Prevention of depression in children
Risk factors of depression in children
We have to identify factors (social and individual) that are known to be
associated with depression in children and young people as a first step to
prevent the occurrence of the disorder.
I. What is meant by risk?
Risk is the degree to which the likelihood of a given adverse outcome
will occur following exposure to a defined toxic agent. The relative
importance of exposure is estimated by the probability of the outcome
occurring in a given population compared with the level of occurrence in a
non-exposed population. Risks for depression occur from a variety of
sources both within and external to the child. For example, individuals may
be born with genes that render them susceptible to depression, acquire
lesions such as head injury that alter their ability to control mood, suffer
infections that result in altered brain metabolism, be exposed to chronic
family discord or to negative peer group environments that alter the
development of emotional processing and self-percept (Goodyer, 2001). In
addition, there may be risks associated with poor housing or living in a
violent or dangerous society. Almost all research concurs that the onset of
clinical depressions occurs as a consequence of multiple rather than single
risk effects that are frequently not independent of each other (Kraemer et al.,
1997). There is however less agreement about how risks exert their effects
over time or what they do to the individual to bring about psychiatric signs
and symptoms and functional impairments.
II. What is the relation between risks over time and the magnitude of their
The size of the association between a risk factor and onset of disorder
indicates its potency and is the maximal discrepancy achievable between
depressed and not depressed groups exposed and unexposed to risk. For
example exposure to severely and personally disappointing life events in
adolescents occurring in the month prior to onset of depression is estimated
to increase the risk for depression about nine times over not being exposed
(Goodyer et al., 2000b). These estimates regarding one type of risk can be
misleading as seldom are all the known adversities measured in one study.
When measuring a range of possible risks in the same study we need
to know three things: i) if risks that occur at a distance in time (i.e. months
and years previously) influence the occurrence and the effects of more recent
adversities such as acute personally undesirable life events; ii) if these distal
processes themselves increase the liability for depression regardless of
proximal risks and; iii) if there is some form of combined effect arising from
exposure or possession of risks occurring distally and proximally not
explained by one set or the other.
For example 60% of all adolescents with depression are exposed to
acutely disappointing life events in the month prior to the onset of the
disorder but more than 90% are already exposed to two or more previous
ongoing risks either in their social environment or within themselves
(Goodyer et al., 2000a; Goodyer, 2001). The impact of the recent adversity
can only best be appreciated by taking into account the contribution of past
risks on both the liability for the recent event and the onset of disorder.
Current evidence from adult studies shows that there are very likely to be
multiple risk pathways that may lead to the emergence of depressive
illnesses (Kraemer et al., 1997). These involve genetic predispositions,
different types of adversities occurring during the first two decades of life
and acute personally disappointing life events not a consequence solely of
past difficulties in the weeks prior to onset (Kendler et al., 2002).
Adolescents at high risk for depression are exposed to, or possess on
average, three psychosocial risks in the 12 months before follow-up
(Goodyer et al., 2000b). Around 1 in 5 of this high psychosocial risk
population will get depressed over the ensuing 12 months.Thus even
amongst those at very high risk a significant number do not immediately
become depressed. The presence of an acute event considerably increases
III. Typology of risk
Environmental risks are invariably classified by their:
_ personal characteristics (e.g. accident, illness including post-infective
mood states, financial etc.)
_ latent psychological process inferred from these (e.g. disappointment,
_ Personal focus (self, parent, friend, etc.)
_ Origin (self-induced, independent of self).
_ time of onset and (less frequently) offset giving duration of exposure.
_ locus of control (uncontrollable by self, controllable).
_ age and developmental stage of exposure (prematurity, infancy, childhood
,adolescence, pre- or post-puberty).
Unfortunately there is no agreed standard definition for classifying risks and
most studies use widely different methods and classification processes.
IV. Social risks
Social adversities that are most associated with the onset of depression
are those that are outside the child’s control, occur as unpredictable
happenings in the daily environment and recur over time. They mainly arise
within family relationships or within friendships and are largely
interpersonal in nature (Rueter et al., 1999; Goodyer, 2001).
