Med Health Care and Philos (2012) 15:41–52
DOI 10.1007/s11019-010-9305-9
SCIENTIFIC CONTRIBUTION
Evolutionary psychiatry and depression: testing two hypotheses
Somogy Varga
Published online: 9 January 2011
Ó Springer Science+Business Media B.V. 2011
Abstract In the last few decades, there has been a genuine ‘adaptive turn’ in psychiatry, resulting in evolutionary
accounts for an increasing number of psychopathologies. In
this paper, I explore the advantages and problems with the
two main evolutionary approaches to depression, namely
the mismatch and persistence accounts. I will argue that
while both evolutionary theories of depression might provide some helpful perspectives, the accounts also harbor
significant flaws that might question their authority and
usefulness as explanations.
Keywords Evolutionary psychiatry Depression Social
navigation hypothesis Rumination
Introduction
In the middle of the nineteenth century, the theory of
evolution that Darwin (1859) and Wallace (1875) put forward, namely that species evolve and that the transmutation of the species occurs, was radically different from the
previous conceptualization of the descent of living beings.
As it is well known, the theory has lead to deep changes in
science and theology. At present, most scientists in the
natural sciences accept some version of the theory of
evolution. Since Darwin and Wallace, evolution is a pivotal
concept in biology and a cornerstone of modern medicine.
S. Varga (&)
Institute of Cognitive Science, University of Osnabrück,
Albrechtstraße 28, 49069 Osnabrück, Germany
e-mail: [email protected]
S. Varga
Center for Subjectivity Research, University of Copenhagen,
Njalsgade 140-142, 2300 Copenhagen S, Denmark
In the last few decades, evolutionary theory has been
increasingly seen as a valuable source in explaining both
individual behaviors and social structures (Nesse 1984).
This is partly because of fundamental progress in the 1960s
and 1970s by proponents like Hamilton (1964) and Wilson
(1975). Their work has managed to deal with unanswered
problems that haunted the original Darwinian account.
Since these publications, there has been an immense
growth of publications in this area, and the study of
behaviors informed by evolutionary theory has become an
independent discipline. Under these circumstances, it is not
surprising that evolutionary theory has begun to inform
psychiatry’s attempts to understand and explain psychopathology. For such approaches that address mental disorders within the framework of contemporary evolutionary
theory, Paul MacLean has coined the term ‘evolutionary
psychiatry’ (MacLean 1985, 219). While few dispute that
the human mind has been shaped by evolution, evolutionary psychiatry attempts to apply insights about evolutionary processes to offer new ways to understand the
origin of mental disorders.
In an initial paper, Cosmides and Tooby (1987) launched an account of evolutionary psychology, which also
became an important reference for the emergence of evolutionary psychiatry. While sharing the general intuition,
the particular attempts are heterogeneous and also conflicting not only in their theoretical orientations and
methodologies, but also in their conclusions. Nonetheless,
possibly helped by a growing dissatisfaction with reductionist views inherent in many biological approaches in
psychiatry, recent years have witnessed increased general
interest in the application of evolutionary theory to issues
in psychopathology (Nesse and Williams 1995; Stevens
and Price 1996; McGuire and Troisi 1998). As Nettle
(2004) notes, there has been a genuine ‘adaptive turn’ in
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psychology and psychiatry, and evolutionary explanations
are being proposed for an increasing number of aspects of
psychopathologies. There are two features of evolutionary
psychiatry that might have contributed to its growing
popularity. First, evolutionary-informed researchers are
surprised to discover that numerous mental disorders seem
to have a genetic basis, while they occur at prevalence rates
that are too high to be explained as mutations. In the
evolutionary optic, high prevalence rates reveal that the
genetic bases of these mental diseases have been promoted
by natural selection. Second, another appealing aspect in
the approach is that evolutionary psychiatry is at least
potentially able to identify not only proximate, but also
ultimate causes. While proximate causes merely explain a
process or structure in an individual organism, ultimate
(evolutionary) causes provide a larger picture, since they
explain the process or a structure in all members of a
species. For instance, the question might be ‘‘what causes
depression?’’ A proximate cause could be given by maintaining that specific imbalances in brain chemistry or particular combinations of environmental precipitants result in
a depressive episode.1 Conversely, ultimate cause can be
given if an explanation of the evolutionary function of
depression is provided, which involves showing how this
ability has improved survival or reproduction possibilities
in the process of natural selection. Thus, while psychiatry
has mostly focused on proximate explanations, some of the
most appealing aspects in the application of evolutionary
principles to psychiatric phenomena are richer explanations
and the possibility of a ‘bigger picture’ that provides a
platform for integrating the diverse levels.
