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Depression as an adaptation for analyzing complex problems (article))


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Maybe interesting for some of you:

Paul W. Andrews and J. Anderson Thomson Jr.:

The bright side of being blue: Depression as an adaptation for analyzing complex problems


Depression ranks as the primary emotional problem for which help is sought. Depressed people often have severe, complex problems, and rumination is a common feature. Depressed people often believe that their ruminations give them insight into their problems, but clinicians often view depressive rumination as pathological because it is difficult to disrupt and interferes with the ability to concentrate on other things. Abundant evidence indicates that depressive rumination involves the analysis of episode-related problems. Because analysis is time consuming and requires sustained processing, disruption would interfere with problem-solving. The analytical rumination (AR) hypothesis proposes that depression is an adaptation that evolved as a response to complex problems and whose function is to minimize disruption of rumination and sustain analysis of complex problems. It accomplishes this by giving episode-related problems priority access to limited processing resources, by reducing the desire to engage in distracting activities (anhedonia), and by producing psychomotor changes that reduce exposure to distracting stimuli. Because processing resources are limited, the inability to concentrate on other things is a tradeoff that must be made to sustain analysis of the triggering problem. The AR hypothesis is supported by evidence from many levels, including genes, neurotransmitters and their receptors, neurophysiology, neuroanatomy, neuroenergetics, pharmacology, cognition and behavior, and the efficacy of treatments. In addition, we address and provide explanations for puzzling findings in the cognitive and behavioral genetics literatures on depression. In the process, we challenge the belief that serotonin transmission is low in depression. Finally, we discuss implications of the hypothesis for understanding and treating depression.

The full article is available here:


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It's an idea I've heard floated before. I think it may come from people who have only had the symptoms described to them, though (lethargy, anhedonia, etc.) rather than having experienced the extraordinary distortions of thought that occur when you're actually depressed ("it'll never get better", etc. not to mention "I'd be better off dead.") It's hard to imagine that full-blown depression results in better thinking about complex problems. They might be able to make a case for depression being an aberration of an otherwise normal process ... Interesting, that introduction says nothing about "analytical rumination's" actual results; whether or not the person's life is improved in the long term by rumination on complex problems. "Depressed people often believe that their ruminations give them insight into their problems", but is that borne out by any experimental evidence?

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Thanks, Mark!

I posted it because I think some people could somehow benefit from this alternative viewpoint. There are many types of depression and at least of them might be primarily seen as a chance to find out key hidden problems and then also some solutions. I think it might be compared to pain: Pain is a signal of a problem (damage), but it doesn't go away as soon as you become aware of the damage and start to "manage it". It's still there, "useless" already, and may be even so strong that one would rather like to die, but at least knowing the cause of the pain can be psychically alleviating to some extent. And it's up to the patient how (s)he bears the pain, if (s)he's trying to heal, ... - and it's also the case of somebody with depression: Knowing that there may be "a reason to be found and solved" and that the symptoms are due to many factors (as distorted thinking based on overly critical parents etc.) and one of them may be also an attempt of the brain to make him/her more focused on the previously unseen need for change in life/thinking/... - that might be motivational.

Of course, it would need a long debate to clearly address all the complicated aspects (and it still would be just a debate of two laymen in this field ;)).

but is that borne out by any experimental evidence?

I doubt that they would write it "just like that", whituout evidence. And I've also read about quite many examples (like those who wrote a book about their successful fight with depression). And it's even logical, I suppose: For instance, if not depressed, not many people would see ("early enough") a therapist and make efforts to gain new insights to their problems (which are often quite hidden to the consciousness)? The symptoms are also a signal of need for help, support and the lack of thereof - thus may motivate to seek them. (I know, this is not about rumination anymre, but...)

In any case, I should have added more about it in the 1st post. For instance:

There are, of course, many articles about this and related topics, but I've chosen that-one because it's free on the web. But to those who have access to scientific journals, here is also a review:

Evolutionary theories of depression: a critical review.


For those who don't, here are some quotes (my emphases):


We critically review evolutionary theories of major depressive disorder (MDD). Because most instances of MDD appear to be caused by adversity, evolutionary theories of MDD generally propose that sadness and low mood evolved as beneficial responses to adversity, and that MDD is dysfunctional sadness and low mood. If so, MDD research should focus much more heavily on understanding the healthy functions of sadness and low mood to better understand how they dysfunction. A debate about the boundary between healthy sadness and MDD is then reviewed. In part, this debate turns on whether MDD's costliest symptoms could provide unknown benefits. Therefore, the review concludes by discussing 2 theories that explore possible benefits of prolonged anhedonia and suicidality.

And here are some author's highlights:

Clinical Implications

• The clinical implications depend on which, if any, of these evolutionary theories of MDD is correct. In general, if MDD is dysfunctional sadness or low mood, then the primary goal of psycho- or chemotherapy would be to restore healthy sadness and low mood, and not simply to reduce MDD symptoms. Conversely, if MDD is functional, then therapy would aim to solve the social problem that triggered the MDD.

• In particular, if MDD is an involuntary subordinate strategy, then therapy should involve encouraging patients to let go of important but seemingly unobtainable life goals that involve conflicts with higher-status people. However, if the analytical rumination hypothesis is correct, then therapy should instead focus on identifying and solving the complex life problem that triggered the MDD. In some patients, and contrary to the involuntary subordinate strategy hypothesis, this may involve redoubling efforts to achieve a seemingly unobtainable life goal.

• Finally, all psychosocial theories of MDD imply that it may be possible to prevent MDD by identifying and avoiding social risk factors. For instance, the credible signalling hypothesis highlights the potent MDD risk posed by the confluence of social conflict, powerlessness, and adversity, each of which, in principle, could be reduced with appropriate interventions.


• The primary limitation of all evolutionary theories of MDD is that, although each is a reasonably parsimonious account of known facts about MDD, few of their novel predictions have been explored. In other words, these theories are largely untested.

More importantly:

All evolutionary theorists agree that sadness and low mood are probably adaptations. Most see MDD as a dysfunction of sadness and low mood. Some, however, argue that much MDD is also functional. Because all mechanisms can dysfunction, all agree, though, that at least some MDD is dysfunctional.

And I'd highlight this, from

Daniel Nettle and Melissa Bateson (2012): The Evolutionary Origins of Mood and Its Disorders, Current Biology 22, R712–R721

Mood systems are no different from any other biological mechanism in that they can go wrong sometimes, becoming

hypersensitive or dysregulated. Horwitz and Wakefield are probably correct to argue that what we currently diagnose

as disordered mood represents a mixture of cases where individuals have had adverse life experiences, but their mood system is itself functioning exactly as it should, and cases where the neurobiological mechanisms subserving mood are dysregulated or diseased. There is unlikely to ever be any simple way of demarcating the boundary between these two sources of mood problems with precision (see [45,98] for further discussion). Note, however, that the criteria for therapeutic concern and medical intervention do not need to depend on being able to distinguish evolved function from dysfunction. In physical pain, for example, administration of analgesia is almost universal, and it is implausible that in all cases this is because of malfunction in people’s pain systems. Rather, we now have technologies to slightly dampen systems that are in fact fulfilling their evolved function, and the justification for doing this is based on suffering, rather than demonstrable dysfunction in the evolutionary sense.

Edited by LaLa3
added intro
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