Download Candidate No.: 124338 Critically evaluate theories of

Candidate No.: 124338
Critically evaluate theories of causation of depression
This essay explores two of the main theories of causation of depression, which are the
cognitive model and the biological model. It gives a definition of depression, then looks at
these models to provide an idea of what causes the disorder. The first model examined is the
cognitive model, with a focus on Beck’s cognitive triad. Several studies are reviewed which
give evidence for this theory, regarding individuals’ negative views of themselves and the
future. This essay then gives criticisms of the cognitive model, such as the difficulty behind
determining if negative thinking is a cause or symptom. Next, this essay moves on to assess
the biological model of causation, emphasizing the function of the monoamine system. It
looks at several ways the monoamine system may affect a depressed individual’s brain
chemistry. Finally, this essay gives critique on the biological model, including its inability to
entirely explain the causes of depression and its oversimplification for the public.
Depression is the colloquial term for the mental disorder known as major depressive
disorder. Major depressive disorder is defined in the DSM-IV as a “depressed mood or a loss
of interest or pleasure in daily activities for more than two weeks”. The change in mood must
be in regards to the person’s baseline mood. For example, a person may have a very negative
personality, but if that is how they normally act, that does not mean they suffer from
depression. It must also impair either the person’s social, occupational, or educational
functioning, or a combination of the three. The DSM also lists specific symptoms that must
be present nearly every day, such as a decreased interest or pleasure in activities, change in
sleep patterns, feelings of worthlessness or inappropriate or excessive guilt, or thoughts of
death or suicide (American Psychiatric Association, 2000).
Researchers have suggested many causes for depression. One of the main theories of
causation of depression is the cognitive model. This theory focuses on the patient’s way of
thinking as the cause of their depression. Supporters of this theory argue that certain patterns
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of thought can lead to a person developing depression. These patterns of thinking are often
based on Beck’s cognitive triad, which states that individuals suffering from depression hold
negative views of the self, world, and future. These views create an encompassing pessimism
that shapes the individual’s actions and interpretations of the world around them. For
example, a person diagnosed with depression may feel excessive guilt because of their
distorted negative view of themselves, which could lead them to have a heightened sense of
their role in their own or others’ failures.
Another aspect of Beck’s cognitive triad that is altered in individuals diagnosed with
depression is their predictions of the future. People with depression have a very negative
outlook on the future, and do not believe that things will ever get better. This tendency is
shown in Strunk and Adler’s (2009) experiment with people’s predictions for the future. In
their experiment, Strunk and Adler asked participants to predict the likelihood of several
positive and negative events happening to them in the next month. At the end of the month,
the researchers then interviewed the participants to determine how many of the events had
actually happened. They found that participants who met the criteria for Major Depressive
Disorder had a much higher percentage of negative predictions, thus showing they had a
more negative bias towards future events. Even within the group of participants categorized
as depressed, individuals who had higher levels of depressive symptoms had more
pronounced negative bias. This shows that people who suffer from depression have a
negatively altered perception of the future, which holds with the cognitive model of
depression.
This negative view is ingrained in the way a person suffering from depression thinks.
This is supported by Wenzlaff and Bates (1998), who say that people at risk for depression
are more likely to produce negative statements, especially when their thought suppression is
undermined by a cognitive load. In their study, they asked participants to unscramble a
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number of sentences, which could form either positive or negative statements. The
participants were asked to unscramble as many sentences as they could in a short time, so
they could not go back to make any changes. Wenzlaff and Bates found that the individuals
who were previously diagnosed with depression were more likely to make the sentences form
negative statements, while individuals not suffering from depression were more likely to
form positive statements. This negative bias was pronounced when participants were asked to
remember a six-digit number, which produced a higher amount of negative statements in all
groups, especially those who were at risk for depression and engaged in thought suppression.
This validates the idea that negative biases are an important part of thinking in individuals
with depression and can lead to depressive symptoms.