V. Family risks
The most common group of adversities to occur within the family,
which are relational in origin and produce negative effects on the child, arise
from dysfunctions between two or more people. Perhaps the commonest of
these are marital discord and emotional difficulties between one parent and
the child, although parental psychopathology may underlie a significant
proportion of these (Hammen & Brennan, 2003; Hammen et al., 2004).
The impact of events within the family on the child, such as physical
maltreatment, are also associated with the onset of depression, but the onset
appears often to be at a considerable distance in time from such abuse events
(Jaffee et al., 2002). However both violence and sexual abuse to the child by
parents, siblings or strangers are associated with depression, as are severe
acute family difficulties such as sudden death, serious physical illness in a
close relative or sudden separation of parents.
In contrast, unhappy marriages, parents being away from home due to work,
low income, poor housing and living in a deprived neighborhood occurring
singly are not strongly associated with clinical depressive onsets in young
people. Overall mild ongoing dysfunctions in family life do not appear on
their own to be markedly associated with the subsequent onset of clinical
depression (Tamplin & Goodyer, 2001).
However, persistent family disagreement through early adolescence
does increase the general level of low mood and depressive symptoms over
time (years) and it is this rising level of non-clinical negative mood and
thoughts that is associated with the onset of later clinical depression in older
adolescents (Rueter et al., 1999).
Those children with higher IQ, better family functioning, closer parental
monitoring, more adults in the household, and higher educational aspiration
are less likely to show depression in the presence of elevated psychosocial
risk (Tiet et al., 1998). In the absence of these protective or buffering factors
the risk for both emotional and behavioral difficulties arises when children
and young people are exposed to adversities. The more the family
environment is chronically emotionally neglectful, involves chronic marital
discord and a lack of authoritative parenting (the ability to be firm and clear
within a positive emotional environment), the greater the risks for
psychiatric disorders in general including personality difficulties in young
adult life. Psychiatric disorder in a parent is another high-risk adversity for
the child, with parental history of recurrent depression over the lifetime of
the child strongly associated with depression in the offspring (Hammen &
Depression runs in families with a resultant increased risk for
depression in the offspring of adults with a history of depression. Adults
with a history of depression may also have a dual diagnosis such as
substance misuse or alcoholism (Stallings et al., 1997). Thus there is an
increased association between depression, substance misuse and alcoholism
in parents and psychiatric disorders in offspring. Children and adolescents
within such families may therefore be at risk for a range of undesirable
outcomes including depression, behavior disorders and substance misuse.
VI. Friendship risks
Non-family-based adversities are also associated with the onset of
depression and other psychopathologies in young people. Children with poor
friendships, characterized by low numbers of friends, infrequent contact and
no intimate relations, are more likely to develop depression as well as
deviant behaviors and increased social isolation from the desired peer
network (Goodyer et al., 1990; Cairns et al., 1995; Bukowski et al., 1996;
This appears to be independent of family strengths and weaknesses.
The most potent form of acute negative life event is that of a recent (last few
weeks) severe personal disappointment (i.e. the failure of a previously held
belief in an expected outcome) with a close friend (Goodyer et al., 2000b).
When recent personal disappointments with a close friend arises its effects
as a risk factor is particularly large in those with previous psychosocial risks
(Goodyer et al., 2000b). Depression is markedly increased in the presence of
multiple adverse experiences involving both longstanding family and more
recent friendship events and difficulties. Under these social conditions, the
child may not perceive an emotionally supportive relationship in their social
VII. Individual risks
1- Genetic risks
Current evidence suggests that while genetic factors appear somewhat
less important in child onset depression, there are genetic contributions to
adolescent depression (Rice et al., 2002). The environmental processes may
be similar in nature but the implication is that these are sufficient to cause
depression in the pre-pubertal child but insufficient in the post-pubertal
adolescent. The studies on which this review is based are twin samples in
which depressive symptoms are the outcome rather than clinical disorders. It
is not clear if genetic factors are low in pre-pubertal children with clinical
depressions, which are rare in this population (Angold & Costello, 2001).
