interven-tions are defined as those efforts that target individuals or a subgroup of the population whose risk for developing the mental health disorder is significantly higher than average. The risk may be immediate or lifelong. Biological, psychological, or social risk factors associated with or related to the specific mental health disorder are used to identify the individual or group level of risk. Those with the identified risk factors are referred to as those “at risk.”

Indicated prevention interventions are defined as those efforts that target high-risk individuals who are identified as having minimal but detectable signs or symptoms that predict the mental disorder or biological markers indicating predisposition to the disorder. For example, individuals who have some symptoms of MDD but do not yet meet criteria for the disorder would fall into this group. Indicated prevention excludes individuals whose signs and symptoms meet diagnostic criteria for the disorder.

The IOM identified three aims or desired outcomes for mental health prevention: (1) reduction in the number of new cases of the disorder; (2) delay in the onset of illness; and (3) reduction in the length of time the early symptoms continue as well as halting the progression of severity so that individuals ultimately do not meet diagnostic criteria. The 1999 Mental Health: A Report of the Surgeon General agreed with the IOM and defined prevention as the “prevention of the initial onset of a mental disorder or emotional or behavioral problem, including prevention of comorbidity” (US-DHHS, 1999). In addition, the report defined other terms that were often imprecisely used in discussions of prevention. They are listed below:

  • First (initial) onset: the initial point in time when an individual's mental health problems meet the full criteria for a diagnosis of a mental disorder

  • Risk factors: “characteristics, variables, or hazards that, if present for a given individual, make it more likely that this individual, compared to someone selected at random from the general population, will develop a disorder” (US-DHHS, 1999). Although risk factors precede the first onset of a disorder, they may change in response to the disorder, development, or stressors.

  • Protective factors: Factors that “improve a person's response to some environmental hazard resulting in an `adaptive outcome.' These factors can be found within the individual or within the family or community. They do not necessarily cause normal development in the absence of risk factors, but they may make an appreciable difference in the influence exerted by risk factors” (US-DHHS, 1999).

  • Risk of onset vs. risk of relapse: The terminologies that refer to the risk of the development of a disorder are often used without specification of the risk of onset vs. the risk of relapse. This is a key distinction because “the risks for onset of a disorder are likely to be somewhat different from the risks involved in relapse of a previously diagnosed condition” (US-DHHS, 1999). Undoubtedly, this same distinction is true for factors that protect against onset or relapse. As will be noted later, not all “prevention” projects have made this distinction between initial and second or subsequent episodes of MDD.

Goals of Prevention Programs

In addition to the IOM's goals of reducing the number of new cases and delaying the onset of MDD and the insidious nature of the onset and course of MDD, there are other ancillary and associated goals of prevention programs. For example, prevention of initial MDD is likely to have an impact on school and work performance, social skills, and quality of life, reduce the need of medical services, and reduce MDD-related substance abuse disorders. In the long run, prevention programs may actually extend the lives of individuals who were at risk but did not develop the disorder, by reducing both the risk of suicide completion and the behavioral and biological sequalae of the disorder.

Another goal of prevention programs is to teach resiliency to the program participants. Individuals at risk for MDD are likely to experience negative and traumatic events, as are other individuals in our society. Prevention programs have a goal of teaching at-risk individuals to become more resilient—to develop skills and abilities to spring back from or adapt to adversity.

A further goal of prevention programs is to enhance and enrich the positive aspects of living. By changing cognitive patterns, enhancing social skills, and increasing resiliency, individuals who otherwise might live a marginally happy life may have the opportunity to develop greater self-esteem and self-efficacy and live a more successful and adaptive life. This positive adaption in life may lead to the development of more adaptive neurological pathways. Emotional intelligence (Goleman, 1995) may also be enhanced by successful preventive programs.

