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According to the analytical rumination hypothesis depressed affect is an evolved response to complex problems.
Analytical rumination involves sustained analysis of the problem which triggered the depressive episode.

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.[1]

Background[edit]

The analytical rumination hypothesis is an extension of the psychic pain hypothesis which is also an evolutionary explanation of depression.[2]

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.[3][1]

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.[1]

The diagram Andrews and Thomson proposed, displaying causal relationships between key variables, for the analytical rumination hypothesis.

Theoretical perspective[edit]

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.[1]

Depressed affect as activated by complex problems[edit]

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.[1]

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.[1]

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.[1][4] 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.[1]

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.[1] Negative affect has been shown to trigger upward counterfactual thinking, and exposure to avoidable stressors does appear to trigger depression.[5][4]

Sustained analysis is promoted by changes in the body system coordinated by depression[edit]

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.[6] 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.[7][8][9][1]

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.[1]

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.[10][1] 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.[11][1] 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.[12][13][14][15]

It appears that no research which specifically tests whether depressed people with higher levels of anhedonia experience less interrupted rumination currently exists.[1] 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.[16]

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.[17] Neurobiological evidence also suggests cognitive processing can be disrupted by oral activity.[18] Psychomotor retardation should also be associated positively with rumination as motor activity does require cognitive resources.[1] Research does show that psychomotor retardation is positively related to problems paying attention to cognitive tasks in the laboratory.[19]

Depressive rumination assists in resolving the triggering problem[edit]

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.[1]

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.[20]

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.[1] 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. [21] This can be attributed to depressed participants being more sensitive to costs of cooperating than normal participants.[1]

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.[22] 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. [23]

Why laboratory task performance is reduced by depressive rumination[edit]

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'.[24] 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.[1]

Paradoxical findings[edit]

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.[25]

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.[1]

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.[26] [27]

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. [28] [29] [30] 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.[1] This extends to complex economic experiments, assessment of health risks and social dilemmas.[20] [31] [32] Literature which examines how depressed individuals perceive facial expression and emotions suggests that depressed individuals may be less accurate at identifying different facial expressions.[33] [34] 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.[35] [36] 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.[37]

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.[38] [39] [1]

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. [1]

References[edit]