The precise genes involved remain unknown. In addition, the genetic risks
may not act directly to produce the disorder, but act through increasing the
liability for other risks in the environment. There may be a complex
patterning of gene-environment interactions combining to cause depressions
in the post-pubertal depressed adolescent (Caspi et al., 2003b). In contrast,
direct associations (and therefore effects) of single genes with depression are
(Henderson et al., 2000; Zill et al., 2002).
Children and adolescents (as well as adults) with a highly emotional
temperamental style (react quickly to everyday events, easily brought to
tears, easily soothed) are more likely to be depressed than those low in these
behavioural characteristics (Goodyer et al., 1993; Hodgins & Ellenbogen,
2003; McWilliams, 2003).
Although this is true for both sexes, more girls than boys have this
temperament and this may be one component that differentially increases the
risk for depression in females over males. The evidence suggests that there
are genetic influences on individual variations in temperament (Eley et al.,
2003; Sen et al., 2004).
The relationships between temperament and personality development over
time suggests that there is coherence across time between the commonest
used in both terms although the precise definitions appear to be somewhat
different (Caspi et al., 2003a; Shiner et al., 2003). The precise relations
between personality and later depression remain unclear but neuroticism
shows an important but complex relationship with depressive onset (Kendler
et al., 2004).
As well as emotional styles, there are thinking styles that increase the
liability for depression. High levels of particular types of self-critical
thoughts known as global self-devaluations (thinking of oneself as
abandoned, a failure, feeble, incapable, a loser, a mess, pathetic, pitiful,
rejected, stupid, unlovable, unwanted, useless, worthless), if present at times
of low mood are significantly associated with clinical depression (Teasdale
& Cox, 2001). A ruminative style, in which young people dwell or even
perseverate on a particular thought, also increases the risk for depression.
Adults and adolescents with both global self-devaluations and a ruminative
style have markedly increased risk for depression (Alloy et al., 1999).
Ruminating lowers mood and increases memory difficulties in adolescents
(Park et al., 2004).
4- Physiological risks
Studies of physiological factors as risk components for depression in
young people are relatively new and few have been published. There is some
evidence that both the monoamines and glucocorticoids are implicated in the
biology of depression in children and adolescents (Birmaher & Heydl,
2001). Children with a positive family history of depression show
abnormalities of serotonin function even when well, suggesting serotonin
vulnerability for subsequent affective disorders. Increased cortisol and a
second adrenal steroid dehydroepiandrosterone (DHEA) are both elevated
and predict the onset of depression in a subset of adolescents at high
psychosocial risk for depression (Goodyer et al., 2000a).
Elevated cortisol levels may themselves arise in part from
interpersonal difficulties in early parenting related to maternal depression
(Halligan et al., 2004). High risk children and young people with no history
of prior depression but with a positive family history for the disorder have
also been shown to have abnormalities in sleep architecture associated with
subtle changes in cortisol secretion (Dahl et al., 1996; Feder et al., 2004).
Overall the evidence suggests biological vulnerabilities in both the serotonin
and the adrenal steroid systems. These are likely to be brought about by a
combination of genetic and environmental influences.
5- Very high-risk groups
Within the child and adolescent population at large there are known
groups at very high risk for mental health difficulties including depression.
These are already the focus of policy review and include looked after
children, refugees, the homeless and asylum seekers. Children and
adolescent offenders, particularly those in secure institutions, are particularly
at risk for mental difficulties. The known numbers of successful suicides in
young offenders strongly indicates high levels of depression that currently
may not be adequately assessed or managed. It is unclear if ethnicity exerts a
specific risk for depression above and beyond the known increase in social,
behavioural and emotional difficulties for selected populations (e.g. Afro-
Caribbean). Maltreatment as risk has already been mentioned but ‘Hidden
maltreatment’ should be considered in children with adolescents with
unexplained mood disorders with no family history of depression and an
absence of other overt social adversities.
6- Special risk groups
Finally there are some families and individuals who have a known set
of risk actors whose precise theoretical mechanism (vulnerability, activating
or formation) is unclear.