The societal goals of depression prevention programs are also numerous. For example, even a modest reduction in new cases of MDD would reduce the economic burden of the disorder. The disorder itself would not have to be treated so frequently, nor would the associated (sometimes self-treatment) problems of alcohol, tobacco, and other forms of substance abuse. Each prevented case of MDD would increase the limited resources available to other health initiatives. Productivity would be increased in the workplace. Thus, the call for effective programs to prevent the first episode of MDD is a forceful and significant one—significant for individuals, families, and society as a whole.


To develop programs for individuals “at risk” for MDD, it is necessary to develop knowledge and understanding of factors and their interactions that render one likely to develop MDD. Chapter 1 provided evidence for many of the risk factors for MDD, so the details will not be reiterated here. These risk factors include dysfunctional parenting and family interactions; gender; personality and temperament; cognitive vulnerabilities; internal and external stress, including negative life events; and poor interpersonal relationships.

In addition to the preceding risk factors, the following risk factors that have implications for prevention of MDD are important and worthy of further detailed review. These include subsyndromal depression, poverty, violence, and cultural factors.

Subsyndromal Depression

Among adults, subsyndromal depression (two or more symptoms for 2 weeks or longer) appears to cause as much health impairment and economic burden as MDD, and these individuals are at increased risk for developing subsequent MDD (Fava, 1999; Johnson, Weissman, & Klerman, 1992; Judd, Akiskal, & Paulus, 1997). In a longitudinal study, subsyndromal depression among adolescents predicted poorer functioning as these individuals became adults (Devine, Kempton, & Forehand, 1994). Subsyndromal depressive symptoms among adolescents predicted MDD later on in adolescence and young adulthood (Pine, Cohen, & Brook, 1999; Rao et al., 1995; Weissman, Warner, Wickramaratne, Moreau, & Olfson, 1997). Lewinsohn, Solomon, Seeley, and Zeiss (2000) found that increasing levels of depressive symptoms among a large sample of nondepressed adolescents (average age of 161 2 ) predicted increased levels of social dysfunction and incidence of MDD, as well as increased substance abuse at age 24. These data indicate that subsyndromal depression renders adolescents at risk for a first episode of MDD, and they are prime candidates for depression prevention programs.


Poverty has been linked with an early onset of depression. It is not clear whether this represents an independent risk factor or can be grouped among the more general examples of diversity that are associated with depression. Results from epidemiological studies have linked lower socioeconomic status with depression and a multitude of other mental health problems (Robins, Locke, & Reiger, 1991). This vulnerability is particularly strong for families living at poverty levels (Bruce, Takeuchi, & Leaf, 1991). This relationship may be explained in part by a phenomenon of selection, whereby those with mental health problems are more inclined to drift toward economic disadvantage and remain there (Dohrenwend et al., 1992). Longitudinal data have also demonstrated that socioeconomic disadvantage is largely a cause of higher vulnerability to psychiatric disorder, particularly for depression (Dohrenwend et al., 1992; Gilman, Kawachi, Fitzmaurice, & Buka, 2002; Johnson, Cohen, Dohrenwend, Link, & Brook, 1999). In a study of over 4,000 Australian families, poverty caused a small but significant increase in risk when other sociological variables were controlled (Spence, Najman, Bar, O'Callaghan, & Williams, 2002); this effect was more pronounced in girls than in boys.

If we consider poverty as a generator for a variety of stressors, the possible mechanisms driving poverty-induced vulnerability appear boundless. A number of mediators between socioeconomic disadvantage and depression have been studied empirically. These include external mediators such as access to health care, quality of social networks and resources, quality of parenting and parent availability, and, of course, level of exposure to violence. Children of families who are of lower socioeconomic status are most likely to witness violence and to be the victims of abuse (Buka, Stichik, Birdthistle, & Earls, 2001; Sedlak & Broadhurst, 1996).

