Depression is an emotional mental state that, at normal levels, can be described as an overall low mood. When it occurs as an expected reaction to life stressors, it is part of the everyday ups and downs of the human experiences. In some cases, depression can occur at a level that impairs daily functioning, relationships, and general health habits. It is characterized by problems with concentration, decreased energy, feelings of hopelessness or guilt, pessimism, insomnia, irritability, excessive sleeping or problems seeing, loss of interest in activities that were once pleasurable, weight gain or loss, physical symptoms, and thoughts of suicide (APA, 2010).

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Cognitive Causes of Depression

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While there are many ideas about what causes depression, the main theories involve a physiological process in which the balance of neurotransmitters in the brain becomes unbalanced. This imbalance then produces the signs and symptoms above. However, medical researchers have recognized the relationship between negative thoughts and the resulting changes in the brain’s neurochemistry. The question is one of which comes first. Does the neurochemical change produce the negative mindset present in depression or does the chemical change occur on its own and thus produce the negative mindset?

A cognitive theory of depression
A cognitive model of treatment for depression has large research base that has implications to a causative model as well. The prominent theorist of a cognitive model of depression is Aaron Beck. His cognitive theory states that the symptoms of depression are produced when an individual attributes circumstances and events through faulty or maladaptive attitudes and belief systems. Beck’s research of individuals with varying levels of depression demonstrated the presence of depressive cognitions preceding the symptoms of depression. Some of these themes that were not as evident among individuals without depression included thoughts of deprivation, low self-image, and exaggeration of problems and difficulties, and desires to run away or die (Butler, Chapman, Forman, Beck, 2006).

Individuals who are depressed, according to Beck’s research, display the “cognitive triad” which consists of negative views of the world, their future, and themselves. Secondly, individuals who are depressed not only have negative thoughts but also patterns thoughts and beliefs that are dysfunctional. These schema lead to errors in thinking that produce an excessively negative and unrealistic view of reality. Beck saw a relationship between the way in which one processes emotions and behaviors and the way in which the individual interprets or places meaning on the event. The level of psychological distress one experiences in dependent upon personality which reflects schemas, the person’s unique cognitive structure, and other genetically acquired traits (Wright, 2006).

The cognitive triad and schema
As mentioned, the cognitive triad is a pattern of negative thoughts. These thoughts reflect a view of oneself as being inadequate, a view of the world that sees the environment as inadequate and defeating, and a view of the future that foresees and continuing pattern of difficulty and suffering. These negative views flavor the person’s perceptions of their experiences and help to establish a negative mood that is interlinked with the biochemical reaction in the brain noted by biomedical researchers. The individual’s schemas or beliefs/attitudes about his situation are developed while experiencing stressors and other life experiences. Beck’s model incorporates a cognitively-oriented form of psychotherapy that places a heavy emphasis on cognitively challenging the beliefs and schemas through testing various hypotheses. The therapist assists the client in developing alternative ways of interpreting their situation (Wright, 2006).

Cognitive behavioral therapies such as that proposed by Beck have become the evidence-based treatments for most mental health problems (Bukh, Bock, Vinberg, Werge, Gether, & Vedel Kessing, 2009).. These approaches challenge the meaning of emotions and place the power for changing them into the hands of the client. Beck and his predecessors do not challenge recent medical findings that have gained validity through the recent improvements in brain imaging and other neuroscience technologies. In fact, they have updated their theories to incorporate these findings.

Beck’s cognitive theory of forty years ago (1967) was updated in 2008 to include recent research into the biological factors that impact depression. Beck argues that depression is produced by a variety of factors including genetics and neurochemical causes that have been more recently identified through the use of modern brain imaging and other technical processes. Whereas neuroscience has produced a strong case regarding the physiological aspects of depression, Beck (2008) highlights other neurobiological factors that also explain the cognitive aspects of depression. For example, studies have indicated that an overly active amygdala is related to the development of a predisposition toward negative viewpoints and outlooks. These patterns, as highlighted in older versions of cognitive theory, can become an underlying cause of depression. Other research indicates that increased activity level in the amygdala coupled with an underactive prefrontal lobe is related to reduced cognitive analyses of situations which contributes to depression. Therefore, Beck concluded that the main biological contributor to depression is the individual’s predisposition to create negative schema and dysfunctional interpretations of the environment and circumstances.

There is little doubt that there is a relationship between one’s cognitions and a depressed mood. There is also little doubt that some individuals are more prone to develop depression as the result of genetically carried predispositions or their environment. However, these relationships in and of themselves do not necessarily make an airtight case for causation. Many proponents of a biomedical model of depression point to the effectiveness of medication in treating depression and therefore determine that the cause must be biological. The problem is that there is no way to absolutely investigate the nature of a person’s thoughts, the time they occur, or the direct relationship between the thought and the biochemical reaction. Medical findings on the neurochemical basis of depression do not refute Beck’s premises. They may instead add support and credence to the idea that negative thinking can indeed produce the objective signs that are identified with depression.

  • Beck. A. T. (2008). The evolution of the cognitive model of depression and its
    neurobiological correlates. American Journal of Psychiatry, 165, 969–977 
  • Butler, Andrew C., Chapman, Jason E., Forman, Evan M., Beck Aaron T., (2006). The empirical
    status of cognitive-behavioral therapy: A review of meta-analyses, Clinical Psychology
    Review 26 (2006) 17– 31.
  • Bukh, J.D., Bock, C., Vinberg, M., Werge, T., Gether, U., Vedel Kessing, L. (2009). Interaction
    between genetic polymorphisms and stressful life events in first episode depression.
    Journal of Affective Disorder, 119(1-3), 107-115.
  • Wright, J.H. (2006). Cognitive Behavior Therapy: Basic Principles and Recent Advances.
    FOCUS, 4, 173-178.