Clinical Characteristics of Mood Disorders

The Social Security Administration (SSA) Listing of Impairments for mood disorders includes within the
same diagnostic category criteria for the following diagnoses: major depressive syndrome, manic syndrome,
and bipolar or cyclothymic syndrome. However, according to the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition (DSM-5) (APA, 2013), the mood disorders that may have a childhood onset
are (1) major depression, (2) persistent depressive disorder (PDD), and (3) disruptive mood dysregulation
disorder (DMDD). In a departure from DSM-IV, DSM-5 treats bipolar disorders as a separate category.
Pediatric bipolar disorder (PBD) will be addressed separately following a discussion of depression.
Go to:

DEPRESSION

Diagnosis and Assessment

Major depression is defined by DSM-5 as the presence of all five symptoms including feeling—or being
observed to feel—sad, empty, or hopeless most of the day (depressed mood); having markedly diminished
interest in most activities (anhedonia); or having severe, recurrent verbal or behavioral outbursts of temper
three or more times per week. Irritability may be a substitute for symptoms of persistent depression for
children, but irritability alone is not a sufficient criterion for major depression in children (Stringaris et al.,
2013). Chronicity is the most easily observed feature of PDD, which may include children diagnosed with
subthreshold depression (formerly known as dysthymia) as well as those diagnosed with chronic major
depression. There is no lower age limit for the diagnosis of either major depressive disorder or persistent
depressive disorder, but the latter is specified as “early onset” if the first episode occurs before age 21.
Disruptive mood dysregulation disorder is applicable only to children between the ages of 6 and 18 years.
DMDD is a new diagnosis that was developed to reduce the risk of misclassifying children with nonepisodic
and chronic irritable mood as having bipolar disorder (Roy et al., 2014). Given that PDD and DMDD are
new diagnostic categories, estimates of prevalence, clinical characteristics, and course may change as these
criteria are applied in future research.
The most important difference between DSM-IV and DSM-5 in the diagnosis of mood disorders is that
“depressive disorders” have been separated from “bipolar and related disorders.” In general, the differences
between depressive disorders in DSM-IV and DSM-5 are very small and unlikely to have a great effect on
estimates of prevalence or incidence.
The diagnosis of a childhood-onset depression disorder requires a comprehensive psychiatric diagnostic
evaluation, including interviews with the child, primary caregivers, and collateral informants such as
teachers (Birmaher et al., 2007). Although screening tools to detect depressive symptoms are available,
findings from these are not a substitute for a clinical diagnosis (Birmaher et al., 2007).
There are no well-established biologic markers for these diagnoses. Research on the biologic correlates of
child depression include studies examining contributing factors such as genetics, sleep, neuroendocrine,
inflammatory, metabolic, and neurotrophic factors. These factors as well as neural networks are in the
exploratory phase of research development (Li et al., 2013a,b; Miller and O'Callaghan, 2013; Mills et al.,
2013; Nivard et al., 2015; Palagini et al., 2013; Penninx et al., 2013; Rao, 2013; Schmidt et al.,
2011; Schneider et al., 2011). Early findings using brain neuroimaging, for example, have suggested that
alterations in the developmental trajectories of limbic and striatal regions may increase the risk of
adolescent-onset depression (Whittle et al., 2014). Luking and colleagues found an attenuated relationship
between the amygdala and cognitive control regions, consistent with the hypothesis of altered regulation of
emotional processing in early childhood–onset major depression (Luking et al., 2011). Preliminary studies
using neuroimaging also raise questions about whether changes in brain white and gray matter differentiate
between early onset unipolar and bipolar depressive disorders (Serafina et al., 2014). None of these research
advances are as yet employed diagnostically.

Demographic Factors and Duration of the Disorder

Age
The age of onset for depression among children and youth is variable because the expression of depressive
symptoms may differ by development stage. Irritability, for example, may be more prominent among
younger depressed children (Birmaher et al., 2009). Preschool children with depressive syndrome may
manifest subthreshold diagnostic criteria for depression of shorter duration (Luby et al., 2014). These early
depressive symptoms are significant because in clinical samples they are predictive of major depressive
disorder in later childhood even after controlling for a maternal history of depression and other risk factors
(Luby et al., 2014). Furthermore, this relationship may persist because subthreshold depressive symptoms
have also been found to be predictive of major depressive disorder (MDD) onset in young adulthood (Klein
et al., 2013). Some of the best established risk factors for MDD include childhood anxiety and parental
depression (Thapar et al., 2012).