These include children with a physical or a learning disability. Disabled
children are more at risk for mental illness and behavioral problems
including depressive disorders, compared with the population at large
(Dekker et al., 2002; Goodman, 1998; Martinez & Semrud-Clikeman, 2004).
Because of their visible handicaps, challenging behaviors and/or their more
overt educational difficulties, mood disorders may be easily missed in such
Likewise adolescents with complex endocrine diseases, adverse reactions to
drug treatments, pervasive developmental disorders, autism and Asperger’s
syndrome are at risk greater than would be expected by chance or by the
effects of being physically or developmentally impaired. Clinical services
may need to consider depressive disorders in these adolescents when social
withdrawal and/or irritability are presenting features or there is a persistent
exaggeration of their obsess ional habits and mannerisms suggesting a mood
1. Risks for depression are multiple in origins and may be correlated with
each other. Single risks resulting in the onset of clinically meaningful
depression are rare.
2. The majority of first depressive episodes arise in adolescents compared
with children and in the presence of at least two and invariably three long-
standing psychosocial risks.
3. Acute life events are key destabilizing elements in those already at high
psychosocial risk evoking relatively sudden onset in about 50% to 70% of
cases. The other third to a half appears to arise more slowly through chronic
persisting interpersonal difficulties.
4. Genetically mediated factors via the serotonin and adrenal steroid systems
may be important features in determining potency of social adversities.
5. The intermediate psychological vulnerabilities for adolescents between
physiology and the social environment are a high level of global self-
devaluative thinking at times of low mood in combination with a ruminative
6. There is increasing evidence that the pattern and potency of risks varies
with development, severity and number of episodes of depression. The
physiological risks for recurrence appear to be greater with an increasing
number of past depressive episodes suggesting an effect of depression on
viii- Risk classification
It is critical to remember when looking at this list that the specificity
of individual risk factors to the onset of depressive disorders is low to
moderate, with the exception of those starred * where specificity is high.
viii-1 Probable vulnerability factors
These increase the general liability to but seldom directly provoke
_ Presence of short arm serotonin promoter gene.
_ Elevated morning cortisol levels.
_ Acquired fetal infections.
_ Maltreatment or emotional neglect through infancy.
_ Maternal postnatal depression.
_ Parental history of depressive disorder*.
_ Brain illnesses in childhood including trauma and infection.
_ Being female*.
_ Being post-pubertal*.
_ Divorced parents.
_ Chronic parental psychiatric illness.
viii-2 Probable activating factors
These are directly implicated in the onset of depressions and in the
presence of vulnerability factors their effects can be large:
_ Personally undesirable life events resulting in permanent change of
interpersonal relationships in friends or family*.
_ Acute brain illnesses.
_ Community disasters such as war, famine and infections.
_ Personal assault.
viii.3 Formation factors
These are responsible for the clinical characteristics of the depressive
_ Past history of depressive symptoms*.
_ High trait levels of neuroticism (Kendler et al., 2004) or emotionality*.
_ Ruminative style of thinking*.
viii-4 Known risk factors whose precise role is currently unclear
These may be vulnerability, activating or formation factors but
currently available information does not permit the classification of their
_ Self-devaluative thinking.
_ Poor school performance.
_ Co-existing medical illnesses.
_ Death of close relative.
_ Death of a pet.
viii-5 Protective factors
These reduce the likelihood of depression in the presence of
vulnerability and activating factors:
_ A good sense of humor
_ Positive friendship networks
_ Close relationship with one or more family member
_ Socially valued personal achievements
_ High normal intelligence.
Preventive models for depression in children
Research and treatment for childhood mood disorders has focused on
clinical trials and longitudinal outcome studies rather than on the prevention
of illness. There are several reasons for this. First, although most research on
mood disorders focuses on intensive clinical endeavors to care for children
and adults already suffering from severe illness, the study of prevention
requires a different, public health, population-based approach. Second, the
methodologies needed to evaluate prevention effects are often more complex
than those used to evaluate treatment because large samples must be
followed over several years. Third, because the study of childhood
depression is relatively recent. As a result, the knowledge of risk factors and
protective resources necessary for preventive interventions has not been
available. Moreover, studies of adult depression have not included
examination of early childhood and adolescent antecedents of depression,
although an understanding of these antecedents is essential to inform
preventive efforts with children (Beardslee and Gladstone, 2001).