In general, the underlying concept of the mind that is
deployed in evolutionary psychiatry rests on the idea of the
‘Modular Mind’, originally developed by Jerry Fodor
(1983). This view shares substantial assumptions with the
so-called functionalist view in philosophy, according to
which mental entities are substrate neutral, best understood
as computation elements (Dennett 1978). Briefly, far from
being an all purpose cognitive device, the human mind is
assumed to be constituted by a numerous separate but
interconnected ‘‘modules,’’ assigned to different information-processing tasks (Gerrans 2002). The mind is conceptualized as bundle with a large number of specialized
components that continually solves difficult and particular
computational tasks (Pinker 1997). There is a myriad of
1
Actually it would be more precise to use the term quasi-proximate
explanation. Maintaining that an imbalance at brain level causes
something at mental level, only qualifies as an explanation if one, like
some biologically oriented psychiatrists, embraces an epiphenomenalist outlook. However, from the point of view of physicalism, which
has become the consensus view in philosophy, identifying a
proximate cause, entails indentifying a physical reason for brainlevel imbalance.
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functionally dedicated modules, like ‘‘specialized systems
for grammar induction, for face recognition, for dead
reckoning, for construing objects and for recognizing
emotions from the face. There are mechanisms to detect
animacy, eye direction, and cheating.’’ In all, there is a
multitude of such ‘‘elegant machines’’ (Tooby 1995, p.
xiv). As Cosmides and Tooby (1994) argue, there are
domain specific computational modules, and—like the case
with organs—all normal members of the species are said to
share the same kind of modules.
The assumption of the modularity of mind is in evolutionary psychology and psychiatry complemented by a
second important hypothesis, namely that mental modules
are genetically specified adaptations (Fodor 2000; Cosmides and Tooby 2000). The modules of the mind are
simply information-processing adaptations to solve the
problems that faced our ancestors. Modules were ‘‘invented
by natural selection during the species’ evolutionary history to produce adaptive ends in the species’ natural
environment’’ (Tooby 1995, p. xiii). In order to stress the
adaptation aspect of the modules posited in evolutionary
approaches, Murphy and Stich (2000) suggest the useful
term ‘Darwinian modules’. So evolutionary psychiatry
assumes that mental modules are both adaptations and
domain-specific computational devices with particular
purposes.
While most accounts share these assumptions, when it
comes to the applications of evolutionary theory to psychopathology, three types of accounts can be distinguished
(Murphy 2005). A breakdown account understands mental
disorder as the malfunction of some component of the
mind/brain in fulfilling its evolutionary function. A mismatch account understands mental disease as connected to
a mechanism that was once adaptive but is no longer
adaptive because of changes in the environment. So the
pathology lies not in some sub-system of an individual, but
in the mismatch between the ancestral environment and our
current environment. A more controversial persistence
account holds that some putative disorders qualify as
adaptive even in the present environment.
In this paper, I will attempt to outline the structure of
evolutionary accounts in psychiatry, limited to the discussion of depression. Generally, it seems that depression is a
good subject in such a discussion: it is suitably prevalent
throughout history to be appropriate to investigate its
evolutionary origins, and, compared to many other mental
disorders, there has been a considerable amount of work
done on the subject. The general aim of the paper will be to
illustrate the benefits and problems of evolutionary
approaches to depression. Two (opposing) paths (mismatch
account and persistence accounts) will constitute the focal
point of the investigation. This focus appears adequate both
because evolutionary-informed investigations have tended
Evolutionary psychiatry and depression
to follow these two paths, and because it is these two
accounts that really distinguish evolutionary psychiatry
from other approaches, while sharing the basic idea that the
mechanisms activated in depression evolved to manage
hostile situations in which flight was impossible. From
here, the two accounts part ways. Guided by this distinction, the first part of the paper will be dedicated the
exploration of the mismatch account defended by
researchers like Nesse (2000) and Gilbert and Allan (1998),
which hypothesizes that in depression an inherited mechanism becomes pathologically over-activated. The second
part of the paper will focus on the persistence accounts of
depression suggested by Price et al. (1994), Hagen (1999)
and Watson and Andrews (2002). Depression in this view
is far from being intrinsically pathological and might be
viewed as fulfilling a specific function, helping to adapt to
changed circumstances, like in the case of changed social
status. In the conclusion of my paper, I will discuss the
usefulness of applications of evolutionary theory to explain
depression.
The mismatch account of depression
The basic assumption that proponents of the mismatch
account of depression assume is that numerous pertinent
characteristics of the human mind evolved in hunter–
gatherer societies that existed around the period of the
Pleistocene (Glantz and Pearce 1989; Cosmides and Tooby
1999). Stevens and Price (1996) emphasize that the human
mind consists broadly of hierarchically organized systems
of very different evolutionary ages, including a ‘reptilian’,
a ‘palaeo-mammalian’ (consisting of the limbic system) a
‘neo-mammalian’ (cerebral neocortex) and unique to the
human mind, mechanisms specialized for language and
symbolic processing. Beneath the threshold of consciousness, these systems are still thought to be active, albeit
sometimes acting in contradictory ways.
The core of their proposal is roughly that both our
ancestors and we are adapted to the hunting and gathering
environment, (genetically) predisposed to behave in ways
that were adaptive in that original environment. Rather
than being helpful in current circumstances, those evolved
genes and patterns of behavior now promote psychopathological conditions (Baptista et al. 2008). Psychopathology
arises in response to a mismatch between behavioral,
cognitive, and affective predispositions and the current
environment with wholly differing social settings. As
Glantz and Pearce (1989, 112) state, ‘‘when culture strays
too far from biology, it also moves away from sanity.’’