Sex
The risk for early-onset depression among children (i.e., 12 years or younger) does not vary by gender;
however, during adolescence the risk among girls substantially increases. Findings from most studies on
children suggest that there are no differences in the rates of depression between boys and girls or only a
slight elevation in boys compared to girls (Brooks-Gunn and Petersen, 1991; Costello et al., 1996; Garrison
et al., 1989; Lewinsohn et al., 1998b; Nolen-Hoeksema et al., 1991; Petersen et al., 1991; Rutter et al.,
1986; Wesselhoeft et al., 2014). In contrast, during adolescence the rate of depression among girls almost
always exceeds that of boys (Avenevoli et al., 2015; Costello et al., 2003; Ferrari et al., 2013; Lewinsohn et
al., 1998b; Offord et al., 1989), and this trend persists into early adulthood (Costello et al., 2003; Ferrari et
al., 2013; Rao et al., 1999; Rohde et al., 2013). There is evidence that hormonal, rather than psychological
or sociological, reasons account for the appearance of this adolescent gender difference, which persists until
menopause (Angold et al., 1998).

Race/Ethnicity
The findings regarding differences in rates of depression among youth by race or ethnicity are mixed, and
the variation is likely due to differences in study design, target populations, and how depression was
identified. Among a nationally representative sample of adolescents, major depression based upon youth-
reported symptoms did not vary by race or ethnicity (Avenevoli et al., 2015). Using data from the National
Health and Nutrition Examination Survey (NHANES) for children ages 8 to 15 years, a study found no
differences in the prevalence of mood disorders by race or ethnicity, possibly because of the small sample
size (Merikangas et al., 2010). In contrast, an analysis of data from the National Comorbidity Study-
Adolescent Supplement (NCS-A) found higher rates of mood disorders among Hispanic adolescents than
among non-Hispanic whites (Merikangas et al., 2010). Furthermore, findings from the National
Longitudinal Study of Adolescent Health indicated that youth from racial or ethnic minority backgrounds
were more likely to report depressive symptoms than non-minority youth (Rushton et al., 2002). This
finding is consistent with that of a study that examined the variation in prevalence rates of depression
among children and youth enrolled in Medicaid (Richardson et al., 2003).

Socioeconomic Status
Although studies of adults suggest that depression is associated with lower social class (Kessler et al.,
2003), results from studies of children and adolescents are inconsistent (Merikangas et al., 2009). Some
studies report a lack of association between depressive and anxiety disorders and social class (Costello et al.,
2003), whereas others report a significant association, at least for the most impoverished groups (Costello et
al., 1996; Gilman et al., 2003; Reinherz et al., 2003). There are also data on lifetime risk of depression that
indicate that a low socioeconomic status (SES) in childhood is related to a higher risk of depression later in
life (Gilman et al., 2002). Consequently the precise nature of the relationship between mood disorders in
children or adolescents and poverty is unknown.

Duration
Childhood-onset depression is a chronic disorder, with an estimated average duration of 6 months. Among a
longitudinal cohort of 816 high school students (ages 14 to 18) with depression, the mean age of onset was
15 years, and the mean duration of a major depressive episode was 26 weeks, but the duration varied widely,
from 2 to 520 weeks (Rohde et al., 2013). The risk factors related to longer depressive episodes were earlier
onset (age 15 years and younger), suicidal ideation, and seeking mental health treatment (Rohde et al.,
2013). These findings are consistent with the NCS-A, which found the mean duration of a major depressive
episode to be 27 weeks among a nationally representative sample of U.S. youth (Avenevoli et al., 2015).
The median duration of major depressive episodes among clinically referred samples has been found to be
considerably longer, most likely reflecting the greater clinical severity among children who access and
receive continuous mental health care. In such samples, the median duration of depression ranged from 7 to
9 months, which was more than three times longer than that found in a community-based sample (Kovacs,
1996).
Adolescent depression also tends to recur. A recent review of outcomes of childhood depression reached the
following conclusions (Costello and Maughan, 2015): (1) One in two children with a diagnosis of
depression had one or more further episodes as an adult; (2) depression alone has a much better prognosis
than depression accompanied by any of the following: anxiety disorders, oppositional defiant disorder, or
substance use disorder; and (3) family conflict predicts continuity of depression into adulthood. Among
adolescents in the community who recovered from a depressive episode, 5 percent experienced another
major depression within 6 months, 12 percent within 1 year, and approximately 33 percent within 4 years
(Rohde et al., 2013). Within clinically referred samples, an estimated 70 percent of depressed young patients
had at least one recurrence within 5 or more years (Kovacs, 1996). These findings are consistent with
international studies that suggest that children and adolescents with depression are more likely to suffer
major depression and to manifest suicidal tendencies as adults (Fergusson et al., 2005; Harrington et al.,
1990).