Converging lines of empirical investigation have changed this,
making possible theoretically driven, empirically justified approaches to the
prevention of depression in youngsters at high risk. a series of longitudinal
investigations suggest strongly that those at highest risk for depression can
be identified both in population-based samples (Lewinsohn et al., 1994) and
in homes with affectively ill parents (Hammen et al., 1990). Remarkable
advances have occurred in the science of prevention, and a consensus has
emerged regarding standard methodologic approaches to research (Institute
of Medicine, 1994) as well as appropriate statistical techniques for the
conduct of prevention trials (Kraemer, 1992). Moreover, there are a number
of well-conducted, methodologically sound prevention trials that
demonstrate significant positive outcomes (Institute of Medicine, 1994). The
scientific advances in both neuroscience and developmental epidemiology
will provide a better empirical knowledge base for the prevention of
Emerging knowledge from the field of developmental
psychopathology provides an important context for the development of
preventive intervention programs as well. In fact, several researchers have
noted that the fundamental working models addressing risk for depression in
youth, and particularly risk created by parental affective illness, are
developmental-transactional models. Thus, although risk factors for
depression are static, the processes that underlie emergence into either health
or illness are dynamic and influenced by developmental shifts throughout
the life span. An understanding of these developmental influences is
essential in the development of prevention programs. Moreover, it is likely
that depression may be most aptly prevented through the use of intervention
programs delivered throughout the life span, targeting the salient issues
particular to each developmental epoch (Carbonell et al., 2000).
An essential element of developmental-transactional models, and the
groundwork for effective preventive intervention, is an understanding of
resilience and protective resources. Luthar et al. (1990) defined resilience as
a "dynamic developmental construct" that refers to competence despite
adversity. They noted that individuals who are resilient in one domain may
exhibit deficits in other spheres and that individuals who exhibit resilience
during one developmental period may exhibit difficulties later in life. Rolf
and Johnson (1990) Argued that resilience can be increased experimentally,
thereby suggesting the important role of intervention research in promoting
adaptation throughout the life span. Moreover, Cicchetti et al. (2000) noted
that outcome studies with resilient youth may provide an important
foundation for preventive intervention research because such studies may
highlight periods of developmental change during which interventions may
be most successful in promoting positive adaptation (Sullivan et al., 2000).
A paradigm from the Institute of Medicine’s (Institute of Medicine,
1994) report on prevention provides a standard sequence for the
development of successful preventive interventions; The first stage is:
identification of risk and protective factors associated with a disorder. The
second stage is: understanding the extent to which variation in a targeted
outcome can be explained by risk factors amenable to intervention. The third
stage is: initiation of pilot and efficacy trials aimed at reducing the identified
risk factors and ameliorating the targeted disorder. The fourth stage is:
conducting effectiveness trials to investigate application of the intervention
at multiple sites and in real-world conditions. The final stage is:
implementation of the prevention strategies in large-scale public health
campaigns and other programmatic initiatives.
Three prevention programs for children with depressed parents:
To date, only three research teams have approached the prevention of
depression in targeted populations of children and adolescents at risk for
disorder, based on new, empirical risk data and following the standards for
prevention research. These studies reflect the fundamental principles of
prevention science, namely, the investigators employed manual-based
interventions with checks for fidelity of intervention delivery, tested
theoretical models, used randomized designs, and evaluated empirical and
well-specified outcomes. In this sense, they were similar to efficacy trial
designs for psychotherapy and psychopharmacology.
I-A group cognitive intervention:
Clarke et al. (1995) developed and evaluated an indicated preventive
intervention program targeting adolescents at risk for future depressive
disorder. This prevention program was based on the risk models for
adolescent depression developed by Lewinsohn et al. (1994) and it aimed to
promote adequate cognitive styles in adolescents identified as "at risk."
