what’s adaptive about depression?

Jonah Lehrer has an interesting article in the NYT magazine about a recent Psych Review article by Paul Andrews and J. Anderson Thomson. The basic claim Andrews and Thomson make in their paper is 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”. Lehrer’s article is, as always, engaging, and he goes out of his way to obtain some critical perspectives from other researchers not affiliated with Andrews & Thomson’s work. It’s definitely worth a read.

In reading Lehrer’s article and the original paper, two things struck me. One is that I think Lehrer slightly exaggerates the novelty of Andrews and Thomson’s contribution. The novel suggestion of their paper isn’t that depression can be adaptive under the right circumstances (I think most people already believe that, and as Lehrer notes, the idea traces back a long way); it’s that the specific adaptive purpose of depression is to facilitate solving of complex problems. I think Andrews and Thomson’s paper received a somewhat critical reception (which Lehrer discusses) not so much because people found the suggestion that depression might be adaptive objectionable, but because there are arguably more plausible things depression could have been selected for. Lehrer mentions a few:

Other scientists, including Randolph Nesse at the University of Michigan, say that complex psychiatric disorders like depression rarely have simple evolutionary explanations. In fact, the analytic-rumination hypothesis is merely the latest attempt to explain the prevalence of depression. There is, for example, the “plea for help” theory, which suggests that depression is a way of eliciting assistance from loved ones. There’s also the “signal of defeat” hypothesis, which argues that feelings of despair after a loss in social status help prevent unnecessary attacks; we’re too busy sulking to fight back. And then there’s “depressive realism”: several studies have found that people with depression have a more accurate view of reality and are better at predicting future outcomes. While each of these speculations has scientific support, none are sufficient to explain an illness that afflicts so many people. The moral, Nesse says, is that sadness, like happiness, has many functions.

Personally, I find these other suggestions more plausible than the Andrews and Thomson story (if still not terribly compelling). There are a variety of reasons for this (see Jerry Coyne’s twin posts for some of them, along with the many excellent comments), but one pretty big one is that is that they’re all at least somewhat more consistent with a continuity hypothesis under which many of the selection pressures that influenced the structure of the human mind have been at work in our lineage for millions of years. That’s to say, if you believe in a “signal of defeat” account, you don’t have to come up with complex explanations for why human depression is adaptive (the problem being that other mammals don’t seem to show an affinity for ruminating over complex analytical problems); you can just attribute depression to much more general selection pressures found in other animals as well.

One hypothesis I particularly like in this respect, related to the signal-of-defeat account, is that depression is essentially just a human manifestation of a general tendency toward low self-confidence and aggression. The value of low self-confidence is pretty obvious: you don’t challenge the alpha male, so you don’t get into fights; you only chase prey you think you can safely catch; and so on. Now suppose humans inherited this basic architecture from our ancestral apes. In human societies there’s still a clear potential benefit to being subservient and non-confrontational; it’s a low-risk, low-reward strategy. If you don’t bother anyone, you’re probably not going to get the girl impress the opposite sex very much, but at least you won’t get clubbed over the head by a competitor very often. So there’s a sensible argument to be made for frequency dependent selection for depression-related traits (the reason it’s likely to be frequency dependent is that if you ever had a population made up entirely of self-doubting, non-aggressive individuals, being more aggressive would probably become highly advantageous, so at some point, you’d achieve a stable equilibrium).

So where does rumination–the main focus of the Andrews and Thomson paper–come into the picture? Well, I don’t know for sure, but here’s a pretty plausible just-so story: once you evolve the capacity to reason intelligently about yourself, you now have a higher cognitive system that’s naturally going to want to understand why it feels the way it does so often. If you’re someone who feels pretty upset about things much of the time, you’re going to think about those things a lot. So… you ruminate. And that’s really all you need! Saying that depression is adaptive doesn’t require you to think of every aspect of depression (e.g., rumination) as a complex and human-specific adaptation; it seems more parsimonious to see depressive rumination as a non-adaptive by-product of a more general and (potentially) adaptive disposition to experience negative affect.  On this type of account, ruminating isn’t actually helping a depressed person solve any problems at all. In fact, you could even argue that rumination shouldn’t make you feel better, or it would defeat the very purpose of having a depressive nature in the first place. In other words, it’s entirely consistent with the basic argument that depression is adaptive under some circumstances that the very purpose of rumination might be to keep depressed people in a depressed state. I don’t have any direct evidence for this, of course; it’s a just-so story. But it’s one that is, in my opinion (a) more plausible and (b) more consistent with indirect evidence (e.g., that rumination generally doesn’t seem to make people feel better!) than the Andrews and Thomson view.