Comorbidities
Comorbid disorders are common among children and youth with depressive disorders, and childhood onset
may increase the risk for comorbidity (Fernando et al., 2011). Children and youth with depression are more
likely to suffer from anxiety disorders, conduct disorder, oppositional defiant disorder, and attention deficit
hyperactivity disorder (ADHD) as well as alcohol and drug abuse (Costello et al., 2003; Fleming and
Offord, 1990; Hipwell et al., 2011; Meinzer et al., 2013). Among a community-based cohort of adolescents
with major depressive disorder, 43 percent also had a lifetime occurrence of another mental disorder. Of
those teens with major depression, for example, 20 percent had an anxiety disorder, 13 percent abused
alcohol, 18 percent abused drugs, 4 percent had conduct disorder, 3 percent had oppositional defiant
disorder, 3 percent had ADHD, 8 percent had core symptoms of bipolar disorder, and 30 percent reported
smoking cigarettes daily (Lewinsohn et al., 1998b). In a study following older teens into adulthood, the rates
of comorbid major depression and of alcohol abuse or dependence were both only 2 percent during
adolescence, but they increased in early adulthood to 11 and 7 percent, respectively (Briere et al., 2014).
Compared to major depression only (i.e., without other diagnoses), the prognosis for youth with combined
depression and substance use disorders is poorer. Youth with both disorders are at higher risk for alcohol
dependence, suicide attempt, impaired role functioning, academic problems, life dissatisfaction, and less
treatment utilization (Briere et al., 2014; Lewinsohn et al., 1998b).

Functional Impairment
A large proportion of children and adolescents with mood disorders have significant levels of functional
impairment, defined as a reduced capacity to meet normal expectations in their roles at home, at school, and
with peers and adults. Based on the NCS-A, 63 percent of youth with past-year major depression reported
significant disability in at least one domain of functioning (Avenevoli et al., 2015). These findings are
consistent with the 2001–2004 NHANES, which found that about half of children with a depressive
diagnosis also showed significant functional impairment (Merikangas et al., 2010). Further, among a large
epidemiologic sample, The Great Smoky Mountains Study of youth aged 9 to 13 found that 73 percent of a
community sample with depression had significant functional impairment (Costello et al., 1996).
In addition, children with depression run a high risk of impaired functioning that continues into adulthood
(Costello and Maughan, 2015). In the Great Smoky Mountains Study, four areas of functioning were defined
as contributing to functional impairment in adulthood: (1) health, (2) education and income (SES), (3) social
relationships, and (4) criminality or self-injurious behavior (Copeland et al., 2015). In all four areas,
participants with early depression were significantly worse off than those with no psychiatric history, and
they were the most likely of any diagnostic group to perform poorly as adults. Results from international
studies are also consistent with these findings. In a Swedish sample (Jonsson et al., 2011) depressed
adolescent females grew into adults who were more likely than other adults to be divorced, to be single
parents, to have miscarried, to have experienced intimate partner violence, or to have had a sexually
transmitted disease. In the Brisbane birth cohort study (Keenan-Miller et al., 2007), even after controlling
for adult depression, early adolescent depression continued to be associated with poorer interviewer-rated
health, poorer self-perceived general health, higher health care utilization, and increased work impairment
due to physical health.

Treatment and Outcomes

Treatments for mood disorders among children and adolescents include evidence-based psychotherapies and
psychotropic medications that may be administered alone or in combination, depending on the clinical
severity, the prior history of treatment response, and parent (or older youth) preference. For mild or brief
depression, education, supportive therapy for 4 to 6 weeks, and case management to address environmental
factors may be sufficient (AACAP, 2007).
For moderate to severe depression, the possible evidence-based psychotherapies for adolescents include
cognitive behavioral therapy (CBT) (Compton et al., 2004; Harrington et al., 1998) and interpersonal
psychotherapy (IPT) (Mufson et al., 1999, 2004; Rossello and Bernal, 1999). These therapies are typically
delivered in six to eight weekly sessions. CBT helps adolescents recognize negative thoughts and unwanted
behavioral patterns and gives them strategies to change their thoughts and actions (AACAP, 1998, 2007).
Interpersonal therapy focuses on strategies to cope with problems in relationships (i.e., family disputes) that
may exacerbate depressed mood (AACAP, 1998, 2007).
For persistent depression that is not improved by psychotherapy alone or for more severe depression,
antidepressant medication is recommended. The medication class commonly used is selective serotonin
reuptake inhibitors (SSRIs), and within this class only a few medications are approved by the Food and
Drug Administration (FDA) for use with children or adolescents. In 2004 the FDA issued a public warning
(i.e., a “black box warning”) about an increased risk of suicidal thoughts or behavior in children and
adolescents treated with SSRI antidepressant medications. In 2007 findings from a comprehensive review of
pediatric trials conducted between 1988 and 2006 suggested that the benefits of antidepressant medications
likely outweigh their risks to children and adolescents with major depression and anxiety disorders (Bridge
et al., 2007).
The results of research on the effectiveness of treatment are mixed but promising. Younger adolescents
respond better to acute treatment than older or multiply comorbid adolescents (Curry et al., 2006). Within
community-based treatment settings, psychotherapy for acute treatment of depressed youth is only modestly
effective (AACAP, 2007; Weisz et al., 2006). Findings from randomized clinical trials comparing the
efficacy of combined CBT and antidepressant medication with medication or psychotherapy alone are
mixed (Curry et al., 2006; Goodyer et al., 2007; Kratochil et al., 2006; March et al., 2004, 2006; Melvin et
al., 2006).
Antidepressant medications from the SSRI class are commonly used. Fluoxetine (Prozac) is the only SSRI
approved by the FDA for use in treating depression in children ages 8 and older. Escitalopram (Lexapro) is
also FDA approved for early-onset depression, but approval is restricted to youth ages 12 and older. The
other SSRI medications and the SSRI-related antidepressant venlafaxine have not been approved for
treatment of depression in children or adolescents, but they may be prescribed on an “off-label” basis. Table
11-1 summarizes the commonly used antidepressant medications for adolescents with depression.

