Critically evaluate theories of causation of depression. This essay explores two of the main theories of causation of depression, which are the

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1 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

2 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

3 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.

4 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

5 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

6 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.

7 Resources American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Retrieved from: doi: /appi.books Dykman, B. M. (1998). Integrating Cognitive and Motivational Factors in Depression. Journal of Personality and Social Psychology, 74(1). Retrieved from: doi: / Eshel, N., & Roiser, J. P. (2010). Reward and Punishment Processing in Depression. Biological Psychiatry, 68(2). Retrieved from: doi: /j.biopsych Haaga, D. A. F., Dyck, M. J., & Ernst, D. (1991). Empirical Status of Cognitive Theory of Depression. Psychological Bulletin, 110(2). Retrieved from: doi: / Krishnan V., & Nestler E. J. (2008). The molecular neurobiology of depression. Nature, 455(7215). Retrieved from: doi: /nature 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: /journal.pmed 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: /j.pnpbp 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: /j.brat