Prominent proponents of the mismatch account of
depression like Price et al. (1994), Nesse and Williams
(1995) argue that depression should be understood as an
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evolved, adaptive response to specific problems that arise
in the small, status-oriented social group of our ancestors.
Clearly, depression is addressed as adaptive, not to the
natural, but to the social environment. Gilbert (2006) notes
that it is not a loss of control over the physical environment
that is particularly depressogenic, but the loss of control in
the social environment. The mismatch account of depression builds on a set of interlocking arguments, proposed by
several proponents. However, two main strains of argument
can be distinguished that understands depression as adaptive responses for the abandonment of unrealistic goals and
for the acceptance of social defeat. In other words, we can
distinguish between an intrasubjective, and an intersubjective social version that complement each other.
Unrealistic goals
It has been suggested that forms of depression assist the
restoration of exhausted resources by pushing the individual
to withdraw (Schmale 1973). Characteristic and well-known
symptoms of depression like psychomotor retardation are
considered as good examples in this case. Nesse (2000) and
Nesse and Williams (1995) propose that depression helps to
maximize payoffs by assisting the adjustment of resource
allocation to activities. The characteristic sense of capability
to fulfill tasks, pessimism, behavioral inactivity, and the
well-documented exaggerated interpretation of the difficulty
of a task, restrains the depressive from allocating resources in
demanding activities with low probability of success (Sloman et al. 2003). Similarly, Stevens and Price (1996) argue
that certain forms of depression are considered to be constructive human responses to situations in which a desired
social goal seems impossible to achieve. It has been long
established that depression is common in people who are
pursuing unattainable goals and fail to yield for example in
the domain of status competition (Randolph and Nesse 2000;
Davis 1970). So in such cases, the distress and the downregulation of positive affect systems that characterize
depression may push the depressed to re-evaluate and
abandon the goal. In this sense, depression could be seen as a
limiting defense mechanism that could help the person disengage from impossible undertakings that have became such
a matter of habit that under normal circumstances it is
unfeasible for the individual to abandon them. Importantly,
for the mismatch theorists, the evolved capacity that has
functioned as a defense mechanism for enabling disengagement from impossible undertakings now causes conflicts that lead to mental disorders.
Submission
The ‘social rank theory’ of depression (Gilbert 1992, 2000)
links involuntary subordination to depression and builds on
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research on the regulators of mood in dominant and subordinate animals in the context of social conflict (Price
1972; Price and Sloman 1987). The central observation that
this account assumes is that depression-like states occur in
animals and humans who have been defeated and lost rank.
More specifically, depression is an adaptive response to the
loss of status in such small social groups that helps to
accept lowered rank once having lost status (Price et al.
1994; Stevens and Price 1996). Once outcompeted, it is of
advantage to self-evaluate, ruminate upon weaknesses, and
alter previous behaviors. The idea is that depressed mood
helps to accept status loss and motivates to alter previous
behaviors in order to ameliorate reproductive chances.
In order to strengthen their point, some accounts make
use of the links between serotonin, social rank, and
depression. It has been established that in a sizeable subpopulation of depressives, serotonin levels are abnormally
low. Also, the level of serotonin seems to be correlated
with negative self-assessment and pessimism. Additionally,
Meyer et al. (2003) have shown that in healthy subjects,
increasing serotonin (5-HT) lowered such dysfunctional
attitudes. Additionally, when animals change their place in
a power hierarchy, their behavioral changes are accompanied by changes in serotonin levels (Kravitz 2000; Drummond et al. 2002). Recently, status-degraded monkeys
display lowered levels of serotonin, and it seems that that
the stress of the new lower social rank produces a downregulation of serotonin level (Shively 1999; Grant et al.
1998; McGuire and Troisi 1998).
The recourse to research on serotonin is supposed to
additionally underpin the central thesis of the ‘social rank
theory’ of depression, namely that depression is both a
mechanism triggered when outcompeted and one that helps
accept lower status and to motivate to change current
behavior to improve reproductive chances. Now the ‘mismatch’ suggestion adds to this that while in such small
groups such an adaptive response might have been a
fruitful strategy resulting in social success, in contemporary and much more sizeable groups, this affect-lowering
response to change in status is a mismatch (Nesse and
Williams 1995). Due to a radically changed social setting,
the inherited mechanism—activated when one believes that
one is outcompeted—is no longer adaptive. On the contrary, as our peer group with whom we compete is much
larger, such a mechanism will be activated inappropriately
in the modern world. In the context of global competition,
the activation of this mechanism whenever we feel outcompeted is neither a satisfactory nor an effective reaction.
Among other aspects, it cannot be effective because it is
difficult to imagine another strategy that one could adopt or
niche one could fill in which one would not be outmatched
in global competition (Murphy 2005). As a result, this
mechanism will not only fail to accomplish the goal it was
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selected to achieve: given modern societal framework, the
depressed affect-lowering response to change is not only
ineffective, but also seriously inhibiting and fitness
decreasing.