Internal individual mediators include self-esteem, health-risk behaviors, cognitive deficits, interpersonal skills, and academic achievement. Several comprehensive reviews on the consequences of poverty and mediating factors demonstrate the vast amount of knowledge we have accumulated on the relation between poverty and depression (Aber, Bennett, Conley, & Li, 1997; Leventhal & Brooks-Gunn, 2000; Turner & Lloyd, 1999). This literature highlights the importance of two larger factors: (a) the need for universal health care with parity for mental illness and physical illness and parity for services for adults and children; and (b) the need to address large-scale public health risk factors that have a strong effect on the occurrence of adolescent depression (i.e., exposure to violence).


Exposure to violence during childhood is a potent risk factor for future psychological and psychiatric disorders (Kilpatrick et al., 2003; MacMillan et al., 2001) as well as physical health-risk behaviors (Felitti et al., 1998), in both the short and long term. The violence to which children are exposed has many forms. This includes being a victim of sexual or physical abuse as well as witnessing violence in the home (Kilpatrick et al., 2003). A large number of children also frequently witness violence in the community (Buka et al., 2001). Children who are exposed to violence are most often exposed to more than one type, and evidence suggests that the amount of violence-related adversities a child encounters has a substantial impact on the severity of the outcome (Felitti et al., 1998). The most disturbing illustration of this accumulation phenomenon is the gradation effect of violence-related adversities on risk for suicide attempt. Results from the Adverse Childhood Experiences Study demonstrated that for every additional adversity experienced as a child, the risk of suicide attempts increased from 2-to 5-fold, such that children or adolescents who encounter seven or more adversities are 50 times as likely to attempt suicide as those without violence exposure (Dube et al., 2001).

Although the mental health consequences of violence exposure are diverse, the most prevalent and commonly studied are posttraumatic stress disorder (PTSD) and major depression. This makes sense, particularly if violence exposure is viewed as a form of trauma. The consequences of our country's recent dealings with terrorism have provided an especially graphic picture of how violence-related trauma is linked to PTSD and depression (North et al., 1999; Schlenger et al., 2002). Survivors of the Okla-homa City bombing, for instance, were studied by North and collegues (1999) about 6 months after the disaster. Of these individuals, 45% had some form of post-disaster psychiatric disorder (34.3% had PTSD, and 22.5% had MDD). Psychiatric comorbidity predicted functional impairment and treatment. Fifty-six percent of depressed subjects had never been depressed before the incident.

Violence-related trauma experienced during childhood can have particularly devastating effects, because the trauma is inflicted during a critical period of development. Neurobiological and neuroendocrine studies of depressed women, which look at the volume of certain brain regions and at hormonal stress-response mechanisms, provide evidence that violence-related trauma experienced during childhood can have profound and lasting effects on brain structure and function (Heim, Newport, Bonsall, Miller, & Nemeroff, 2001; Vythilingam et al., 2002). These alterations, in turn, increase vulnerability to stress-related disorders like depression.

Depression that is comorbid with PTSD or other disorders, as well as depression that has an established neurobiological etiology like that experienced by childhood victims of trauma, are forms of the disorder that are particularly resistant to treatment and are associated with increased levels of impairment (Mervaala et al., 2000; Petersen et al., 2001). Thus, it is essential that prevention strategies attend to violence exposure.

Cultural Factors

The role of ethnocultural factors has been understudied. Some ethnic groups appear to have higher rates of adolescent depression than others. For example, Mexican Americans and African-American adolescents appear to have higher risk for depression whereas American adolescents of Chinese descent may be at lesser risk (Barrera & Craighead, 2004; Roberts, Roberts, & Chen, 1997). It appears that some groups (such as African-American or Hispanic adolescents) may not show the gender disparity following puberty that is seen among Caucasian adolescents (Hayward, Gotlib, & Schraedley, 1999).


During the past decade, a number of promising strategies for the prevention of childhood depression have emerged. The overarching principles of these programs are similar, and the specifics of preventive interventions for children and adolescents have taken into account the development level of the participants. The evaluated preventive strategies are based primarily on cognitive behavioral and family-educational approaches that seek to reduce risk factors and enhance protective and resiliency factors associated with depression in youth.