  1. ^ a b c d e f g h i j k l m n o p q r s t u v w Andrews, P.W.; Thompson, J.A. (2009). "The bright side of being blue: depression as an adaptation for analyzing complex problems". Psychological Review. 116 (3): 620–654. doi:10.1037/a0016242. PMC 2734449. PMID 19618990.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ Hagen, E. H. (2011). "Evolutionary theories of depression: A critical review". Canadian journal of psychiatry. Revue canadienne de psychiatrie. 56 (12): 716–726. PMID 22152640.
  3. ^ Thornhill NW, Thornhill R (1991). "An evolutionary analysis of psychological pain following human (Homo sapiens) rape: IV. The effect of the nature of the sexual assault". J Comp Psychol. 105 (3): 243–52. doi:10.1037/0735-7036.105.3.243. PMID 1935004.
  4. ^ a b Hammen, C. (1992). "Life events and depression: The plot thickens". American Journal of Community Psychology. 20 (2): 179–193. doi:10.1007/BF00940835. PMID 1605133.
  5. ^ Epstude, K.; Roese, N. J. (2008). "The Functional Theory of Counterfactual Thinking". Personality and Social Psychology Review. 12 (2): 168–192. doi:10.1177/1088868308316091. PMC 2408534. PMID 18453477.
  6. ^ Treynor, W. (2003). "Rumination Reconsidered: A Psychometric Analysis". Cognitive Therapy and Research. 27 (3): 247–259. doi:10.1023/A:1023910315561.
  7. ^ Gray, J. R.; Chabris, C. F.; Braver, T. S. (2003). "Neural mechanisms of general fluid intelligence". Nature Neuroscience. 6 (3): 316–322. doi:10.1038/nn1014. PMID 12592404.
  8. ^ Carter, O. L.; Burr, D. C.; Pettigrew, J. D.; Wallis, G. M.; Hasler, F.; Vollenweider, F. X. (2005). "Using Psilocybin to Investigate the Relationship between Attention, Working Memory, and the Serotonin 1A and 2A Receptors". Journal of Cognitive Neuroscience. 17 (10): 1497–1508. doi:10.1162/089892905774597191. PMID 16269092.
  9. ^ Winstanley, C. A.; Chudasama, Y.; Dalley, J. W.; Theobald, D. E.; Glennon, J. C.; Robbins, T. W. (2003). "Intra-prefrontal 8-OH-DPAT and M100907 improve visuospatial attention and decrease impulsivity on the five-choice serial reaction time task in rats". Psychopharmacology. 167 (3): 304–314. doi:10.1007/s00213-003-1398-x. PMID 12677356.
  10. ^ Drevets, W. C. (2000). "Neuroimaging studies of mood disorders". Biological Psychiatry. 48 (8): 813–829. doi:10.1016/S0006-3223(00)01020-9. PMID 11063977.
  11. ^ Vollmayr, B.; Henn, F. A. (2003). "Stress models of depression". Clinical Neuroscience Research. 3 (4–5): 245. doi:10.1016/S1566-2772(03)00086-0.
  12. ^ Amat, J.; Baratta, M. V.; Paul, E.; Bland, S. T.; Watkins, L. R.; Maier, S. F. (2005). "Medial prefrontal cortex determines how stressor controllability affects behavior and dorsal raphe nucleus". Nature Neuroscience. 8 (3): 365–371. doi:10.1038/nn1399. PMID 15696163.
  13. ^ Canli, T.; Lesch, K. P. (2007). "Long story short: The serotonin transporter in emotion regulation and social cognition". Nature Neuroscience. 10 (9): 1103–1109. doi:10.1038/nn1964. PMID 17726476.
  14. ^ Barton, D. A.; Esler, M. D.; Dawood, T.; Lambert, E. A.; Haikerwal, D.; Brenchley, C.; Socratous, F.; Hastings, J.; Guo, L.; Wiesner, G.; Kaye, D. M.; Bayles, R.; Schlaich, M. P.; Lambert, G. W. (2008). "Elevated Brain Serotonin Turnover in Patients with Depression: Effect of Genotype and Therapy". Archives of General Psychiatry. 65 (1): 38–46. doi:10.1001/archgenpsychiatry.2007.11. PMID 18180427.
  15. ^ Rajkowska, G. (2000). "Postmortem studies in mood disorders indicate altered numbers of neurons and glial cells". Biological Psychiatry. 48 (8): 766–777. doi:10.1016/S0006-3223(00)00950-1. PMID 11063973.
  16. ^ Dubal, S.; Pierson, A.; Jouvent, R. (2000). "Focused attention in anhedonia: A P3 study". Psychophysiology. 37 (5): 711–714. doi:10.1017/S0048577200001943. PMID 11037048.
  17. ^ Guastella, A. J.; Moulds, M. L. (2007). "The impact of rumination on sleep quality following a stressful life event". Personality and Individual Differences. 42 (6): 1151. doi:10.1016/j.paid.2006.04.028.
  18. ^ Jacobs, B.; Fornal, C. A. (1999). "Activity of Serotonergic Neurons in Behaving Animals". Neuropsychopharmacology. 21 (2): 9S–15S. doi:10.1016/S0893-133X(99)00012-3. PMID 10432483.
  19. ^ Lemelin, S.; Baruch, P. (1998). "Clinical psychomotor retardation and attention in depression". Journal of Psychiatric Research. 32 (2): 81–88. doi:10.1016/S0022-3956(98)00002-8. PMID 9694003.
  20. ^ a b >Au, K.; Chan, F.; Wang, D.; Vertinsky, I. (2003). "Mood in foreign exchange trading: Cognitive processes and performance". Organizational Behavior and Human Decision Processes. 91 (2): 322. doi:10.1016/S0749-5978(02)00510-1.