TABLE 11-1
Commonly Prescribed Antidepressant Medications for Depressive Disorders Among Adolescents.
Overall, the phases of treatment for depressive disorders are conceptualized as acute, continuation, and
maintenance and are defined by the goal to be achieved. The goal of the acute phase is to achieve response
(i.e., the patient having no symptoms or a significant reduction in symptoms for at least 2 weeks) and,
ideally, full symptomatic remission (i.e., a period of at least 2 weeks and less than 2 months with no or few
depressive symptoms) (AACAP, 2007). Continuation treatment is required for all depressed youths in order
for them to avoid relapses (AACAP, 2007). This phase typically lasts 6 to 12 months. The goal of the
maintenance phase is to avoid recurrences, especially among youth with depression of greater clinical
severity. This phase may last 1 year or longer, and little research is available to guide national
recommendations for when treatment during the maintenance phase should end (AACAP, 2007).
Go to:

PEDIATRIC BIPOLAR DISORDER

Diagnosis and Assessment

DSM-5 conceptualizes bipolar and related disorders as a distinct diagnostic group which includes (1) bipolar
I disorder, (2) bipolar II disorder, (3) cyclothymic disorder, and (4) other specified. The hallmark
characteristic of bipolar I disorder is meeting criteria for a manic episode. Bipolar II disorder is
characterized by a history of at least one major depression and at least one hypomanic episode. Given the
chronicity of depression and mood instability, teens with bipolar II disorder may also experience serious
impairment in social, academic, and occupational functioning (APA, 2013). The diagnosis of cyclothymic
disorder is given to persons who experience both hypomanic and depressive periods without ever fulfilling
the criteria for mania, hypomania, or major depression (APA, 2013). The latest guidelines for diagnosing
bipolar disorder in children were issued in 2007 by the American Academy of Child and Adolescent
Psychiatry, and they are currently being updated to reflect new DSM-5 criteria. The diagnosis of PBD
requires a comprehensive psychiatric diagnostic evaluation, including a psychiatric interview with the child
or youth, the primary caregiver, and collateral informants, such as teachers. There are no well-established
biologic markers for PBD. Pediatric bipolar disorder is a rare condition in childhood but it can lead to
significant impairments (Goldstein, 2012).
A thorough evaluation is needed to rule out organic conditions. A pediatric examination should include a
thorough neurological evaluation, especially in the presence of either psychotic symptoms or catatonia.
Medical conditions that mimic either mania or depression, such as metabolic, endocrine, or infectious
disorders or acute intoxication or withdrawal, need to be evaluated as indicated.

Comorbidities
Comorbid disorders among teens with bipolar disorder are common and include ADHD, anxiety disorders,
oppositional defiant disorder, and substance use disorders (Bernardi et al., 2010; Birmaher et al., 2009; Jolin
et al., 2008; Masi et al., 2006; Pini et al., 2006; Sala et al., 2014; Stephens et al., 2014). In a national
household sample, rates of ADHD and alcohol use were three times higher among adolescents with bipolar
disorder who received treatment than among those who received no treatment; those who received treatment
often had much more severe bipolar disorder (Khazanov et al., 2015). Among youth hospitalized for their
first manic episode, the rate of comorbid substance abuse is high. In one study, almost one-half (48 percent)
of youth hospitalized for bipolar disorder had a substance use disorder either at baseline or within the
following year (Stephens et al., 2014). Furthermore, early onset of mania may increase a youth's risk for
substance abuse (Gao et al., 2010), and combined bipolar and substance use disorders is associated with
legal and academic difficulties, pregnancy, and suicidality (Goldstein and Bukstein, 2010).
Functional Impairment
The extent of functional impairment among children with pediatric bipolar disease is influenced by the
severity of the child's illness and by the complexity of the disorder. Because PBD is a chronic and serious
disorder, severe impairments in functioning are very common. Youth with PBD have documented
impairments in academic functioning and achievement due to executive functioning deficits (Biederman et
al., 2011; Perlman et al., 2013). Research also shows that children and adolescents with PBD have
difficulties reading facial expressions (Schenkel et al., 2012; Whitney et al., 2013), which is key to effective
social functioning. Current longitudinal studies underway (see Findling et al., 2010 will elucidate the extent
of functional impairments associated with this diagnosis.