In general, progress in the field of prevention science has been made through the introduction of rigorous standards for the development and evaluation of manualized preventive strategies that are based on well-established theoretical frameworks and proceed through a series of orderly stages. This is best described in the 1994 IOM's Report on the Prevention of Mental Disorder. The IOM suggested that prevention development and evaluation proceed through five stages. The first and second stages are identifying risk factors and describing the relative contributions of different factors to the disorder. The third stage is applying strategies developed in pilot studies and completing efficacy trials to evaluate the overall effectiveness of these approaches. The fourth stage, carrying out effectiveness trials, involves the examination of such strategies in multiple sites in large-scale investigations under nonideal, real-world conditions. The final stage consists of implementing such strategies in large-scale public health campaigns. Following this sequence and the articulation of a set of rigorous empirical standards by which to test preventive intervention approaches, a number of important strategies for prevention of depression have emerged. These have begun to be tested in randomized trial designs according to the recommended guidelines.

Consideration of the prevention of depression also must take place in the context of the remarkable progress in developmental neuroscience, the sequencing of a human genome, and in psychiatric epidemiology. As these important scientific advances unfold, they will offer important opportunities for future prevention programs. These findings will need to be integrated with adolescents' developmental, social, cultural, and family contexts in the development of preventive interventions.

To date, there have been two major conceptual frameworks that have guided most of the development of the prevention studies. First, cognitive behavioral programs have been used and show considerable promise—e.g., those of Seligman and Clarke in the United States, programs of Shochet and Spence in Australia, and the program of Arnarson and Craighead in Iceland. In addition, Beardslee and colleagues have developed and evaluated a program designed to prevent depression in the family context. All of these programs have in common a strong theoretical orientation—an orientation toward building of strengths and resiliency; they have all been written into manuals for dissemination; and they have been or are being tested with randomized trials designs.

Penn Prevention Program

In the Penn Prevention Program, Seligman and colleagues (Gillham & Reivich, 1999; Gillham, Reivich, Jaycox, & Seligman, 1995; Jaycox, Reivich, Gillham, & Seligman, 1994) developed and evaluated a school-based “indicated” prevention program targeting 10-to 13-year-old children in school districts in the Philadelphia suburbs. The youth were defined as at risk for depression on the basis of elevated self-reported depressive symptomatology, self-reported parental conflict, or both. This prevention program was based on a model of explanatory style introduced by Seligman and colleagues (Nolen-Hoeksema, Girgus, & Seligman, 1992) and on research identifying core cognitive deficits associated with youth depression, including negative self-evaluation, dysfunctional attitudes, poor interpersonal problem solving, and low expectations for self-performance (Garber, Weis, & Shanley, 1993; Kaslow, Rehm, & Siegel, 1984; Quiggle, Garber, Panak, & Dodge, 1992). Participants recruited for the treatment group were assigned to one of three treatment programs: a cognitive training program, a social problem-solving program, or a combined program. Eighty-eight students, whose scores were matched to prevention participants, were recruited from nearby schools and comprised the no-participation control group. Assessments included child self-report, teacher-report, and parent-report questionnaires.

Results indicated that relative to control participants, children who participated in any of the treatment groups reported significantly fewer depressive symptoms immediately following the program and at the 6-month and 2-year follow-ups, but not at the 12-month and 3-year follow-ups. Moreover, teacher reports at follow-up revealed better classroom behavior in treatment participants than in control participants. Finally, overall treatment effects were more significant for children who, at the screening phase of the study, reported more significant depressive symptomatology and more significant parental conflict at home. The major limitations of the study are the lack of randomization to intervention conditions, the use of only self-report measures, attrition of approximately 30% of partici pants during follow-up, and the failure to include diagnoses for clinical depression.

More recently, Seligman and his group at Penn have focused on “positive psychology” programs, which are likely to have an indirect effect of preventing episodes of MDD. These programs are included in Part VII of this book.

