My picture on Depression

What is depression?

Beck's Cognitive Theory of Depression Features Underlying Dysfunctional Beliefs

Beck's main argument was that depression was instituted by one's view of oneself, instead of one having a negative view of oneself due to depression. This has large social implications of how we as a group perceive each other and relate our dissatisfactions with one another. Abela and D'Alessandro's (2002) study on college admissions is a good example of this phenomenon. In their study they found that the student's negative views about their future strongly controlled the interaction between dysfunctional attitudes and the increase in depressed mood. The research clearly backed up Beck's claim that those at risk for depression due to dysfunctional attitudes who did not get into their college of choice then doubted their futures, and these thoughts lead to symptoms of depression. Therefore, the students' self-perceptions became negative after failing to get into college, and many showed signs of depression due to this thinking. Other aspects of this study did not match up well with Beck.

They elaborate: "As for participants' more enduring mood reactions, our findings are incongruent with Beck's...theory.... Therefore, one possible explanation of discrepancies between these studies is that immediately following the occurrence of a negative event, cognitively vulnerable individuals show marked increases in depressed mood. At the same time, the do not yet exhibit increases in other symptoms of depression.... However, in vulnerable individuals…such depressed mood may be to be accompanied by a host of other depressive symptoms.... Their level of depressed mood, however, was simply not more severe than individuals who did not possess dysfunctional attitudes" (Abela & D'Allesandro, 2002, p.122). What occurred is that the requirements, according to Beck, for depressive symptoms were there but they did not occur regardless. Findings like this show that Beck's theory may not be as complete as we would like, and there is likely to be factors which are unaccounted for in play in situations like this.

http://www.personalityresearch.org/papers/allen.html

Environmental Theory Depression

Environmental causes of depression are concerned with factors that are outside of ourselves. They are not directly related to brain function, inherited traits from parents, medical illnesses, or anything else that may take place within us. Instead, environmental events are those things that happen in the course of our everyday lives. These may include situations such as prolonged stress at home or work, coping with the loss of a loved one, or traumatic events. Sometimes researchers refer to these as sociological or psychosocial factors since they bring together events that happen out in society with the inner workings of a person's mind.


It has long been understood that experiences we have in our lives can affect our state of mind. The relationships we have with others, how we are brought up, losses we have, and crises we encounter all may affect our thoughts, emotions, and behaviors. How we react to these environmental events may influence the development of clinical depression.

http://www.allaboutdepression.com/cau_04.html

Biological Theory of Depression

There have been a variety of theories concerning the neurobiologic etiology of depression. The classic biogenic amine theory of depression suggests that a shortage of noradrenalin (NA) and serotonin (5-HT) in the synaptic clefts is the neurobiological basis of depression (Schildkraut 1965, Bunney & Davis 1965, Coppen 1967). Although the serotonin system is still the most widely studied system, there is evidence suggesting that other neurotransmitter systems also play important roles (Barros et al. 2002). It is suggested that instead of being a consequence of a simple decrease in some crucial cerebral transmitter concentrations depression may be the result of a disturbed balance between different regulatory systems and consequent transmitter overactivity in some brain regions (Syvälahti 1994). According to a hypothesis by Harro & Oreland (1996) the neurobiological starting-point of depression lies in the malfunction of the noradrenergic innervation from the locus coeruleus, which, in turn, leads to dysregulation of serotonergic and dopaminergic neurotransmission. A molecular and cellular theory of depression posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, the neurotrophic factors necessary for the survival and function of particular neurons (Duman et al. 1997).


As reviewed by Sheline (2000), there is increasing evidence for structural brain changes associated with major depression. Brain changes associated with early-onset major depression have been reported in the hippocampus, amygdala, caudate nucleus, putamen, and frontal cortex, which structures are extensively interconnected. Furthermore, several studies utilizing the magnetic resonance imaging (MRI) technology have reported losses of left and right hippocampal volumes in subjects with a history of severe recurrent depression. (Sheline 2000.) Moreover, functional neuroimaging studies have identified abnormal blood flow in the medial prefrontal cortex in patients with depression. The medial prefrontal cortex is a region where activity is crucially modulated by the neurotransmitters believed to be implicated in depression. (For a review, see Elliott 1998.) Depression is often accompanied by certain biological alterations, which may well explain the comorbidity of depression and various diseases. The corticosteroid overdrive and noradrenergic hyperactivity present in depression may impair the normal functions of the immune system (Syvälahti 1994).

http://herkules.oulu.fi/isbn9514270215/html/x294.html