As I have noted in the beginning of this paper, an
appealing aspect of the evolutionary psychiatry approach
lies in its ability to provide not only proximate, but also
ultimate causes. The mismatch account of depression certainly lives up to these expectations, since depressive
responses can be seen as the results of systems performing
their originally evolved functions, but in a mismatched
context. It allows a ‘bigger picture’ that provides a platform that has potentials to integrate diverse levels. For
instance, against the background of the mismatch thesis
and the work of Nesse (1999), we could speculate that there
is a link between the growing globalization (and hence
growing peer groups) and the alleged increase in depression in the last few decades.2 However, there are seriously
inhibiting aspects about the mismatch model. First, the
mismatch theory of depression does not address the individual and social factors and thus does not address why
some rather than others are affected. It would seem that the
proponents of the mismatch theory of depression would
need to show that those individuals on the international job
market that are taking part in global competition would be
more vulnerable to depression. Yet, no such evidence is
given. On the contrary, it is well known that socio-economic deprivation is connected to a high prevalence mental
illness such as depression (Thornicroft et al. 1992; Acheson
1998), and many studies show higher rates of depression is
associated with lower socioeconomic status (Stansfeld
et al. 1998; Kessler et al. 1994; Bebbington et al. 1981),
area deprivation (Eachus et al. 1996), unemployment
(Meltzer et al. 1995) and employment grade (Stansfeld and
Marmot 1992). It is quite easy to see that such a picture
does not fit very well with the implications of the mismatch
theory of depression. It seems that contrary to the point of
the mismatch theory of depression, underprivileged and
unemployed individuals that typically do not take part in
the global competition on international job market are more
vulnerable to depression.
First, we could legitimately maintain that mismatch
theory of depression needs to provide an explanation to
why not more individuals afflicted by the condition. Second, mismatch theory of depression departs on the
assumption that it can identify something like a static
2
The view that there has been an increase in depressive illness
during the last decades is controversial. Taking seriously epidemiological theory and the conceptual shifts that the definition of mental
disorder (particularly depression) has undergone in the last decades,
the uncertainties with such statements are immense. However,
whether this is actually the case or not does not play any role for
my argument.
Evolutionary psychiatry and depression
moment in human evolution, with an ideal match between
genes and environment. These are both problematic issues
that would require substantial scientific evidence. Up to
now, no such evidence has been provided. Without convincing evidence, and given the dynamic and ongoing
nature of evolutionary processes, it seems unpersuasive
that such a static moment in human evolution can be
crystallized. Also, due to these dynamic and intertwining
interactions between human biology, behavior, and environment, the idea of an almost perfect adaptation at a
certain time in history appears improbable.
Third, a more broad-spectrum objection could be raised
that both the mismatch and the persistence account of
depression are vulnerable to. While I will deal with this
issue at length in connection to the persistence account, let
me just mention that it seems unlikely that depression
really results in the positive process of re-evaluating and a
changing of one’s behavior.
In conclusion, the mismatch model as a specific application of evolutionary theory to depression might shed
light on single aspects of depression and might help to
integrate diverse aspects. But overall, if it is to provide a
credible option, the mismatch model needs to provide
convincing answers to the problematic issues that have
been raised. However, this does not mean that we should
reject all applications of evolutionary theory to depression.
In the following section, I will illustrate the benefits and
problems of the competing, persistence account of
depression.
The persistence explanation of depression
The competing application of evolutionary theory to
depression is the persistence account of depression that I
am going to expound here maintains that depression cannot
be viewed as the impairment of particular mechanisms.
Thus, the genetic material involved is somehow adaptive.
Concerning depression, the adaptive view is that depression is not intrinsically pathological: even though it causes
serious pain and distress, it can be viewed as adaptive, as
having a specific function, namely the adaptation to
changed circumstances. Researchers like Price et al.
(1994), Hagen (1999) and Watson and Andrews (2002)
hold this admittedly more daring claim. On this view,
alleged psychopathologies like depression represent adaptive behavioral strategies and function adaptively in the
present environment, as they did in the ancestral environment. The fact that distinctive features of depression have
been shown to exist almost worldwide (Hadley and Patil
2008; Kohrt et al. 2005; Patil and Hadley 2008; Watson
and Andrews 2002) and that there is a higher prevalence of
45
depression in Western societies (Horwitz and Wakefield
2007; Patel 2001) is taken to support the persistence view.