Clarke and Colleagues

Clarke and colleagues (Clarke et al., 1995) in Oregon were among the first to study prevention of MDD among adolescents. In an excellent study, 150 adolescent students from 9th and 10th grades were assigned randomly to either a “prevention” or “usual-care” group. The prevention program, entitled “Adolescent Coping with Stress Course” was delivered in groups and was a prevention-focused version of this group's “Adolescent Coping with Depression Course” (Clarke, Lewinsohn, & Hops, 1990). The 5-week intervention was conducted within the adolescents' school setting and comprised fifteen 45-minute group sessions (3 after-school meetings per week). The usual-care youngsters were free to continue with preexisting treatment or seek new treatment. This program employed both behavioral and cognitive coping techniques designed to reduce vulnerability to future depressive episodes.

Participants were followed for 1 year, and the results were positive. Namely, significantly (p < .05) fewer prevention group (14.5%; 8 of 55) subjects were diagnosed with MDD or dysthymia than control group subjects (25.7%; 18 of 70). The major strengths of this program include random assignment of subjects, adequate sample sizes, diagnoses of clinical mood disorders, and encouraging outcomes. It is important to note, however, that approximately 36% of their participants had suffered a prior episode of MDD. Because 30% to 50% of adolescents who have had a prior episode can be expected to have a relapse or recurrence of the disorder during the time (18 months) of this study (Hart, Craighead, & Craighead, 2001; Lewinsohn, Rohde, Seeley, & Fischer, 1993; Rao et al., 1995), it very well may be that Clarke and colleagues actually had their biggest impact on preventing relapse or recurrence rather than on preventing a first episode of MDD. In addition, it should be noted that there was differential dropout between conditions in this study (Clarke et al., 1995), but as the authors suggested, this probably operated against their favorable outcomes.

In an expansion of this program, Clarke and associates (2001) applied this approach to a health maintenance organization (HMO) population of adolescents of parents with diagnosed depression and youngsters already manifesting symptoms. They screened all those at risk and divided them into three groups: low or no depressive symptomatology, medium symptomatology, and those already in episode. Those already meeting criteria for MDD were referred for treatment, and those with no depressive symptomatology were excluded. In this trial, those adolescents (ages 13–18) with moderate symptomatology were randomized into a usual-care condition (N = 49) or their cognitive behavioral intervention group (N = 45). As in their previous study, prevention group subjects participated in 15 group sessions.

This intervention yielded substantial preventive effects, with significant treatment-by-time effects in the expected direction on the Center for Epidemiological Studies–Depression (CES-D) and the Global Assessment of Functioning scales—i.e., adolescents in the prevention condition did much better than those in the usual-care condition. Survival analysis indicated that over a 15-month follow-up period, there was a cumulative rate of major depression of only 9% in the experimental group in contrast to 28% in the usual-care condition (Clarke et al., 2001). Even though this is the most sophisticated prevention study to date, its specific implications for prevention are limited by the choice to include adolescents who had previously suffered from an episode of depression; these subjects comprised 67% of the adolescents in this study. Thus, as with the prior study, it is impossible to determine if the study prevented first episodes or relapse and recurrence of prior episodes of MDD. Currently, Clarke, Garber, Beardslee, and Brent are conducting a four-site effectiveness study of this preventive intervention.

Programs in Australia

Two prevention programs in Australia have recently been described and evaluated: one by Shochet and colleagues, and the other by Spence and associates. Shochet and colleagues (2001) evaluated a “universal” prevention program applied in a school setting in Australia. This was a skills-based program of 11 sessions offered by a psychologist and based on a downward extension of principles of cognitive behavior therapy (CBT) and interpersonal therapy (IPT). The student sessions could be supplemented with three parental sessions, but not many parents took advantage of this offer. There were 240, 12-to 15-year-old subjects, who were assigned to assessment-only control, prevention without parental sessions, or prevention with parental sessions.