One common aspect of depression is that, because they have such a negative view of
themselves, sufferers may look for validation from others. Generally, people diagnosed with
depression are validation oriented rather than goal oriented. This is because they have such a
poor outlook on the future that they believe they will fail at any goal they set for themselves.
Instead, they focus on support they get from other people. They hope that others will be able
to boost their self-esteem and assure them that they are worth something. This is shown in
Dykman’s (1998) study on validation oriented people as compared to goal oriented people.
Dykman tested how participants would act leading up to, during, and after a stressful event.
He found that validation seeking people are more likely to become more anxious in
anticipation of a stressful event, and have greater self esteem loss, task disengagement, and
depression after a negative event. This fits in with Beck’s model for depressive thinking, as
people diagnosed with depression have such a negative view of themselves and their future
actions, which is then perpetuated by their perceived failures. If they also believe others think
poorly of them, their depressive symptoms will only be further exacerbated.
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Although there are many studies that provide evidence for the cognitive theory of
causation for depression, there are many other researchers who disagree and find issues with
this model. One such issue is the difficulty of testing whether the negative thinking involved
in Beck’s cognitive triad is a cause of depression or a symptom (Haaga, Dyck, & Ernst,
1991). Because the majority of studies are conducted on individuals who have already been
diagnosed with depression, it is difficult to determine whether the person’s negative thinking
was present before their diagnosis. The only way to conclusively test if Beck’s cognitive triad
is truly causal is if researchers were to study thought patterns in individuals who have never
been diagnosed with depression before, and see if those individuals with negative thought
patterns are eventually diagnosed. However, this is highly impractical, as there is the
possibility that the individuals being studied will never be diagnosed, and therefore valuable
time and resources will have been wasted.
Another main theory of causation of depression is the biological model. This model
focuses on unusual brain structures or brain chemistry as the cause of depression. It argues
that there is something physically different in a person’s brain that would lead to them
developing the symptoms of depression. One main focus is on the monoamine system and
related neurotransmitters. The monoamine system includes the neurotransmitters dopamine,
norepinephrine, and serotonin. These neurotransmitters affect many different areas of the
brain, but they all play a role in the appearance of depressive symptoms.
One aspect of the monoamine system that may affect depression is the relation
between serotonin and norepinephrine. According to the permissive hypothesis, serotonin has
a controlling affect on norepinephrine, and can dampen or inhibit its uptake, therefore
altering the amount present in the brain. If there are low serotonin levels, the neurotransmitter
is not able to prevent the reuptake of norepinephrine, causing there to also be abnormally low
levels of norepinephrine. These low norepinephrine levels can lead to the development of the
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symptoms of depression, such as the dysregulation of emotion (Shah, Eisner, Farrell, &
Raeder, 1999).
The disrupted uptake of other neurotransmitters also plays a part in causing the onset
of depression. Catecholamines such as dopamine, along with norepinephrine and serotonin,
have an effect on an individual’s mood according to how much of the substance there is in a
person’s brain. If the level of dopamine in presynaptic stores is altered, leaving a deficiency
of the neurotransmitter, symptoms of depression may emerge. The decreased levels of
dopamine affect the way the brain communicates information about pleasurable experiences.
Because dopamine is involved in reward based behavior, a reduction of this substance would
cause patients diagnosed with depression to feel less pleasure in their activities or
environment (Sperner-Unterweger, Kohl, & Fuchs, 2014).
In a study by Eshel and Rosier (2010), the researchers found that depressed patients
have abnormal functioning in their frontostriatal systems modulated by the monoamine
systems. In comparison to individuals not diagnosed with depression, the brain structures
most affected by the neurotransmitters in the monoamine system, such as the striatum and
prefrontal cortex, responded differently to the effects of drugs that manipulated the levels of
monoamine neurotransmitters. This abnormal functioning leads people with depression to
react inappropriately to reward and punishment, with a maladaptive response to punishment
and hyposensitivity to reward. This makes them unable to use affective information to guide
their behavior, which may predispose them to developing depression.