The other thing that struck me about the Andrews and Thomson paper, and to a lesser extent, Lehrer’s article, is that the focus is (intentionally) squarely on whether and why depression is adaptive from an evolutionary standpoint. But it’s not clear that the average person suffering from depression really cares, or should care, about whether their depression exists for some distant evolutionary reason. What’s much more germane to someone suffering from depression is whether their depression is actually increasing their quality of life, and in that respect, it’s pretty difficult to make a positive case. The argument that rumination is adaptive because it helps you solve complex analytical problems is only compelling if you think that those problems are really worth mulling over deeply in the first place. For most of the things that depressed people tend to ruminate over (most of which aren’t life-changing decisions, but trivial things like whether your co-workers hate you because of the unfashionable shirt you wore to work yesterday), that just doesn’t seem to be the case. So the argument becomes circular: rumination helps you solve problems that a happier person probably wouldn’t have been bothered by in the first place. Now, that isn’t to say that there aren’t some very specific environments in which depression might still be adaptive today; it’s just that there don’t seem to be very many of them. If you look at the data, it’s quite clear that, on average, depression has very negative effects. People lose friends, jobs, and the joy of life because of their depression; it’s hard to see what monumental problem-solving insight could possibly compensate for that in most cases. By way of analogy, saying that depression is adaptive because it promotes rumination seems kind of like saying that cigarettes serve an adaptive purpose because they make nicotine withdrawal go away. Well, maybe. But wouldn’t you rather not have the withdrawal symptoms to begin with?

To be clear, I’m not suggesting that we should view depression solely in pathological terms, and should entirely write off the possibility that there are some potentially adaptive aspects to depression (or personality traits that go along with it). Rather, the point is that, if you’re suffering from depression, it’s not clear what good it’ll do you to learn that some of your ancestors may have benefited from their depressive natures. (By the same token, you wouldn’t expect a person suffering from sickle-cell anemia to gain much comfort from learning that they carry two copies of a mutation that, in a heterozygous carrier, would confer a strong resistance to malaria.) Conversely, there’s a very real danger here, in the sense that, if Andrews and Thomson are wrong about rumination being adaptive, they might be telling people it’s OK to ruminate when in fact excessive rumination could be encouraging further depression. My sense is that that’s actually the received wisdom right now (i.e., much of cognitive-behavioral therapy is focused on getting depressed individuals to recognize their ruminative cycles and break out of them). So the concern is that too much publicity might be a bad thing in this case, and, far from heralding the arrival of a new perspective on the conceptualization and treatment of depression, may actually be hurting some people. Ultimately, of course, it’s an empirical matter, and certainly not one I have any conclusive answers to. But what I can quite confidently assert in the meantime is that the Lehrer article is an enjoyable read, so long as you read it with a healthy dose of skepticism.

ResearchBlogging.org
Andrews, P., & Thomson, J. (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

11 thoughts on “what’s adaptive about depression?”

  1. RE: rumination. You write:

    it seems more parsimonious to see depressive rumination as a non-adaptive by-product of a more general and (potentially) adaptive disposition to experience negative affect.

    I believe that ‘biologically fit’ is a more parsimonious assumption than superfluous. It is quiet possible that however long humans have had awareness of distress, we have ruminated.

    Depression itself is positively correlated with posttraumatic growth (Dolbier et al. 2009). Watkins (2008) suggests rumination predicts reduced levels of depression. Nolan-Hoeksama (2008) also accepts that rumination can have positive effects on depression. The literature about rumination has shifted a fair amount in the past two years.

    You write:

    the very purpose of rumination might be to keep depressed people in a depressed state

    Struggling with the consequences of trauma can be considered the main source of posttraumatic growth (Tedeshi & Calhoun 2004). Trauma is often regarded as a violation of basic assumptions and believe. So recovery from trauma would, in part, involve the abandonment of old beliefs and the creation of new ones. The emotion sadness helps break down attachments and identifications, so in that sense, depression would have value. Constructive rumination, on the other hand, would be part of building new beliefs.

    Rumination is the consequence of trauma and distress. If you ruminate about “your co-workers hate you,” you are rumination of the very primal concern about the availability and sustainability of social-bonds and meaningful attachments. A trivial representation does not mean the source of the distress is trivial.

    You site the losses which occur from depression. Those losses occur from trauma, and depression is one of its consequences. Depression itself can be a condition which supports recovery from the debilitating distress of the trauma.

    One point, CBT is shifting in favor of a “mindfulness” component, and rumination is no longer regarded as something to be “broken out of” or suppressed. The idea is to be aware but not reactive. Trauma literature often discusses the concept of “window of tolerance,” and this CBT+mindful approach would have the quality of trying to help expand the window of tolerance and maintain the ruminations within it.