Students who completed either prevention program (no differences were obtained between the two prevention groups) showed fewer depressive symptoms on one measure of depression (but not another) than controls. The prevention program subjects also reported less hopelessness at the end of the project. All of these effects were maintained at a 10-month follow-up. The limitations of this program include the lack of random assignment of subjects (controls participated in one academic year, and intervention subjects in the next academic year), a small sample size, and assessments conducted at different times of the year in different conditions. The findings, though limited, were encouraging for such a short program and short follow-up period.

A very sophisticated study evaluated the long-term impact of a universal, teacher-implemented, and school-based prevention program that was developed by Spence, Sheffield, and Donovan (2003) in Australia. The program, Problem Solving for LIFE (PSFL), is a combination of cognitive restructuring and problem-solving approaches, and it is designed to prevent a first episode of depression. Subjects were 1,500 eighth-grade (ages 12–14; mean = 12.9) students attending 16 participating high schools in the Brisbane region of Queensland, Australia. The eight 1-hour classroom-session program was implemented by 28 teachers in eight randomly assigned schools (N = 751), while the control subjects (N = 749) attended the other eight schools. There were approximately equal numbers of girls and boys.

Appropriate data analyses indicated that the program significantly decreased depressive symptoms between the beginning and end of the program. This finding, however, was only true for those adolescents who had elevated (“high risk,” defined as 13 or higher on the Beck Depression Inventory) depression scores at the beginning of the study. Unfortunately, this difference was not maintained at a 12-month follow-up.

These two well-conducted studies are not particularly encouraging for the effectiveness of “universal” prevention programs for MDD. There are some hints, however, that similar studies conducted with at risk samples (i.e., selected or indicated prevention programs) might be more effective. For example, in the Spence study (replicating the Penn Study) it appears that students with greater depressive symptomatology (but not MDD) may respond better to prevention programs.

Arnarson and Craighead (Iceland)

Because of the stable population of Iceland and because most of the citizens live in one city, Reykjavik, Arnarson and Craighead have spent the past several years translating and standardizing the assessment instruments and developing a manualized, developmentally based, behavioral and cognitive program designed to prevent depression. It has been labeled the “Thoughts and Health” program, and it includes a student workbook as well as a program manual. The program consists of 15 group sessions (6–8 students per group) that are delivered in the school setting by the local school psychologists.

In their most recent report of this work (Arnarson & Craighead, 2004), they had studied 72 students at risk for MDD. At risk was defined as scoring above 13 on the Children's Depression Inventory or at the 75th percentile or higher on the negative composite of the Children's Attributional Style (CAS) Questionnaire (see Alloy et al., 2000). Thirty-two of the subjects from five schools were randomly assigned (within their respective schools) to the prevention program, and 40 subjects were randomly assigned (within their respective schools) to an assessment-only control condition. All at risk subjects were interviewed with the Children's Assessment Scale, and any subjects who were currently depressed or had suffered a previous depressive episode were excluded (currently depressed subjects were referred for treatment), as were subjects with attention deficit hyperactivity disorder or conduct disorder.

At the end of the intervention, there were no differences between the two groups on depressive symptoms or attributional style. However, at the 6-month follow-up interview (CAS interview), 18% of the assessment-only control subjects had developed MDD or dysthymia, whereas only one (3%) of the prevention program subjects had developed either disorder. Arnarson and Craighead are currently evaluating their prevention program with 96 at-risk (as previously defined) students in six schools in Iceland. They are also developing a similar program for use with 16-to 18-year-old students in a commercial or trade school setting.

Beardslee and Associates

Beardslee and associates, following the IOM stages, first studied risk and resilience, then developed pilot interventions and conducted a large efficacy trial, and are now exploring the effectiveness phase. Their prevention programs were designed to be public health interventions and useful to all families in which a parent is depressed. The programs are to be used by a range of health practitioners, including internists, pediatricians, school counselors, and nurses, as well as by mental health practitioners such as child psychiatrists, child psychologists, and family therapists. Moreover, this approach includes a strong emphasis on treatment, given that so much depression is undiagnosed and untreated.