Youngsters were chosen based on scores from a widely used self-report
measure of depressive symptomatology and on high symptom levels from a
structured diagnostic interview.
In this study, 150 students from the 9th and 10th grades who were
considered at risk for future depression were assigned randomly to one of
two intervention groups. The active intervention program, titled the Coping
With Stress (CWS) course, consisted of 15, 45-min group sessions. This
approach was theoretically driven, was based on the cognitive distortion
theory of depression, and was modeled after an effective cognitive
behavioral treatment for depression (Clarke et al., 1990). In the usual care
condition, adolescents were free to continue with preexisting treatment or to
seek new treatment opportunities. Participants were reassessed for diagnostic
status at 1-year follow-up. Results indicated that based on survival analysis,
a highly significant difference emerged between the incidence of major
depressive disorder or dysthymia in the usual care group (25.7%) versus the
active intervention group (14.5%).
ii-A school-based prevention program:
In the Penn Prevention Program, Seligman et al. (1994) developed and
evaluated a district-wide, school-based indicated prevention program
targeting 10- to 13-year-old children at risk for depression based on elevated
self-reported depressive symptomatology, self-reported parental conflict, or
both. This prevention program was based on a model of explanatory style
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.
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 were recruited for
the no-participation control group. Assessments included child self-report,
teacher-report, and parent-report questionnaires.
Results indicated that relative to control subjects, children who
participated in any of the treatment groups reported significantly fewer
depressive symptoms immediately following the program and at the 6-month
follow-up, even controlling for initial levels of symptomatology. Moreover,
teacher reports at follow-up revealed better classroom behavior in treatment
participants relative to 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. (Jaycox et al., 1994).
iii-A family-based prevention program:
In contrast to the two indicated prevention programs described above,
Beardslee et al. (2001) developed and evaluated a family-based selective
prevention program targeting nonsymptomatic early adolescents at risk for
future depression because of the presence of significant affective disorder in
one or both parents. This work, based on a public health model, draws from
earlier investigations of risk and resilience in the adolescents of affectively
ill parents. Two intervention programs (i.e., clinician based and lecture)
were designed to address all children within a family, not simply those
already manifesting symptoms. The clinician-based program was
administered to families on an individual basis, whereas the lecture program
was delivered to parents in a group format.
Both programs aimed to:
1) Decrease the impact of family and marital risk factors.
2) Encourage the promotion of resilience-related behaviors and attitudes in
the children through enhanced parental and family functioning.
3) Prevent the onset of depression or related psychopathology. Families
were assigned randomly to one of the two preventive intervention programs.
Results with a portion of the sample indicated that both interventions
are safe and feasible and are associated with positive change in both parents
and children (Beardslee et al., 1997). In addition, participants in the
clinician-facilitated condition reported significantly greater levels of
assessor-rated and self-reported change than did participants in the lecture
condition. Most important, greater parental benefit from intervention (in
terms of changes in illness-related behaviors and attitudes) was associated
with significant global change among children, including enhanced
understanding of parental illness and improved communication with parents.
These findings indicate that providing parents with factual information
regarding risk and resilience in children, and linking this factual information
to family members’ illness experiences, can result in behavioral and
attitudinal changes among parents that ultimately translate into more optimal
functioning among children.
iv-Two prevention programs for adults:
Similar preventive approaches used with adults yield promising findings.
Moreover, these adult studies may instruct preventive work with children of
depressed parents because they involve as subjects parents at high risk for
A-A study of prevention with adults in a primary care setting:
Munoz et al. (1995) conducted a selective preventive intervention trial
with a low-income minority population of adult patients recruited from
primary care clinics in the San Francisco area. Participants were randomized
to either a cognitive-behavioral or a control condition. They found that
relative to control participants, experimental participants became less
pessimistic, reported more positive and fewer negative thoughts, and
engaged in more pleasant activities at follow-up. Munoz and colleagues
concluded that this study provides support for the utility of a randomized,
controlled study of a preventive intervention for major depression in adults,
in that they were able to reduce significantly depressive symptoms in a
nonclinically depressed population.