Treatment and Outcomes

Treatment for bipolar disorder includes psychotherapy and medication. Recommended evidence-based
psychotherapies are family-focused therapy (FFT), CBT, and IPT. FFT has a strong evidence base and
targets reduction of highly charged emotions and stressors while promoting family problem-solving and
conflict resolution (AACAP, 2009). FFT in combination with mood-stabilizing medications has been found
to improve symptoms of mania, depression, and behavior problems (Miklowitz et al., 2006). CBT helps
adolescents avoid stressful situations that may trigger mania (AACAP, 2009) and develop strategies to
change thoughts and actions. IPT focuses on strategies to improve the stability of daily routines, such as
maintaining a regular sleep schedule; it may also reduce a teen's vulnerability to new episodes of mania
(AACAP, 2009).
Medications for bipolar disorder in older children and youth include mood stabilizers and atypical
antipsychotic medication (see Table 11-2).

TABLE 11-2
Commonly Prescribed Medications for Bipolar Disorder in Adolescents.
Although the short-term efficacy of recommended first-line mood stabilizers and antipsychotic medication
treatment has been established, there are few, if any, studies examining the long-term efficacy of medication
treatment. Among a cohort of 263 children and adolescents with bipolar spectrum disorders, approximately
70 percent recovered from their index episode, but 50 percent had at least one syndromal recurrence,
particularly depressive episodes (Birmaher et al., 2006). Clinically, the extent of improvement is likely
influenced by clinical severity and complexity (i.e., comorbid substance abuse), timely access to care,
treatment adherence, and environmental factors such as social support, family functioning, and schooling.
The duration of treatment for this chronic disorder also varies from individual to individual. Common short-
term goals for treatment usually include a reduction in target symptoms. Longer-term goals include
improvement in social and academic functioning, which may include a reduction in high-risk behaviors such
as substance abuse.
 FINDINGS
 Diagnosis requires a comprehensive psychiatric diagnostic evaluation. Screening tools are available
to detect symptoms of depression, particularly in adolescents. There are no well-established
laboratory tests for mood disorders.
 Mood disorders of childhood may occur in children of all ages. However, the risk of mood disorders
increases during adolescence, especially among girls. A younger age of onset is a risk factor for
increased severity and duration.
 While symptoms may wax and wane, mood disorders cause significant functional impairment that
often persist or recur through childhood and into adulthood.
 Mood disorders frequently co-occur with other mental disorders.
 There is evidence for the effectiveness of medication treatment and psychotherapies for mood
disorders. Improvements in functional impairments are enhanced with a combination of evidence-
based psychotherapy and medication.
 Bipolar disorder in children and youth is classified by the DSM-5 as a diagnosis distinct from
depression. Severe impairments in functioning are very common and frequently persist, even with
treatment.

Psychologists
Theories
Studies
Research Methods

1. Atypical Psychology

2. Depression
Psychological Theories of
Depression
By Saul McLeod, published 2015

Depression is a mood disorder which prevents individuals from leading a normal life, at
work socially or within their family. Seligman (1973) referred to depression as the
‘common cold’ of psychiatry because of its frequency of diagnosis.
Depending on how data are gathered and how diagnoses are made, as many as 27% of
some population groups may be suffering from depression at any one time (NIMH, 2001;
data for older adults).

Behaviorist Theory
Behaviorism emphasizes the importance of the environment in shaping behavior. The
focus is on observable behavior and the conditions through which individuals' learn
behavior, namely classical conditioning, operant conditioning and social learning theory.
Therefore depression is the result of a person's interaction with their environment.
For example, classical conditioning proposes depression is learned through associating
certain stimuli with negative emotional states.Social learning theory states behavior is
learned through observation, imitation and reinforcement.