A variety of studies from different theoretical points of view have in common the finding that children of depressed parents are at risk for depression and other conditions. Rates of depression are two to four times higher in children of depressed parents than those for children of parents with no illness (Beardslee, Versage, & Gladstone, 1998). To understand the transmission of depression, it is important to recognize that in many instances, depression in parents serves as an identifier of a constellation of risk factors that, taken together, cause poor outcomes. In Rutter's classic epidemiologic studies, six factors were identified, including maternal psychiatric disorder. When only one was present, there was no increased risk to the child, but when two or more risk factors were present, the risk went up dramatically. In a random HMO sample over a 4-year period, Beardslee and associates (1996) demonstrated that the same principles were evident in predicting who became depressed. They devised an adversity index consisting of parental major depression, parental nonaffective illness, and a prior history of disorder in the child. When no risk factors were present, less than 10% of the children became ill. When all three were present, 50% of the children became ill, with a gradation in between.

In studying resilience, Beardslee and associates identified three characteristics that described resilient children of depressed parents. The three characteristics, which were incorporated into the preventive intervention, were (1) support for activities and accomplishment of developmental tasks outside of the home; (2) a deep involvement in human relationships; and (3) the capacity for self-reflection and self-understanding, in particular, in relationship to the parent's disorder. Resilient youth repeatedly said that understanding that their parent was ill, that the disorder had a name, and that they were not to blame for it contributed substantially to their doing well. This, then, became a central part of the preventive intervention.

Initial studies of these intervention programs revealed that they were safe and feasible, and that families believed them to be helpful. In an initial random assignment study of the first 20 families enrolled, promising effects were observed 6 months after intervention, and a further follow-up study of parents' reports showed sustained effects over 3 years. In addition, pilot studies revealed that greater benefits were associated with the clinician-facilitated intervention than with the lecture condition. More recent reports on a portion of the sample at the third assessment point have indicated that both conditions resulted in family improvements, and that parents in the clinician-facilitated condition reported significantly greater levels of assessor-rated and self-reported change in family understanding and problem-solving strategies than did participants in the lecture condition.

Most recently, Beardslee, Gladstone, Wright and Cooper (2003) presented findings from follow-up interviews conducted with their entire sample of families at the fourth data point, nearly 2.5 years after intervention. They chose this interval because it was long enough to begin to see substantial, sustained changes in several main domains hypothesized to be affected by participation in the prevention programs. They focused on effecting change in a mediating variable that they described as parental child-related behavior and attitude change.

Results revealed several important findings about the primary prevention of depression and other forms of psychopathology in children at risk for dysfunction due to parental mood disorder. They found that these programs did have long-standing effects in how families problem solve about parental depression (i.e., behavior and attitude change). There was evidence that the clinician-facilitated program was initially more beneficial than the lecture program, and that the amount of change in parent's child-related behaviors and attitudes increased over time. They also found that children reported an increased understanding because of the intervention. They found a significant relation between the amount of child-related behavior and attitude change manifested by parents and the amount of change in understanding manifested by children, even though change was rated entirely separately by assessors blind to the knowledge of the other subjects' reports. Finally, they found that children who participated in the intervention programs reported decreased internalizing symptomatology over time.

After the success of the randomized trial, Beardslee and associates examined the mechanisms by which change took place. Briefly, they found that when families did make changes, they talked repeatedly about depression. Often, breaking the silence about depression led the families to talk and strategize successfully about many other things. This process was named the “emergence of the healer within.” Similarly, they found that what works for a child at 12 does not work for the same child at 16. In this sense, understandings of depression change both as the course of parental illness changes and as children grow and mature. Finally, many parents, despite the negativism and self-doubt of depression, end up functioning effectively as parents. In essence, they made peace with their disorder and moved on.


  • 1. The number of empirical studies of effectiveness of preventive interventions needs to be dramatically increased.