B-A study of prevention with adults experiencing job loss:
Price et al. (1995) conducted an intervention program targeting
unemployed workers that also prevented severe depressive symptomatology
in many of the participants. Briefly, designed as a job search seminar, the
JOBS Intervention Project enhanced job-search skills, self-esteem, and sense
of control; improved job-search self-efficacy; and provided strategies to
assist participants in coping with setbacks. The investigators found that a 1-
week job-search intervention program that promotes reemployment and
mastery among unemployed persons also has significant mental health
benefits for participants labeled high risk. In this regard, the findings are
important because they show significantly less depression as a by-product of
a successful intervention for job loss.
Relation between treatment and prevention
Finally, it must be emphasized that there is no tension between
treatment of known illness and prevention. In fact, adequate treatment of
depression in parents is preventive of many difficulties in children. It is
crucial that adequate treatment for children and adults be incorporated into
any prevention approach. This treatment effort must involve all those who
suffer from the disease. Thus, from a public health point of view, those
concerned about the prevention of depression can find common ground with
others in advocating for adequate health care for all children and their
caregivers. This need for universal health care is underscored by the
overwhelmingly powerful evidence of how impairing untreated parental
depression can be and by the fact that the majority of youngsters with full-
blown depressions are not receiving adequate treatment (Luthar et al., 2000).
Careful empirical evaluation of risk factors for depression suggests
that the most promising approach for preventive research targets those at
highest risk for affective illness. The true promise of prevention will evolve
as developments in neuroscience and epidemiology better identify not just
risks but protective factors and crucial periods for intervention. Above all, a
long-term life span–developmental perspective is needed because such a
perspective will highlight opportunities for intervention at different points in
Could child depressive symptoms relapse?
Community-based studies indicate that children and adolescents
experience continuity of symptoms, if not disorder, from early to later
adolescence (Ialongo and Kellam, 2001). Risk factors for onset identified
previousely. Data are limited, but clinic-based and community samples
suggest a relapse rate of between 46% and 63% (Klein and Gotlib, 2000).
These rates should be interpreted cautiously, however, as these studies have
had limited period of follow-up, and recurrence and chronicity rates by mid-
adulthood are not yet known.
Relapse Prevention Strategies
The most widely used strategy for preventing depressive relapse is the
continuation of the treatment that achieved acute phase remission. Effective
maintenance antidepressant therapy can reduce relapse rates by up to 50 %
(Agency for Health Care Policy and Research Depression Guidelines Panel,
1993). Short-term psychotherapies such as Cognitive Behavioral Therapy
(CBT) and Interpersonal Therapy (IPT) modified for use after remission is
achieved also protect against relapse.
CBT with continuation psychotherapy significantly reduced relapse
compared to CBT without continuation. Patients with earlier initial onset and
with less robust remission showed even greater reductions. Similar findings
have been reported for continuation phase IPT.
New strategies have focused on using specific treatments for different
phases of depression, that is, switching patients to a different therapy after
acute phase remission is achieved. Examples include following
antidepressant medication with CBT and starting nortriptyline after
discontinuing ECT (Haskett et al., 2001).
CBT-based preventative interventions sequenced with antidepressants
provided comparable relapse protection to continuation pharmacotherapy.
One study did not find this for IPT vs. maintenance pharmacotherapy,
although IPT was significantly more effective compared to maintenance
medication in which an active drug was replaced with placebo. Thus,
multiple interventions may be more effective at relapse prevention than
simply continuing single interventions. Further study is needed, especially in
light of the under treatment of depression in non specialty settings
(Maidment and Baxter, 2001).
Continuation treatments may be indicated for subgroups of depressed
patients. Specifically, patients with earlier onset and greater chronicity, those
with more than two episodes, and those with incomplete response to acute
phase intervention are at highest risk, suggesting that tailoring and testing
treatments specific to these groups may be indicated. Some workshop
participants were more cautious about endorsing the need for continuation
treatments, while emphasizing the value of enhancing acute treatment
outcomes. A number of studies, including those testing sequencing
approaches, indicate a relapse preventative effect when a complete or robust
acute phase recovery is achieved, consistent with observations that
incomplete recovery increases risk of relapse (Kupfer and Frank, 2001).