    Can I be skeptical of your skepticism?

  2. Hi Cole,

    Thanks for the comment! A couple of thoughts:

    I believe that ‘biologically fit’ is a more parsimonious assumption than superfluous. It is quiet possible that however long humans have had awareness of distress, we have ruminated.

    I suppose what “seems” adaptive to one is ultimately somewhat subjective (which is a major limitation of all of these just-so stories). My point was that if you posit that depression is adaptive specifically because it promotes rumination, you have a discontinuous hypothesis that doesn’t explain depression-like traits in other animals. It seems more plausible to me to have just one story that explains the range of depression-like behavior across the board, and then view the human-specific rumination as a by-product of another trait that clearly seems adaptive (intelligence). But I don’t really see any way to reconcile differing opinions on this point; unfortunately it’s not a question that lends itself to easy empirical validation.

    I think it’s something of a mischaracterization to say that “Nolan-Hoeksama (2008) also accepts that rumination can have positive effects on depression”. Nolen-Hoeksema’s more recent work (and that of others) suggests that the effects of rumination aren’t uniformly negative (mainly because in some cases they’re neutral–not because they’re positive!), and that rumination bears some relation to more adaptive forms of reflection. But she specifically draws a distinction between rumination and adaptive self-reflection (which surely makes sense, unless you think that non-depressed people never have to solve self-relevant problems!). And her overarching point still remains that depressed people’s ruminative pattern is generally quite maladaptive; she emphasizes repeatedly (both in the 2008 paper and others) that there are all sorts of other cognitive distortions associated with ruminative tendencies. So on balance, the preponderance of evidence going back several decades (much of which she reviews) still clearly indicates that rumination is overwhelmingly a negative thing.

    Trauma is often regarded as a violation of basic assumptions and believe. So recovery from trauma would, in part, involve the abandonment of old beliefs and the creation of new ones. The emotion sadness helps break down attachments and identifications, so in that sense, depression would have value. Constructive rumination, on the other hand, would be part of building new beliefs.

    Recovery from trauma isn’t the same thing as depression. Actually, in many cases, it’s an exclusion criterion. If someone close to you dies suddenly, you may experience trauma and be very upset for a couple of weeks (that would be within the normal range of human response), but you generally wouldn’t consider that depression unless the person didn’t recover in a timely manner. So I’m not sure that’s relevant here. There’s also the question I alluded to with my cigarettes analogy of whether depression is more likely to lead to trauma in the first place (which is generally the case: dispositionally negatively people react more aversively to all kinds of major life events). So even if it were true that depression-induced rumination ultimately helps you get out of your bind (which, to reemphasize, I don’t think is the case), that’s not much consolation if your depressive tendencies are what got you into that bind to begin with.

    Lastly, no one’s going to dispute that sadness often serves a valuable purpose, but there’s a world of difference between feeling sad (which everyone does from time to time) and being in a state of clinical depression. The Andrews and Thomson argument isn’t that sadness is adaptive, it’s that full-blown depression is adaptive specifically in virtue of promoting rumination. There’s very little evidence for the latter claim, and much against it.

    At any rate, I appreciate the comment, and of course you can (and should) be skeptical of my skepticism. :)

  3. Thanks tal for you lengthy response. This response and other commentary leads confirm some of my biases :)

    1. Depression is really code for some maladaptive or pathological condition rather than the whole class of persistent sadness which occur after significant loss (small-d depression in a sense). The study and alleviation of this big-D Depression is of great importance.

    2. Most of the studies are of big-D Depression and probably have a disproportionately small cohort of small-d depression sufferers.

    3. Big-D Depression is a condition, but small-d depression is more of a symptom.

    In this way, we are talking about somewhat different but overlapping issues.

    4. The idea that trauma and depression (either big- or small-d) are exclusive is bunk :)

    5. I agree that my reference to Nolan-Hoeksema was a distortion of the 2008 article and her general concept of depression and rumination. But she did acknowledge both Watkins 2008 and also the possible value of rumination:

    In light of the effectiveness of distraction and behavioral activation interventions for rumination and depression, it seems paradoxical that interventions designed to focus attention on distressing emotions and thoughts, such as experiential or mindfulness therapies, also have positive effects on depression in some studies…

    6. My general POV is embodied-cognition, yet most of the discussion is in a more classical POV, so I resort to indulging my cognitive biases :). Your writing and responses are much more deserving of the quality-impartiality labels.

  4. Tal, I agree that depression is an evolved trait, I completely disagree that “rumination” is the benefit it evolved to achieve.