Importantly, the authors do not argue that depression is not
an impairment. Rather, they maintain that impairment can
also be caused by appropriately functioning defense
mechanisms. In order to secure the best allocation of
resources to different systems that deal with adaptive
challenges, particular stressors trigger evolved stress
response mechanisms. Involuntary responses to environmental challenges like negative emotions constitute good
examples for the activation of stress response mechanisms,
which then coordinate bodily and cognitive resources to
manage the task (Cosmides and Tooby 2000; LeDoux
1996). Differently than in the case of negative emotions,
such mechanisms can also generate impairments when
responding to a particular stressor. Fever might be seen as
an impairment in multiple domains, reducing metabolism,
sexual and social activity, etc., although it is an adaptation
that evolved to increase fitness by a specific immune system response (Hasday et al. 2000). In much the same way,
depression impairs a large array of life aspects: it is aversive and disruptive, and in many senses it interrupts normal
function. So at first sight, it is difficult not to consider it a
maladaption. However, one might argue that a brief look at
a wide array of our functional capacities, like experiencing
fatigue, nausea, or pain, reveals that it is exactly the
aversive and disruptive character of such capacities that is
the key to their adaptive capacity: it is the disruptive
character that helps us avoid potentially dangerous and
fitness-decreasing situations. Following the same path of
thought, Darwin (1859/2000, 431) himself considered
depression as an adaptive function: ‘‘Pain or suffering of
any kind, if long continued, causes depression and lessens
the power of action; yet it is well adapted to make a
creature guard itself against any great or sudden evil.’’ But
the crucial question must be: how does it give a selective
advantage? Any kind of unyielding answer can only be
given when considering the situations in which its various
characteristics offer fitness advantages.
As was the case with the mismatch account of depression, the persistence account is also based on different sets
of interlocking arguments, proposed by several proponents,
but also here intrasubjective and intersubjective main
strains of argument can be fleshed out. The intrasubjective
version of the persistence account of depression maintains
that the down-regulation of positive affect systems in
depression helps the depressed to re-evaluate and abandon
unachievable life goals or depressive rumination promotes
sustained analysis of the triggering problem. The intersubjective version holds that to the depressive, the connectedness to others becomes a crucial issue to pursue; the
members of the social network are urged to engage with the
depressed person in a new manner. This reshapes to a
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certain extent the relationships within the social network.
Let us first turn to the intrasubjective argument.
Depressive rumination
As already mentioned, among others Stevens and Price
(1996) maintain that certain forms of depression are conceivable as constructive human responses to situations in
which a desired social goal is unachievable. This view
gains some additional credence through the fact that
depression is common in people who are pursuing unattainable goals and fail to yield for example in the domain
of status competition (Randolph and Nesse 2000; Davis
1970). Additionally, depression can become graver and
chronic when individuals remain committed to poor pay off
goals and tasks they cannot fulfill (McGuire and Troisi
1987; Leahy 2000). Against the background of evolutionary aspects and empirical findings, proponents of the persistence view of depression have proposed that the distress
and the down-regulation of positive affect systems that
characterize depression may push the depressed to reevaluate and abandon impossible undertakings that have
became overly habitual. In this case, depression would be
an adaptive response to social circumstances, enhancing
our ability to navigate in the social context. D.A. Hamburg,
an early exponent of this view, has summarized possible
functions of depression, maintaining that in a case where
the individual estimates that the probability of achieving a
goal is very low, ‘‘the depressive responses can be viewed
as adaptive’’, because ‘‘feelings of sadness and discouragement may be a useful stimulus to consider ways of
changing (the) situation’’ (Hamburg 1974, 240). So
depressive pessimism, the down-regulation of positive
affect, diminished responsiveness and the lack of motivation may be seen as fostering disengagement from the
unachievable challenges of a chosen path of life, which at
the end would exhaust and harm the individual. In this
sense, depression helps to conserve resources.
More recently, in their rich and well-crafted paper,
Thompson and Andrews (2009) have put forward a new
hypothesis that points into the same direction. It is widely
acknowledged that depression produces specific impairments, such as maladaptive cognitions (Alford 2009). Also,
often depressive cognitive processed are characterized by
persistent ‘depressive rumination’, recyclic negative
thinking resistant to distraction and that by many is considered as important in the development, maintenance, and
relapse of recurrence of depression (Treynor et al. 2003)
and difficult to suppress (Nolen-Hoeksema 1991; Wenzlaff
and Luxton 2003). Conversely, Thompson and Andrews
(2009) aim to explain the cognitive impairments associated
with depression, by hypothesizing that depression is an
evolved stress-response mechanism and that depressive
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rumination harbors a beneficial cognitive effect. They
summarize their ‘analytical rumination hypothesis’ as
follows:
In summary, we hypothesize that depression is a
stress response mechanism (a) that is triggered by
analytically difficult problems that influence important fitness-related goals; (b) that coordinates changes
in body systems to promote sustained analysis of the
triggering problem, otherwise known as depressive
rumination; (c) that helps people generate and evaluate potential solutions to the triggering problem; and
(d) that makes trade-offs with other goals to promote
analysis of the triggering problem, including reduced
accuracy on laboratory tasks. Collectively, we refer
to this suite of claims as the analytical rumination
hypothesis (2009, 623).
In other words, when facing complex social problems,
natural selection is argued to have promoted specific
behaviors and cognitive patterns that force individuals to
withdraw, to abandon formerly pleasurable and even fitness
increasing activities. The withdrawal from activities and
commitments to depressive rumination enables the
depressed individual to engage in a profound analysis of
the triggering problems. The adaptive aspect of depressive
rumination is that it assists problem solving before
re-engaging in social activities and commitments.