The need to determine the active ingredients in effective treatments, as
well as designing preventative treatments that can be provided to recovered
patients, regardless of type of acute treatment, were also highlighted. For
example, Mindfulness Based Cognitive Therapy (MBCT), a therapy
provided during recovery that teaches patients to disengage from cognitions
linked to relapse, has shown effectiveness, particularly among patients with
3 or more episodes (Hollon et al., 2001).
Markers of relapse risk:
Research to date has focused on relapse risk factors that are largely
clinical features of depression. For example, number of past depressive
episodes, quality of remission, and psychiatric co morbidity are the most
reliable and robust predictors of relapse to date. Thus, this raises the
challenge as to whether such high-risk patients can be identified and treated
accordingly. Participants also stressed that identifying markers of relapse
risk is vital to treatment development. Basic science paradigms could be
used to model relapse processes, especially in searching for mechanisms
thought to mediate symptom return. Embedding tests of these models into
ongoing prevention trials could provide direct, outcomes-based data to
measure the effect of modifying these factors (Segal et al., 2000).
Cognitive models of relapse vulnerability have tested predictions derived
from Teasdale’s Differential Activation Hypothesis, which suggests that risk
of severe, persistent depression depends in part of information processing
patterns activated during mild dysphoric states. Those who have
experienced, in conjunction with depression, events interpreted in themes of
severe loss, self-denigration, and hopelessness become predisposed to the
reactivation of these cognitions during later periods of dysphoria. Thus,
current experiences become more likely to trigger depressive cognition,
though during non-depressed periods the affected individuals may not show
such thought patterns (Cooper et al., 2001).
Empirical studies of this model commonly use laboratory-based
challenges to induce transient dysphoric mood in groups at high and low
relapse risk. As hypothesized, formerly depressed subjects had a more
depressogenic cognitive style when feeling sad, but were comparable to low-
risk subjects during times of euthymia (Segal et al., 2003) reported that the
degree of laboratory mood-linked cognitive reactivity significantly predicted
relapse up to 30 months later. These are among the first clinical data
suggesting that challenges in cognitive processing arising from the
experience of dysphoria can predict symptom return.
With regard to findings on the neurobiology of relapse, new research is
underway on changes in regional brain activation following successful
treatment of depression is developing. To date, there are no biological
markers predicting relapse vulnerability during maintenance treatment.
Recent neuroimaging studies describe frontal and cingulate metabolic
abnormalities in depression, with striatal and amygdala-hippocampal
changes also noted. Medication seems to normalize these changes, and some
change may occur with structured psychological treatment (Salmon et al.,
Mayberg et al. (2002) studied concordant and functional change after
provocation of sadness in healthy volunteers and resolution of chronic
dysphoria in depressed patients. With sadness, increases in limbic-
paralimbic blood flow and decreases in neocortical regions were identified.
With depression remission, the reverse was seen. Data showed a significant
inverse correlation between subgenual cingulate and right dorsolateral
prefrontal activity in both conditions. The presence and maintenance of
functional reciprocity between these regions may mediate the relationship
between mood and attention seen in normal and pathological conditions.
These areas may also be implicated in the amplification of transient
dysphoric mood into depressed states.
Zindel Segal, Jane Pearson, and Michael Thase organized the workshop.
Greg Siegle produced a written record of the meeting. Virginia Lindahl
assisted Jane Pearson and Zindel Segal in developing this summary.
James C. Coyne, Ph.D., University of Pennsylvania Health System
Jan Fawcett, M.D., Rush Presbyterian St. Luke’s Medical Center, Chicago
Ellen Frank, Ph.D., University of Pittsburgh, Western Psychiatric Institute
Richard G. Frank, Ph.D., Harvard Medical School
Joseph J. Gallo, M.D., M.P.H., University of Pennsylvania
Connie Hammen, Ph.D., University of California Los Angeles
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