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The analytical rumination hypothesis presents depression as an evolutionary response which causes the focalization of attention toward the analysis of the complex problems faced by the depressed individual. Analytical rumination is self-reflective and gives the depression-activating problem prioritized access to processing resources, thereby decreasing the individual's participation in those activities that would otherwise be distracting.

Background
The analytical rumination hypothesis is an extension of the psychic pain hypothesis which is also an evolutionary explanation of depression.

Depression is thought to be an illness that causes much mental pain and distress, as does physical pain, and physical pain is unarguably an evolved function. It motivates withdrawal from the source of the pain and teaches avoidance of similar pain-eliciting situations in the future. The psychic pain hypothesis argues that like physical pain, depression alerts the sufferer to a threat to biological fitness, and motivates the sufferer to halt those activities that lead to the threatening situation. While proponents of the psychic pain hypothesis focus mostly on low mood and regard clinical depression as an extreme of low mood that is dysfunctional, proponents of the analytical rumination hypothesis may view much of major clinical depression as functional.

Major proponents of the analytical rumination hypothesis include Paul W. Andrews and J. Anderson Thomson who, in 2009, published a large and extensive psychological review which presents both theoretical arguments and empirical evidence for the hypothesis.



Theoretical perspective
The analytical rumination hypothesis specifically defines depression as an adaptive stress response mechanism that: is caused by problems that are analytically difficult and related to important fitness related goals,  promotes enduring analysis, or rumination, of the triggering problem by coordinating changes in body systems, assists the affected individual in the generation and evaluation of potential solutions to the problem causing the depression, and causes cognitive resource trade-offs with other goals to advance analysis of the triggering problem.

Depressed affect as activated by complex problems
A complex problem can be viewed as an analytically difficult problem, especially as it is seen to be related to important fitness-related goals, for example, in the case of social dilemmas. One solves an analytic problem by breaking it up into smaller parts that are more easily studied. This involves paying greater attention to detail and processing more slowly and methodically.

Effective psychotherapies for depression, which are often just as, if not more, effective than medication, and unlike medication, have enduring effects even after treatment has stopped, often help the depressed individual identify and attempt to solve the problems that caused their depression. Being able to address the cause of depression instead of just the symptoms, and this leading to better long-term outcomes, suggests that the cause of depressive episodes is not the negative cognitions, but the problems that people have so much difficulty solving on their own.

Social dilemmas have an analytical structure in that the goals involved tend to work against each other, as in the case of pursuing self-interest, while trying to maintain cooperative bonds. There is some evidence suggesting that social dilemmas tend to cause depression. For example, many of the problems faced by depressed people are social in nature and conflict of the interpersonal variety is frequently associated with depression. The fact that conflict with close social partners, that the depressed individual has an otherwise cooperative and helpful relationship with, is also associated with higher levels of depression suggests that it is difficult social dilemmas that are tending to cause depression.

Avoidable stressors pose the problem of understanding how to prevent them in the future – attaining this type of understanding, particularly in the case of social problems, often requires upward counterfactual thinking, which in turn requires analysis. This type of thinking helps the individual focus on how a situation could have turned out differently, and better, if different actions had been taken. Negative affect has been shown to trigger upward counterfactual thinking, and exposure to avoidable stressors does appear to trigger depression.

Sustained analysis is promoted by changes in the body system coordinated by depression
The analytical rumination hypothesis predicts that depression coordinates body system changes which encourage or trigger an analytical problem solving approach, specifically to deal with the complex problems which are causing the depression. Two rumination factors, both which involve analysis, have been identified in depression, problem analysis or reflection, and counterfactual analysis or brooding. Key to sustaining rumination is maintaining its high working memory load. Doing so require greater attentional control – this control is regulated by the left ventrolateral prefrontal cortex (VLPFC), as well as serotonin (5-HT), and the 5-HT1A receptor which is a subtype of 5-HT receptor that binds serotonin.

Three types of body system changes in depression that promote analysis by reducing the disruption of information in working memory are the enhancement of attentional control, anhedonia, and psychomotor changes.

The claim that depression enhances attentional control is supported by consistent findings of neuroimaging studies that have found that depressed affect usually shows a high neuroimaging signal in the VLPFC, the same region activated during processing that necessitates high working memory loads, such as analysis. Further, depression may also coordinate processes in the brain that sustain neural firing in the VLPFC, as well as decrease apoptosis there. No studies in humans currently exist that show this, but studies of behavioural depression in rats support this claim. Apoptosis may also be reduced by sustained serotonin transmission, but this conflicts with the view that depression in humans is characterized by low brain serotonin. This claim appears to be based on circumstantial evidence and Andrews and Thomson, in their 2009 paper, in support of the analytical rumination hypothesis, argue that it is more plausible that serotonin is high in depression. Their evidence comes from studies with rats which clearly show that behavioural depression results in sustained serotonin transmission, studies which study the genetic factors influencing high levels of synaptic serotonin, studies of jugular blood in participants with major depression which show higher overflow a neuronal metabolite of serotonin, and postmortem studies.