    First, if “rumination” (i.e. long term cognitive problem solving and planning) were the primary benefit, then animals that don’t do long term cognitive problem solving and planning (i.e. just about all animals) should not exhibit depressive symptoms. Rumination might be a human adaption to use time spent in a depressive state productively, but that can’t be the feature that depression evolved to achieve because animals that don’t plan still can get depressed.

    Second, a state of compulsive rumination need not be accompanied by the state of anti-hedonia that accompanies depression. It is not simply the absence of feeling good, it is active feelings of feeling bad, feeling so bad that death via suicide is perceived to be a desirable and sought for outcome. The only way that a state that induces a significant risk of death (as in suicide from depression) could evolve is if that state saves more lives that it costs. By what mechanism specifically does anti-hedonia decrease death sufficiently that deaths from suicide could be balanced and produce a net benefit?

    Maybe individuals could be saved from death in trial by combat by giving up so they are spared by the victor. How does this translate into increased reproductive opportunities? If the fights are over females (essentially the only thing worth fighting to the death over), then depression should be sex-linked with females not exhibiting it. This is not observed. It should only be observed in sexually mature individuals, and not in children. It should not be observed in post-menopausal women, it should not be observed in the elderly. It should not be observed in individuals not undergoing mate selection stress.

    I have a much simpler explanation. When an organism is being chased by a predator, the “fight or flight” state is triggered. In the extreme case, the organism can run itself to death. From an evolutionary standpoint, being caught by a predator and running oneself to death are “the same”, death and loss of all future reproductive possibilities. However the ability to run oneself to death is a very strong survival feature because the organism doesn’t need to run itself to death, it only needs to run until it has escaped from the predator. If the predator gets tired and stops before the organism runs itself to death, then the organism has survived and may have future opportunities to reproduce. Any injury or damage short of death is infinitely better than being caught by the predator. Death from exhaustion is only equivalent to being caught.

    In order to induce a state where an organism can run itself to death, physiology must induce a state of euphoria. A state where the euphoria over rides all of the normal pain and fatigue warning signals so they can be ignored and the organism can willingly and euphorically run itself to death. I think this is the euphoria of the “runner’s high”, the euphoria of autoerotic asphyxiation, the euphoria of solvent huffing, the euphoria of stimulant abuse, the euphoria that near drowning produces. I call this the Euphoric Near Death State, ENDS. I see this state as brought about solely by extreme metabolic stress, near death metabolic stress.

    During this physiological state, a state which may occur only a few times (or never) in an organism’s life span, there is not an emergency energy source that comes online, saved only for that emergency. That would be grossly inefficient. No, what happens is that essential systems get turned off for a short period of time. Things that are not needed while running from a predator can be turned off, and their metabolic resources diverted to running. It is the turning off of essential pathways that leads to eventual death from exhaustion. For example, is continued healing useful while running from a predator? No, if the organism is caught, that healing is useless. If the healing is turned off and the predator is escaped from, then healing can be turned back on. Any inefficiencies due to turning stuff off during the attempted escape are worth it if it produces escape. Any damage due to turning stuff off during the attempted escape is worth it if it leads to escape. It is this turning off of essential physiological pathways that causes death from exhaustion. There are degrees of course, and physiology is pretty good at ranking physiological pathways and needs so that only the longest time scale pathways are turned off first.

    With healing and repair turned off, damage occurs and accumulated during this period. When enough damage accumulates, the organism dies.

    Because the organism has to run while enduring extreme damage, broken bones, cuts, bleeding, muscle necrosis, etc, the state of euphoria has to be pretty extreme to counter all the signals that in other situations would produce inaction. Damaging a broken foot by running on it is a bad idea, unless a bear is chasing you.

    Because the near death metabolic state has to be euphoric, and has to shut off all the “safeties” that normally protect an organism from self-injury, it is an extremely dangerous state for an organism to enter. If organisms could enter that euphoric state, at will, they would because it is an euphoric state. If they did enter that state at will, they would uselessly risk death. Organisms don’t enter that euphoric state at will, readily or easily. Therefore there must be an aversive state between the state “at rest” and the euphoric near death state. This aversive state provides a barrier to the easy entering of the euphoric state. It is my hypothesis that this necessary aversive state is the depressive state.

    The hypothesis that depression is the aversive state between at rest and a near death metabolic state fits all the data. Depression is associated with reduced metabolic activity in the brain, reduced blood flow, reduced glucose oxidation, reduced ATP levels. It explains how metabolic compromise by itself (as in vascular depression) can cause depression. It explains the reduced metabolic activity, reduced immune system activity, lethargy, and other metabolic disturbances. It also explains the insomnia that sometimes accompanies depression. A state of stress, metabolic or otherwise is not a good time to sleep, if there are other things that can be done to reduce stress.