Crucially, Watson and Andrews (2002) claim that depressive rumination provides adequate cognitive means to
solve difficult analytical problems. The evolutionary benefits of depressive rumination are great enough to compensate for the substantial costs (2009, 643).
Social navigation hypothesis
For other proponents of the adaptation view, there is
another intersubjective sense in which depression can be
viewed as adaptive. It has both been suggested that adults’
depression conveys a plea for help to others, to arouse pity
in them interpreted as a communication designed to
manipulate others into providing resources. Focusing on an
adaptationist stance on postpartum depression, Hagen
(1999) has maintained that depressed mothers obtain
greater care from both their partners and their social network. In their ‘‘social navigation hypothesis’’, Watson and
Andrews (2002) extend this idea to depression generally
and argue that depressive responses have this function of
obtaining a re-vitalizing of social relationships.
Watson and Andrews (2002) review evidence that
depression is associated with social problems and suggest
that complementary to focusing limited cognitive resources, it plays a crucial role in motivating close social partners (who have a positive fitness interest in the normal
Evolutionary psychiatry and depression
functioning of the depressed) to provide help and to make
concessions in favor of the depressed. Disinterest in normal
fitness-related activities, anhedonia and psychomotor perturbation does not only impose costs on the depressed:
Social partners are aware of the costs imposed on them
when a partner is depressed (Segrin and Dillard 1992). The
costs of depression motivate members of the depressive’s
social network to make investments that they under normal
circumstance would hesitate to make. They might understand the benefits of assisting and ending of the depressive
episode, to avoid escalating costs. Besides specific partners, depression is also thought to be designed to and able
to motivate the entire social network, depending on the
configuration of the network and in the way the costs of
depression are distributed in it. In this sense, depression
may be an extortive means to motivate within the network
to overcome their reluctance to help (Hagen 1999). The
fact that there is overwhelming empirical evidence maintaining that individuals in conflict with significant peers are
more likely to become depressed seems at least partly to
support the persistence position. For instance, while interpersonal conflict is commonly associated with depression
(Hammen 1992), it is striking that in unhappily married
people the risk for major depression is about 40 times
greater than in happily married ones (Weissman 1987).
Overall, even if depression might cause abandonment and
sometimes produce social deterioration, the main idea
underlying the social navigation hypothesis is that
depression has evolved to serve a social motivation
function.
Having explored the main lines of thought underlying
the persistence account of depression, the next part of the
paper will be dedicated to a critical examination of such an
account.
Problems with the persistence account of depression
To begin with, I would like to mention a positive aspect of
both versions of the persistence account. Just as it was the
case in the mismatch account of depression, the persistence
account might be seen as appealing version of evolutionary
psychiatry, at least considering its ability to provide both
proximate and ultimate causes. Additionally, both the
mismatch and the persistence accounts have speculated on
how the change of social environments could affect the
prevalence of depression. However, while the mismatch
account allowed some speculation on a link between the
transformation into globalized societies and the increase in
depression, this advantage remained speculative since the
mismatch account failed to address the individual factors.
In other words, it failed to address why some rather than
others are affected. This aspect is much better integrated in
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the persistence account, where concrete individual causing
factors such as complex social problems come into play. As
such, it might lend some support to preliminary reflection
on the growing rates of depression. As Watson and
Andrews (2002) suggest, it might be the case that modern
social complexity increases the context for ruminative and
motivational depression: while there is a larger number of
positive fitness partners, these partners simultaneously
become more replaceable, reducing the average fitness
interest among them. On the background of the persistence
account, it seems reasonable to think that living in social
networks with reduced fitness interests among partners may
contribute to growing prevalence of depression. However,
this positive feature of the application of evolutionary
theory to depression should not blind our gaze to what
might seem as an insurmountable bulk of problems. The
following assessment will focus on the persistence explanation, but some of the concerns I am going to raise also
afflict the mismatch reading.
Depressive rumination deals with complex social
problems
Although depressive rumination is widespread, it seems
that Watson and Andrews (2002, 2009) overestimate its
outcome. The vigor with which the persistence explanation
is maintained does not fit well with the evidence that the
authors draw together in order to sustain it. In my critical
assessment of this position, I will attempt to follow a
bifocal approach with two different sets of arguments.
First, I will present a more philosophical elaboration of
some of the underlying assumptions of the persistence
account. First, as I see it, the persistence account needs to
show both that depressive rumination deals with problems
(a) and that they are complex social problems that are to be
dealt with in an analytical manner (b), depression promotes
a productive analysis that helps people solve underlying
problems (c). However, I will argue that these claims
appear unsubstantiated. Second, I will draw on an established body of research that sheds doubt on the persistence
approach. Instead of helping to provide solutions, rumination maintains and exacerbates depression: it impairs
problem-solving capacities (d), hinders instrumental
behavior, (e) and undermines social support (f).