  21. ^ Axelrod, R.; Hamilton, W. (1981). "The evolution of cooperation". Science. 211 (4489): 1390–1396. doi:10.1126/science.7466396. PMID 7466396.
  22. ^ Hayes, A. M.; Feldman, G. C.; Beevers, C. G.; Laurenceau, J. P.; Cardaciotto, L.; Lewis-Smith, J. (2007). "Discontinuities and cognitive changes in an exposure-based cognitive therapy for depression". Journal of Consulting and Clinical Psychology. 75 (3): 409–421. doi:10.1037/0022-006X.75.3.409. PMID 17563158.
  23. ^ Graf, M. C.; Gaudiano, B. A.; Geller, P. A. (2008). "Written emotional disclosure: A controlled study of the benefits of expressive writing homework in outpatient psychotherapy". Psychotherapy Research. 18 (4): 389–399. doi:10.1080/10503300701691664. PMID 18815991.
  24. ^ Brittlebank, A. D.; Scott, J.; Williams, J. M.; Ferrier, I. N. (1993). "Autobiographical memory in depression: State or trait marker?". The British Journal of Psychiatry. 162: 118–121. doi:10.1192/bjp.162.1.118. PMID 8425125.
  25. ^ Nolen-Hoeksema, S. (1991). "Responses to depression and their effects on the duration of depressive episodes". Journal of Abnormal Psychology. 100 (4): 569–582. doi:10.1037/0021-843X.100.4.569. PMID 1757671.
  26. ^ Ambady, N.; Gray, H. M. (2002). "On being sad and mistaken: Mood effects on the accuracy of thin-slice judgments". Journal of Personality and Social Psychology. 83 (4): 947–961. doi:10.1037/0022-3514.83.4.947. PMID 12374446.
  27. ^ Austin, M. -P.; Mitchell, P.; Goodwin, G. U. Y. M. (2001). "Cognitive deficits in depression: Possible implications for functional neuropathology". The British Journal of Psychiatry. 178 (3): 200. doi:10.1192/bjp.178.3.200.
  28. ^ Ackermann, R.; Derubeis, R. J. (1991). "Is depressive realism real?". Clinical Psychology Review. 11 (5): 565. doi:10.1016/0272-7358(91)90004-E.
  29. ^ Alloy, L. B.; Abramson, L. Y.; Viscusi, D. (1981). "Induced mood and the illusion of control". Journal of Personality and Social Psychology. 41 (6): 1129. doi:10.1037/0022-3514.41.6.1129.
  30. ^ Msetfi, R. M.; Murphy, R. A.; Simpson, J.; Kornbrot, D. E. (2005). "Depressive Realism and Outcome Density Bias in Contingency Judgments: The Effect of the Context and Intertrial Interval". Journal of Experimental Psychology: General. 134 (1): 10–22. doi:10.1037/0096-3445.134.1.10. PMID 15702960.
  31. ^ Keller, P. A.; Lipkus, I. M.; Rimer, B. K. (2002). "Depressive Realism and Health Risk Accuracy: The Negative Consequences of Positive Mood". Journal of Consumer Research. 29: 57. doi:10.1086/339921.
  32. ^ Kirchsteiger, G.; Rigotti, L.; Rustichini, A. (2006). "Your morals might be your moods". Journal of Economic Behavior & Organization. 59 (2): 155. doi:10.1016/j.jebo.2004.07.004.
  33. ^ Leppänen, J. M. (2006). "Emotional information processing in mood disorders: A review of behavioral and neuroimaging findings". Current Opinion in Psychiatry. 19 (1): 34–39. doi:10.1097/01.yco.0000191500.46411.00. PMID 16612176.
  34. ^ Venn, H. R.; Watson, S.; Gallagher, P.; Young, A. H. (2005). "Facial expression perception: An objective outcome measure for treatment studies in mood disorders?". The International Journal of Neuropsychopharmacology. 9 (2): 229. doi:10.1017/S1461145705006012.
  35. ^ Bouhuys, A. L.; Geerts, E.; Mersch, P. P. A. (1997). "Relationship between perception of facial emotions and anxiety in clinical depression: Does anxiety-related perception predict persistence of depression?". Journal of Affective Disorders. 43 (3): 213–223. doi:10.1016/S0165-0327(97)01432-8. PMID 9186792.
  36. ^ Frewen, P. A.; Dozois, D. J. A. (2005). "Recognition and Interpretation of Facial Expressions in Dysphoric Women". Journal of Psychopathology and Behavioral Assessment. 27 (4): 305. doi:10.1007/s10862-005-2410-z.
  37. ^ Harkness, K.; Sabbagh, M.; Jacobson, J.; Chowdrey, N.; Chen, T. (2005). "Enhanced accuracy of mental state decoding in dysphoric college students". Cognition & Emotion. 19 (7): 999. doi:10.1080/02699930541000110.
  38. ^ Storbeck, J.; Clore, G. L. (2005). "With Sadness Comes Accuracy; with Happiness, False Memory: Mood and the False Memory Effect". Psychological Science. 16 (10): 785–791. doi:10.1111/j.1467-9280.2005.01615.x. PMID 16181441.
  39. ^ Ellis, H. C.; Ottaway, S. A.; Varner, L. J.; Becker, A. S.; Moore, B. A. (1997). "Emotion, motivation, and text comprehension: The detection of contradictions in passages". Journal of Experimental Psychology: General. 126 (2): 131. doi:10.1037/0096-3445.126.2.131.
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