Operant Conditioning
Operant conditioning states that depression is caused by the removal of positive
reinforcement from the environment (Lewinsohn, 1974). Certain events, such as losing
your job, induce depression because they reduce positive reinforcement from others (e.g.
being around people who like you).
Depressed people usually become much less socially active. In addition depression can also
be caused through inadvertent reinforcement of depressed behavior by others.
For example, when a loved one is lost, an important source of positive reinforcement has
lost as well. This leads to inactivity. The main source of reinforcement is now the sympathy
and attention of friends and relatives.
However this tends to reinforce maladaptive behavior i.e. weeping, complaining, talking of
suicide. This eventually alienates even close friends leading to even less reinforcement,
increasing social isolation and unhappiness. In other words depression is a vicious cycle in
which the person is driven further and further down.
Also if the person lacks social skills or has a very rigid personality structure they may find
it difficult to make the adjustments needed to look for new and alternative sources of
reinforcement (Lewinsohn, 1974). So they get locked into a negative downward spiral.

Critical Evaluation
Behavioral/learning theories makes sense in terms of reactive depression, where there is a
clearly identifiable cause of depression. However, one of the biggest problems for the
theory is that of endogenous depression. This is depression that has no apparent cause (i.e.
nothing bad has happened to the person).
An additional problem of the behaviorist approach is that it fails to take into account
cognitions (thoughts) influence on mood.
Psychodynamic Theory
During the 1960's psychodynamic theories dominated psychology and psychiatry.
Depression was understood in terms of:
1. inwardly directed anger (Freud, 1917),
2. introjection of love object loss,
3. severe super-ego demands (Freud, 1917),
4. excessive narcissistic, oral and/or anal personality need (Chodoff, 1972),
5. loss of self-esteem (Bibring, 1953; Fenichel, 1968), and
6. deprivation in the mother child relationship during the first year (Kleine, 1934).

Freud’s psychoanalytic theory is an example of the psychodynamic approach. Freud (1917)

prosed that many cases of depression were due to biological factors. However, Freud also
argued that some cases of depression could be linked to loss or rejection by a parent.
Depression is like grief, in that it often occurs as a reaction to the loss of an important
relationship.
However, there is an important difference, because depressed people regard themselves as
worthless. What happens is that the individual identifies with the lost person, so that
repressed anger towards the lost person is directed inwards towards the self. The inner
directed anger reduces the individual’s self-esteem, and makes him/her vulnerable to
experiencing depression in the future.
Freud distinguished between actual losses (e.g. death of a loved one) and symbolic losses
(e.g. loss of a job). Both kinds of losses can produce depression by causing the individual to
re-experience childhood episodes when they experienced loss of affection from some
significant person (e.g. a parent).
Later, Freud modified his theory stating that the tendency to internalize loss objects is
normal, and that depression is simply due to an excessively severe super-ego. Thus, the
depressive phase occurs when the individual’s super-ego or conscience is dominant. In
contrast, the manic phase occurs when the individual’s ego or rational mind asserts itself,
and s/he feels control.
In order to avoid loss turning into depression, the individual needs to engage in a period of
mourning work, during which s/he recalls memories of the lost one. This allows the
individual to separate him/herself from the lost person, and so reduce the inner-directed
anger. However, individuals very dependent on others for their sense of self-esteem may be
unable to do this, and so remain extremely depressed.
Critical Evaluation
Psychoanalytic theories of depression have had a profound impact on contemporary
theories of depressions. For example, Beck's (1983) model of depression was influenced by
psychoanalytic ideas such as the loss of self-esteem (re: Beck's negative view of self), object
loss (re: the importance of loss events), external narcissistic deprivation (re:
hypersensitivity to loss of social resources) and oral personality (re: sociotropic
personality).
However, although being highly influential, psychoanalytic theories are difficult to test
scientifically. For example, many of its central features cannot be operationally defined
with sufficient precision to allow empirical investigation. Mendelson (1990) concluded his
review of psychoanalytic theories of depression by stating:
'A striking feature of the impressionistic pictures of depression painted by many writers
is that they have the flavor of art rather than of science and may well represent
profound personal intuitions as much as they depict they raw clinical data' (p. 31).
Another criticism concerns the psychanalytic emphasis on unconscious, intrapsychic
processes and early childhood experience as being limiting in that they cause clinicians to
overlook additional aspects of depression. For example, conscious negative self-
verbalisation (Beck, 1967), or ongoing distressing life events (Brown & Harris, 1978).

Cognitive Approach
This approach focuses on people’s beliefs rather than their behavior. Depression results
from systematic negative bias in thinking processes.
Emotional, behavioral (and possibly physical) symptoms result from cognitive
abnormality. This means that depressed patients think differently to clinically normal
people. The cognitive approach also assumes changes in thinking precede (i.e. come
before) the onset of depressed mood.

