What is the etiology of depression (Major Depressive Disorder)?

Learned helplessness explains the etiology of depression

Question: What is the etiology of depression (Major Depressive Disorder)?
Position‹2 of 3›: Depression has a cognitive etiology
Argument‹2 of 2: Learned helplessness explains the etiology of depression

According to the theory of learned helplessness, 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 environments, even when escape is possible.

The argument

Martin Seligman proposed a cognitive explanation of depression called learned helplessness in 1974. Learned helplessness occurs when an individual continuously faces a negative, uncontrollable situation and stops trying to change their circumstances, even when they can do so. Seligman based this theory on experiments conducted on dogs. When dogs were subjected to mild electric shock delivered through the floor of their housing but had access to a partitioned area, escape was possible by crossing over to the shock-free area. When restrained, however, and escape was no longer possible, they eventually stopped attempting to escape. When subjected to repeated inescapable shocks in this way, they failed to escape even when it was later possible to do so. They also exhibited some symptoms associated with depression in humans, such as loss of appetite. Abramson, Seligman, and Teasdale (1978) reformulated this hypothesis. They included a cognitive process whereby an individual could attribute the cause for an event. The attribution model is based on three causal dimensions: whether the cause is internal or external to the individual, whether the cause is stable and permanent or transient in nature, and whether it is global or specific. Abramson et al. argued that people who attributed failure to internal, stable, and global causes were more likely to become depressed. This is because they would conclude that they could not influence or control the situation for the better. Abramson, Metalsky, and Alloy (1989) further revised the model, integrating Beck’s theory with a reformulated learned helplessness model to derive the ‘hopelessness theory of depression’. The theory considers depression to arise when people with a negative attributional style interpret a stressful life event negatively. These interpretations give rise to hopelessness, an immediate cause of depression.

Premises

[P1]Seligman's learned-helplessness theory holds that repeatedly facing uncontrollable negative situations leads people (and, in his experiments, dogs) to stop trying to escape even when escape becomes possible, mirroring symptoms of human depression. [P2] Later reformulations added attributional style, arguing that people who attribute failure to internal, stable, and global causes fall into the hopelessness that immediately precedes depression. [C] Depression has a cognitive etiology, which learned helplessness helps explain.

Counter-arguments

This theory presents helplessness/hopelessness as a cause of depression. However, whether they are symptoms (or manifestations) rather than a cause of depression remains unclear. Gotlib and Colby (1987) found that people who were formerly depressed are 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. Additionally, it may be that negative thinking generally is also an effect rather than a cause of depression.

Rejecting the premises

[Rejecting P1] The animal work established that uncontrollable aversive events produce passivity, which is a model of one feature of depression rather than of the disorder, and the inference from restrained dogs to a human condition defined by mood, cognition and self-evaluation is the step most in need of support. [Rejecting P2] Attributional style faces the direction-of-causation problem the theory was reformulated to escape but did not: measured during an episode it may be an effect rather than a cause, and the finding that formerly depressed people do not differ from the never-depressed in attributional style is evidence against its being the standing vulnerability the account requires.