One issue with the monoamine system aspect of the biological model is that it does
not entirely explain the onset of depression. Although many studies have found that an
imbalance of the neurotransmitters involved can effect the development of the symptoms of
depression, this only happens in individuals who have a history of major depressive disorder
in their families. A decrease in the concentration of monoamines in depressed patients may
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somewhat lower their mood, but it does not have an effect on the mood of healthy people.
Manipulating the levels of neurotransmitters in individuals without a history of depression
does not have any noticeable consequence on their mental health. This suggests that
deficiency in the monoamine system is not sufficient cause for depression to develop
(Krishnan & Nestler, 2008).
Another problem is that this model has been oversimplified to market to the general
public. In the United States, selective serotonin reuptake inhibitor (SSRI) antidepressants are
advertised directly to consumers. These marketing campaigns have revolved around the claim
that depression is caused by a “chemical imbalance” in a person’s brain. However, in reality
the causes are much more complicated. Much about the brain is unknown, and it is difficult
to truly understand how the numerous chemicals and neurotransmitters work together. It is
therefore almost impossible to simplify the process of the development of depression down to
a simple chemical imbalance. Some argue that this theory allows for too much potentially
harming misinformation (Lacasse & Leo, 2005).
This essay has examined two major theories of causation of depression. It first looked
at the cognitive model, with specific focus on Beck’s cognitive triad. It gave several
examples of studies that provided evidence for this theory, dealing with the negative thought
processes of individuals diagnosed with depression. Next, this essay critiqued the cognitive
model, relating the difficulty of determining if this negative pattern of thought is a cause or
symptom. This essay then focused on the biological model of causation, with special interest
in the monoamine system. It showed several ways that the neurotransmitters involved in the
system could affect the onset of depression. Finally, this essay gave criticisms against this
theory, such as it incomplete explanation of the cause of depression and its oversimplification
for the general audience.
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Resources
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental
disorders (4th ed., text rev.). Retrieved from:
doi:10.1176/appi.books.9780890423349.
Dykman, B. M. (1998). Integrating Cognitive and Motivational Factors in Depression.
Journal of Personality and Social Psychology, 74(1). Retrieved from:
doi:10.1037/0022-3514.74.1.139
Eshel, N., & Roiser, J. P. (2010). Reward and Punishment Processing in Depression.
Biological Psychiatry, 68(2). Retrieved from: doi:10.1016/j.biopsych.2010.01.027
Haaga, D. A. F., Dyck, M. J., & Ernst, D. (1991). Empirical Status of Cognitive Theory of
Depression. Psychological Bulletin, 110(2). Retrieved from: doi:10.1037/00332909.110.2.215
Krishnan V., & Nestler E. J. (2008). The molecular neurobiology of depression. Nature,
455(7215). Retrieved from: doi:10.1038/nature07455.
Lacasse J. R., & Leo J. (2005). Serotonin and Depression: A Disconnect between the
Advertisements and the Scientific Literature. PLoS Med 2(12). Retrieved from:
doi:10.1371/journal.pmed.0020392
Shah N., Eisner T., Farrell M., & Raeder C. (1999). An overview of SSRIs for the treatment
of depression. Journal of the Pharmacy Society of Wisconsin.
Sperner-Unterweger B., Kohl C., & Fuchs D. (2014). Immune changes and neurotransmitters:
Possible interactions in depression?. Progress in Neuro-Psychopharmacology and
Biological Psychiatry, 48. Retrieved from: doi:10.1016/j.pnpbp.2012.10.006
Strunk, D. R., & Adler, A. D. (2009). Cognitive biases in three prediction tasks: A test of the
cognitive model of depression. Behaviour Research and Therapy, 47(1). Retrieved
from: doi:10.1016/j.brat.2008.10.008