It appears that no research which specifically tests whether depressed people with higher levels of anhedonia experience less interrupted rumination currently exists. There is some indirect support which indicates that individuals who score high on anhedonia have a decrease in the amplitude of the P300 event-related potentials of ERP signals. This type of decrease is frequently viewed as evidence of a highly focused state of attention.

A decrease in the interruption of analysis through psychomotor changes in the depressed individuals is also quite plausible. Depressed individuals often prefer solitude, feel fatigued, and experience changes in appetite and sleep patterns. Such symptoms can be viewed as reducing exposure to distracting stimuli. For example, it has been reported that people who ruminate more tend to see a reduction in the amount they sleep. Neurobiological evidence also suggests cognitive processing can be disrupted by oral activity. Psychomotor retardation should also be associated positively with rumination as motor activity does require cognitive resources. Research does show that psychomotor retardation is positively related to problems paying attention to cognitive tasks in the laboratory.

Depressive rumination assists in resolving the triggering problem
This is not a claim that has been tested thouroughly, but one experiment does somewhat directly address it, and other evidence exists that supports it.

In a mood induction experiment, which tested how carefully investment opportunities were analyzed, sad participants made the most accurate decisions, followed by neutral and happy participants.

Performance in social dilemma-type experiments is also better in depressed or sad mood participants. Greater information processing on cost and risks, as well as more context dependent behaviour is displayed by such participants. For example, in a study which used a modified prisoner's dilemma game, where people played against one other in dyads, depressed participants performed significantly better than control participants. This can be attributed to depressed participants being more sensitive to costs of cooperating than normal participants.

A peak and intensity in processing and insights were found to be associated with long-term improvements in terms of depressive outcomes, while a peak in avoidance was found to be associated with poorer long-term outcomes. Interestingly the processing peak was also associated with a drastic rise of depressive symptoms; the temporary increase was actually viewed as a positive and as part of growth in the treatment. While this evidence is correlational, other controlled experiments that were longitudinal and used subclinical and outpatient samples reported that the expressive writing about emotionally heavy matters helped resolve depressive symptoms over time.

Why laboratory task performance is reduced by depressive rumination
Fewer autobiographical and more overgeneral memories are recalled by depressed individuals in response to cue words, in comparison to control participants. When depressed individuals were first given a distracting task, such as thinking of a black umbrella, their performance improved to the level of control participants'. Distracting depressed individuals from their ruminations allows them to use those cognitive resources tied up by the ruminations to perform normally on the laboratory task at hand. Since studies which show that depressed individuals, perform more poorly on problem-solving and other cognitive laboratory tasks do not account for the fact that these individuals are using some of the cognitive resources to ruminate about other things in the meanwhile, these studies are unable to prove that general cognitive processing in depressed individuals is worse than that of control individuals or that depressed people would be worse at solving the problems about which they are ruminating because of the depressed affect.

Paradoxical findings
The following are three examples of paradoxical findings of the effects of depression on cognition that can be explained by the analytical rumination hypothesis.

1. Depression is associated with both persistent ruminations and with difficulty concentrating.

As processing priority will be given to problems that are related to the depressive episode, fewer resources will be left for other things, explaining the difficulty concentrating, as well as the persistent ruminations.

2. Depressed affect fosters an analytical processing style which increases performance on a variety of cognitive tasks, but also causes performance reduction on many cognitive laboratory tasks.

When do depressed individuals show enhanced performance on laboratory tasks - when the task has an analytical structure to it. A good example is the judgement of control task in which depressed individuals outperform control participants, as well as zero contingency situations in which subclinically and experimentally induced depressed participants outperformed normal participants. It appears that depressed people have a tendency to perform better at more difficult tasks – where long intervals increase working memory demands and the need for attentional control is high. Depressed individuals also show more rational decision-making, where the systematic evaluation of options is important, and the highly analytical processing style therefore comes into play. This extends to complex economic experiments, assessment of health risks and social dilemmas. Literature which examines how depressed individuals perceive facial expression and emotions suggests that depressed individuals may be less accurate at identifying different facial expressions. It appears though, that this only true when anxiety is not controlled for, when exposure to the stimuli is very brief, and when quick judgements are required from participants that allow for very little processing. Subclinical participants showed better interpretation of facial cues related to emotion than controls when the cues were subtle and attention to detail and analysis were important to the interpretation.

3. Depending on the procedure used to induce depressed affect, performance on the experimental tasks with an analytical component are affected differentially – sometimes enhanced and sometimes reduced.

This can be explained by the qualitatively different methods used to induce depressed affect. Self-referent methods, where participants read statements for example, that result in them interpreting their current situation in life in negative, depressing ways, lead participants to imagine that they have complex and important problems in their lives. This in turn causes off-task rumination which lowers task performance by taking up the limited cognitive resources that would otherwise be used to enhance performance on the laboratory task. Those experiments which showed that depressed affect increases task performance of analytically difficult tasks, seemed mostly to use sad music or film clips to induce the sad mood. Since this does not cause individuals to ruminate about the problems they imagine they have, task performance is not impacted negatively and participants perform better.