a) At first look, one might object that the issues that
depressive rumination deals with do not fit into our usual
definition of real problems. Rather, it seems that typical
ruminations such as ‘‘Why am I such a bad person?’’ are
often of hypothetical nature. Such ‘problems’ often do not
emerge from what we would consider real problems that
neither need analytical attention nor need to be solved at
all. In the vast literature on therapeutical approaches to
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48
depression based on Cognitive Theory, there is an overflow
of evidence that such phrases do no really reflect beliefs,
but are rather expressions of underlying emotional states
(see Varga forthcoming). However, by a problem we
usually mean an unresolved obstacle, which makes it difficult to achieve a desired goal. In other words, a necessary
condition for a problem to exist is the existence of a conscious belief that identifies a gap between what actually is
and what is desired. So overall, it might not be that obvious
that depressive rumination actually deals with problems at
all.
b) In order to lend credence to its conclusions, the
persistence account of depression needs to establish that
the problems that depressive rumination both is triggered
by and deals with complex social problems that that are to
be treated and solved in an analytical manner. To start
with, the first part of the assumption is not as straightforward as it first seems. The fact seems to be ignored that
often there is no apparent external trigger for a depressive
episode that can be identified and ruminated on. Additionally, while biologically informed psychiatrists and
psychologists would argue that there might not even be
such a trigger, proponents of the cognitive theory or psychoanalysis would maintain that what really matters is not
the external trigger, but the relevant metacognitive aspects.
Nevertheless, in this context, I will focus on the second
part of this claim. Watson and Andrews (2002) and
Andrews and Thompson (2009) claim that social dilemmas
have an analytical structure, because there are multiple
goals like maintaining cooperative bonds, and pursuing
self-interest. that must be satisfied. As an example for such a
complex social problem, the authors invoke the case of
sexual infidelity. The bottom line is that the adequate way of
dealing with a complex social problem like sexual infidelity
is analytic. In the spirit of Rational Choice Theory, the
authors argue that the problem must be broken down and
studied with respect to each goal the individual might have
(decision) making the most rational (i.e., utility-maximizing) decision requires the systematic evaluation of options.
Specific costs and benefits of possible strategy must be
carefully considered and weighed against each other to
identify the best likely choice. So the complexity of such
choices is a quantitative one: since such choices involve a
myriad of possible outcomes, and this is why the authors
compare such choices with playing chess (2009, 627).
However, I would like to question the assumption that
such complex choices like in the case of sexual infidelity
are adequately thought of as ones that need analytical
processing and costs and benefits analysis. The complexity
of a problem does not necessarily warrant the conclusion
that it is analytically difficult (claim 1). The underlying
problem here is one that has been discussed in philosophy
and particularly in ethics, dealing with the problem
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S. Varga
whether all choices can be conceptualized within the
framework of rational choice theory that is proposed here. I
cannot provide a complete argument against such a position here, I can nevertheless briefly mention some central
points. The point is that the kinds of choices that Andrews
and Watson discuss are ‘existential’ choices that are categorically different from choices between options. At least
since the work of Frankfurt (1988), it has become common
to think that some second-order choices constitute ourselves as the persons we are. However, if we acknowledge
that some choices constitute the basis for sets of preferences, then holding that every choice is made on the basis
of preferences gets us into an infinite regress. Indeed, there
is a difference in kind between such an existential choices
and calculative choices, because it involves fundamental
commitments that make up who we are, which are not
calculative in the sense of rational choice theory. The
person in question probably faces a situation, where the
task is not to execute a calculative, preference-based choice
between options, in principally the same way (but much
more complex) as choosing which of several different
meals to eat. Rather, such choices involve the sense of who
we are as persons and who we want to be, moral, ethical, or
possibly religious issues—questions that cannot be established by purely calculative means. To conclude this short
detour, it might not be the case that such complex choices
are adequately treated by analytical processing involving
costs and benefits analysis.
Equally severely challenging the persistence account,
according to an established body of research, instead of
helping to provide solutions, rumination maintains and
exacerbates depression: it impairs problem-solving capacities (d), hinders instrumental behavior, (e) and undermines
social support (f). Before dealing with evidence on these
issues, let me mention that longitudinal studies have shown
that generally, people engaging in rumination as a reaction
to stress are more vulnerable to develop depressive disorders and to have prolonged periods of depression (Just and
Alloy 1997; Kuehner and Weber 1999; Nolan et al. 1998;
Nolen-Hoeksema 2000; for an overview see Nolen-Hoeksema and Lyubomirsky 2005). It seems that rumination
exacerbates and prolongs distress, particularly depression
(Nolen-Hoeksema 1991).
d) A central challenge of the persistence account is to
show that rumination helps solving the problems that
actually trigger the depressed episode. However, there is
lack of support studies that show directly that. Andrews
and Thompson cite evidence such as the work of Hayes
et al. (2005) to underpin their point. But the interpretation
of the results of the work of Hayes et al. (2005) seems
exaggerated. In order to construct an alternative integrative
therapeutic approach, Hayes et al. (2005) maintain that
expressive writing ‘‘might facilitate processing by having
Evolutionary psychiatry and depression
clients articulate their thoughts and feelings about their
depression, as they also verbalize them in the sessions’’
(120). Importantly, and unsupportive of the interpretation
of Andrews and Thompson, they hold that ‘‘important tasks
in treating depression are to reduce the patterns of avoidance and rumination and to facilitate processing’’ (112).