    This hypothesis also explains all the disorders that are associated with depression, heart disease for example. If there is starting to be metabolic stress sufficient to induce depression, there aren’t enough metabolic resources to keep the heart and vasculature in good repair, so it degenerates.

    The problem is that metabolic state that can produce depression can occur via multiple paths and that some states that are adaptive in the short term can cause depression in the long term. It is mostly a problem of the regulation of the metabolic state. The simplest way to look at it is as a problem of ATP regulation. ATP is exquisitely well regulated. It is so well regulated that a myth has developed about its regulation, the myth of homeostasis. I have a blog on that, from a few years back. Because physiology must control the ATP consumption of so many different pathways, and regulate them all “in sync” with ATP supply and demand, physiology must use the ATP level as a control parameter to regulate ATP consumption. At high ATP levels non-voluntary pathways like healing are fully on. At low ATP levels they are off, but voluntary pathways like muscle activity are on. This regulation is what allows muscle to consume ATP until it necroses. This is a feature in the short term, but to regulate the ATP levels in an entire tissue compartment (necessary to let all the cells work “in sync”), there must be a diffusible signal that communicates ATP status between adjacent cells. If this signal is not working properly, then the tissue compartment may enter a state of low ATP and be unable to leave it. It is the long term dis-regulation of ATP that causes depression.

    Fix the ATP levels and you fix the depression. This is more difficult than it sounds. The primary stress response is to lower NO levels. This lowers ATP levels (via sGC) and raises the aerobic ATP generation rate by mitochondria (by disinhibiting cytochrome c oxidase). No doubt it also triggers many other stress responses. Ending the “fight or flight” state requires increasing NO levels. This is what is not easy. NO is extremely well regulated. There is no generally recognized way to raise NO levels. I think that topical ammonia oxidizing bacteria is the only way that will be effective.

    In summary, depression is the feature that allows the near death euphoria that allows an organism to run itself to death while trying to escape from a predator. It is the feature that allowed the physiology to evolve that lets a parent to lift a car off their child. It allows all metabolic resources to be devoted to a single task for a short period of time, even if that diversion would cause death if extended for too long.

  5. daedalus2u,

    The point of my post wasn’t to advocate for any particular evolutionary account of depression, it was to point out that the rumination hypothesis discussed in the link article seems (to me) less plausible than many others. So I don’t think we disagree on that point, and I’m not sure how you got that impression. As for your ATP conjecture, I don’t find it particularly convincing, but I think it’s an open empirical question. I think there are any number of possible explanations for depression that remain viable, and time will tell.

  6. I am highly surprised that this many words can be spent on discussing whether something is adaptive or not without ever talking about how it directly affects reproductive ability. What’s the correlation between happiness and fitness?

  7. Here is my “just so story” which explains evolutionary roots of depression. The benefits of the phenomenon are only present at the pack level and not at the individual level.

    The goal of depression is to drive least valuable members of the pack to suicide. This has a number of potential benefits:

    1. First and foremost the pack can only be as numerous as the resources allow, if the reproduction rate is higher then what can be sustained then it is a sound idea to sacrifice the least important members.

    2. The symptoms of depression – severance of social contacts, no food, no procreation, no will to act, suicidal thoughts, are consistent with the individual wanting to die. Such an individual would naturally make an easy target for predators and in that way could offer some protection for the more valuable members.

    This is much more beneficial then an outright killing of unwanted members of the pack since the latter would promote internal conflicts and infighting as the individuals closer to the singled out target would try to defend him or retaliate. By having the individual commit suicide this problem is averted. What’s more as the individual get’s depressed he actively tries to sever the ties with those who were close to him before and it can be interpreted as an attempt to limit their suffering when he will eventually die.

    This hypothesis would also explain why social exclusion can often lead to depression since if this hypothesis is correct it would be the exclusion by individuals perceived as authoritative and influential in the group to which one aspires that would be the signal inducing depression.

    So to sum it up the benefits are:
    1. It is beneficial for the pack to have a way to get rid of unwanted individuals in a non-violent manner, the reasons may be lack of resources, internal conflicts, removal of individuals who’s behavior puts the group in danger, etc.
    2. It may be beneficial for the pack to single out certain individuals as a sacrifice for predators to make other more valuable individuals safer.
    3. It could also serve as a mechanism protecting other members from diseases if the diseased individuals where to get depressed and leave the pack to die but this poses the problem of why healthy individuals suffer from depression.

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