Beck's (1967) Theory

One major cognitive theorist is Aaron Beck. He studied people suffering from depression
and found that they appraised events in a negative way.
Beck (1967) identified three mechanisms that he thought were responsible for depression:
1. The cognitive triad (of negative automatic thinking)
2. Negative self schemas
3. Errors in Logic (i.e. faulty information processing)
The cognitive triad are three forms of negative (i.e. helpless and critical) thinking that
are typical of individuals with depression: namely negative thoughts about the self, the
world and the future. These thoughts tended to be automatic in depressed people as they
occurred spontaneously.
For example, depressed individuals tend to view themselves as helpless, worthless, and
inadequate. They interpret events in the world in a unrealistically negative and defeatist
way, and they see the world as posing obstacles that can’t be handled. Finally, they see the
future as totally hopeless because their worthlessness will prevent their situation
improving.

As these three components interact, they interfere with normal cognitive processing,
leading to impairments in perception, memory and problem solving with the person
becoming obsessed with negative thoughts.
Beck believed that depression prone individuals develop a negative self-schema. They
possess a set of beliefs and expectations about themselves that are essentially negative and
pessimistic. Beck claimed that negative schemas may be acquired in childhood as a result
of a traumatic event. Experiences that might contribute to negative schemas include:
 Death of a parent or sibling.
 Parental rejection, criticism, overprotection, neglect or abuse.
 Bullying at school or exclusion from peer group.

However, a negative self-schema predisposes the individual to depression, and therefore

someone who has acquired a cognitive triad will not necessarily develop depression. Some
kind of stressful life event is required to activate this negative schema later in life. Once the
negative schema are activated a number of illogical thoughts or cognitive biases seem to
dominate thinking.
People with negative self schemas become prone to making logical errors in their
thinking and they tend to focus selectively on certain aspects of a situation while ignoring
equally relevant information.
Beck (1967) identified a number of systematic negative bias' in information processing
known as logical errors or faulty thinking. These illogical thought patterns are self-
defeating, and can cause great anxiety or depression for the individual. For example:
1. Arbitrary Inference. Drawing a negative conclusion in the absence of
supporting data.
2. Selective Abstraction. Focusing on the worst aspects of any situation.
3. Magnification and Minimisation. If they have a problem they make it appear
bigger than it is. If they have a solution they make it smaller.
4. Personalization. Negative events are interpreted as their fault.
5. Dichotomous Thinking. Everything is seen as black and white. There is no in
between.

Such thoughts exacerbate, and are exacerbated by the cognitive triad. Beck believed these
thoughts or this way of thinking become automatic. When a person’s stream of automatic
thoughts is very negative you would expect a person to become depressed. Quite often
these negative thoughts will persist even in the face of contrary evidence.

Critical Evaluation
Alloy et al. (1999) followed the thinking styles of young Americans in their early 20’s for 6
years. Their thinking style was tested and they were placed in either the ‘positive thinking
group’ or ‘negative thinking group’. After 6 years the researchers found that only 1% of the
positive group developed depression compared to 17% of the ‘negative’ group. These
results indicate there may be a link between cognitive style and development of depression.
However such a study may suffer from demand characteristics. The results are also
correlational. It is important to remember that the precise role of cognitive processes is yet
to be determined. The maladaptive cognitions seen in depressed people may be a
consequence rather than a cause of depression.

Learned Helplessness
Martin Seligman (1974) proposed a cognitive explanation of depression called learned
helplessness. According to Seligman’s learned helplessness theory, depression occurs when
a person learns that their attempts to escape negative situations make no difference.
As a consequence they become passive and will endure aversive stimuli or environments
even when escape is possible.
Seligman based his theory on research using dogs.

A dog put into a partitioned cage learns to escape when the floor is electrified. If the dog is
restrained whilst being shocked it eventually stops trying to escape.
Dogs subjected to inescapable electric shocks later failed to escape from shocks even when
it was possible to do so. Moreover, they exhibited some of the symptoms of depression
found in humans (lethargy, sluggishness, passive in the face of stress and appetite loss).
This led Seligman (1974) to explain depression in humans in terms of learned helplessness,
whereby the individual gives up trying to influence their environment because they have
learned that they are helpless as a consequence of having no control over what happens to
them.
Although Seligman’s account may explain depression to a certain extent, it fails to take into
account cognitions (thoughts). Abramson, Seligman, and Teasdale (1978) consequently
introduced a cognitive version of the theory by reformulating learned helplessness in term
of attributional processes (i.e. how people explain the cause of an event).
The depression attributional style is based on three dimensions, namely locus (whether the
cause is internal - to do with a person themselves, or external - to do with some aspect of
the situation), stability (whether the cause is stable and permanent or unstable and
transient) and globalor specific (whether the cause relates to the 'whole' person or just
some particular feature characteristic).
In this new version of the theory, the mere presence of a negative event was not considered
sufficient to produce a helpless or depressive state. Instead, Abramson et al. argued that
people who attribute failure to internal, stable, and global causes are more likely to become
depressed than those who attribute failure to external, unstable and specific causes. This is
because the former attributional style leads people to the conclusion that they are unable
to change things for the better.