  • 2. We need to continue to expand the study of cognitive behavioral and educational approaches based on public health principles. The promising interventions described here need much further study, but the core principles are likely to be highly applicable.

  • 3. A number of methodological issues need to be clarified: (1) how to increase retention of participants in prevention studies; and (2) how to identify who drops out of prevention studies (dropouts may be those at highest risk—e.g., high family conflict, more negative life events, and greater depressive symptoms).

  • 4. The optimal timing of prevention interventions needs to be established. Current data suggest that ages 13–14 may be the best time, because this is the age just before a sharp upturn (ages 15–18) in initial episodes of MDD and bipolar disorder.

  • 5. The low rate of “caseness” of mood disorders must be taken into account in calculating the sample sizes necessary for prevention studies. At-risk samples are likely to result in 40%–50% of individuals (ages 13–14) with MDD during a 3-year follow-up, whereas, universal programs are more likely to see a control group caseness in a much lower range.

  • 6. We need continually to expand the science base of depression, particularly regarding the question of its heterogeneity. It is important to identify robust subtypes of depression because specific programs for some of these subtypes are likely to be more effective than general prevention programs for a heterogenous overall MDD. Robust subtypes of MDD are also likely to yield important genetic information. It is likely that certain vulnerabilities to depression are conveyed by multiple genes acting in concert and expressed in stressful situations. Promising leads include the work of Garber (Garber & Martin, 2002) on the stress diathesis hypothesis, work by Goodman and associates (Goodman & Gotlib, 1999) on ways in which genes and the stressors in families with parental depression interact, and Reiss and colleagues' (Reiss, Neiderhiser, Hetherington, & Plomkin, 2000) work on behavioral genetics. Recent work points to other subtypes and suggests that depression may represent an underlying dysregulation of emotion (Dahl, 2001), or that it may be part of a general phenomenon of inhibition (Kagan & Snidman, 1991). The more we understand risk factors and risk mechanisms (i.e., how risks come together), the better we will be able to mount preventive interventions.

  • 7. It is also very important to remember that better treatments make a huge difference in the lives of families—e.g., quicker recoveries, less misunderstanding. And, as better interventions are found, they will contribute to the prevention of depression among other family members.

  • 8. We need more study of prevention programs in different contexts with an awareness of cultural, racial, and ethnic differences.

  • 9. The occurrence of depression in either a parent or a child requires educational support from the other family members. Important opportunities exist for prevention in these situations. Some groups have found that adult family members with MDD do not want their children to know of the disorder; this attitude needs to be overcome by reducing stigma associated with mood disorders.

  • 10. Prevention of depression is closely related to other preventive efforts—in particular, the prevention of suicide and the consideration of victimization by violence. The work by Marikangas and colleagues suggests the possibility that MDD may be prevented by preventing the development of anxiety, which is a risk factor for subsequent development of MDD (Marikangas, Avwneoli, Dierker, & Grillon, 1999).

  • 11. Community/political intervention. Although the prevention of adolescent depression is a common goal in adolescent health, it is rarely approached in a comprehensive and systematic manner that includes continuous attention to all aspects of prevention. Most often, adolescent depression rises to the attention of the local or national health agenda after a series of well-publicized adolescent suicides. National and local advocacy groups have been effective in raising the public visibility of issues such as teenage pregnancy and drug abuse. A similar approach is needed for the prevention of adolescent depression. Three specific approaches are needed:

    • a. Campaigns to educate local and national governmental agencies and institutions and assist them in developing policies and programs that ensure utilization of effective and comprehensive models that prevent adolescent depression at all stages.

    • b. Advisory groups that work with national professional organizations to assist them to develop protocols and professional standards that place a higher priority on the prevention of adolescent depression. These efforts should include all professions that interact with youth—health care, education, social service, and juvenile justice.

    • c. Self-help groups that work on the local level with families, communities, and youth development agencies to assist them in the development of effective prevention interventions.