Critical Evaluation
Gotlib and Colby (1987) found that people who were formerly depressed are actually no
different from people who have never been depressed in terms of their tendencies to view
negative events with an attitude of helpless resignation.
This suggests that helplessness could be a symptom rather than a cause of depression.
Moreover, it may be that negative thinking generally is also an effect rather than a cause of
depression.

Humanist Approach
Humanists believe that there are needs that are unique to the human species. According
to Maslow (1962) the most important of these is the need for self-actualization (achieving
out potential). The self actualizing human being has a meaningful life. Anything that blocks
our striving to fulfil this need can be a cause of depression. What could cause this?
1. Parents imposing conditions of worth on their children. I.e. rather than accepting
the child for who s/he is and giving unconditional love, parents make love conditional
on good behavior. E.g. a child may be blamed for not doing well at school, develop a
negative self-image and feel depressed because of a failure to live up to parentally
imposed standards.
2. Some children may seek to avoid this by denying their true self and projecting an
image of the kind of person they want to be. This façade or false self is an effort to
please others. However the splitting off of the real self from the person you are
pretending to be causes hatred of the self. The person then comes to despise
themselves for living a lie.
3. As adults self actualization can be undermined by unhappy relationships and
unfulfilling jobs. An empty shell marriage means the person is unable to give and
 receive love from their partner. An alienating job means the person is denied the
opportunity to be creative at work.

Download this article as a PDF

References
Abramson, L. Y., Seligman, M. E., & Teasdale, J. D. (1978). Learned helplessness in
humans: critique and reformulation. Journal of abnormal psychology, 87(1), 49.
Alloy, L. B., Abramson, L. Y., Whitehouse, W. G., Hogan, M. E., Tashman, N. A., Steinberg,
D. L., ... & Donovan, P. (1999). Depressogenic cognitive styles: Predictive validity,
information processing and personality characteristics, and developmental
origins. behavior research and therapy, 37(6), 503-531.
Beck, A. T. (1967). Depression: Causes and treatment. Philadelphia: University of
Pennsylvania Press.
Beck, A. T., Epstein, N., & Harrison, R. (1983). Cognitions, attitudes and personality
dimensions in depression. British Journal of Cognitive Psychotherapy.
Bibring, E. (1953). The mechanism of depression.
Brown, G. W., & Harris, T. (1978). Social origins of depression: a reply. Psychological
Medicine, 8(04), 577-588.
Chodoff, P. (1972). The depressive personality: A critical review. Archives of General
Psychiatry, 27(5), 666-673.
Fenichel, O. (1968). Depression and mania. The Meaning of Despair. New York: Science
House.
Freud, S. (1917). Mourning and melancholia. Standard edition, 14(19), 17.
Gotlib, I. H., & Colby, C. A. (1987). Treatment of depression: An interpersonal systems
approach. Pergamon Press.
Klein, M. (1934). Psychogenesis of manic-depressive states: contributions to
psychoanalysis. London: Hogarth.
Lewinsohn, P. M. (1974). A behavioral approach to depression.
Maslow, A. H. (1962). Towards a psychology of being. Princeton: D. Van Nostrand
Company.
National Institute of Mental Health. (2001). Depression research at the National Institute
of Mental Health. Retrieved
from http://www.nimh.nih.gov/health/publications/depression/complete-index.shtml.
Seligman, M. E. (1973). Fall into helplessness. Psychology today, 7(1), 43-48.
Seligman, M. E. (1974). Depression and learned helplessness. John Wiley & Sons.
Further Information
Abnormal Psychology CBTA-level Psychology Psychopathology Revision
NotesPsychoanalysisMedical Model of AbnormalityBehavioral TherapyCognitive
TherapyList of Support GroupsCampaign against Living MiserablyMen do cry: one man’s
experience of depressionNHS Self Help Guides
Download this article as a PDF

How to reference this article:

McLeod, S. A. (2015, Jan 14) Psychological theories of depression. Retrieved from
https://www.simplypsychology.org/depression.html

Home | About | A-Z Index | Privacy Policy | Contact Us

Back to top

This workis licensed under a Creative Commons Attribution-Noncommercial-No

Derivative Works 3.0 Unported License.
Company Registration no: 10521846
Print Download
Article Content
Behaviorist Theory Psychodynamic TheoryCognitive TheoryHumanistic TheoryReferences