More directly, they state that rumination inhibits processing (114). It seems that the results of the work they cite
contradicts the conclusions they make on its background.
With another argument, the authors attempt to make the
same point, maintaining that if depressive cognition were
generally unproductive, then the disruption of depressive
rumination should be associated with better outcomes.
However, this does not follow.
In another strategy to show that shows that people in
depressed states perform better in social dilemmas, the
authors rely on experimental research (for example Hertel
et al. 2000). Unfortunately, these experiments might not
provide good evidence for the conclusions the authors draw.
The fact that happy or secure participants show shorter
decision latencies in the chicken dilemma, whereas sad or
insecure participants exhibit more systematic and rational
behavior (tending to defect when others’ cooperation is high,
but to increase their investment for the common when others’ cooperation was low) does only say something about
cognition in depression, if one subscribes to the controversial thesis that there is no qualitative difference in processing
in sad mood and depression. Additionally, even if this were
the case, showing that depressed individuals engage in better
processing of information on costs and risks does not warrant the conclusion that they are better at solving the complex social problems. This only stands if one embraces the
assumption that complex social problems are best solved in a
calculative, cost-benefit equation. However, as I have
mentioned above, it is doubtful that this really is the case.
Additionally Nolen-Hoeksema and Lyubomirsky (2005)
have cited overwhelming evidence showing that rumination strategy and the typical negative depressive outlook
hampers problem-solving abilities rather than being solution-oriented. Because the ruminating person will be
focused on her depressive symptoms, which typically
involves negative self-ascriptions, the conclusion will often
be that he/she lacks the capacity to engage in constructive
activities. Ruminating depressives will lack confidence in
their solutions that might be the reason why they often do
not pursue them. Studies have confirmed this, showing that
rumination tends to result in an assessment of the particular
problems as overpowering and impossible to solve and
consequently people do not succeed in problem solutions
(Lyubomirsky et al. 1999; in clinically depressed patients
see: Donaldson and Lam 2004). Thus, it seems that ruminative responses in depression also interfere with good
solutions through the inhibition of instrumental behavior.
49
Studies reveal that even if the ruminator acknowledges that
a certain activity would have an effect, they have trouble in
motivating themselves to actually engage in these activities
(Lyubomirsky and Nolen-Hoeksema 1993). Taken together, it seems difficult to hold that depression is a kind of
source of cognitive regeneration leading to new behavior:
in fact, it is well established that long-drawn-out decisionmaking and decreased concentration are essential features.
And this brings me to another issue: in order to increase
plausibility, the persistence account would have to explain
the endurance of a depressive episode. Even taking into
account the complexity of the problems that are ruminated
on, it seems exaggerated to claim that they in some cases
require months of rumination.
While these points seem to shed doubt on one of the key
aspects of the persistence account, namely the usefulness of
depressive rumination, let me add a last point. For the sake
of argument, let us assume that depression is an adaptation.
Knowing that every depressive episode dramatically
increases the risk of another episode, this means that
individuals facing complex problems are more likely to
face such problems again. So even if it were true that
depression is an adaptation to allow optimal functioning, it
certainly does not seem to be effective.
e) Central symptoms like sexual dysfunction, physical
pain, and greatly increased risk of suicide are highly
unlikely to bring about advantages (DSM-IV-TR,
349–352). We have to bear in mind that statistically, those
who suffer from major depression are 20 times more likely
to commit suicide than individuals in the general population (Lonnqvist 2009). Curiously, the issue of suicide is not
discussed in adaptationist texts, like the otherwise informative paper of Andrews and Thomson (2009).
f) While on the adaptationist ‘‘social navigation hypothesis’’, Watson and Andrews (2002) interpret depression as a
mechanism designed to manipulate others into providing
resources, which may be useful in solving the complex social
problem at the core of depression. Depressed individuals
impose costs on close social partners who depend on them.
Therefore, to stop the imposition of costs, close social partners
are motivated to provide help and to make concessions to the
depressed individual (Hagen 1999, 2003; Watson and
Andrews 2002). However, the picture seems very different. In
fact, long-term depressive ruminations appear to have negative influence on social relationships. Quite conceivably, the
continued ruminations result in a decreasing emotional support from others (Nolen-Hoeksema and Davis 1999).
Conclusion
In the last few decades, there has been a genuine ‘adaptive
turn’ in psychology and psychiatry, which has led to
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50
evolutionary accounts for an increasing number of psychopathologies. If true, an appealing aspect in the application of evolutionary principles to psychiatric phenomena
is that such accounts make possible a more comprehensive
‘big picture.’ In this paper, I have attempted to explore
evolutionary accounts of depression, which due to its
suitable prevalence is seen to be an appropriate object of
evolutionary investigation. The general aim of the paper
was to explore the benefit and problem of evolutionary
approaches to depression, namely the mismatch and persistence accounts. Both accounts were found to harbor
significant flaws that might question their credibility and
usefulness as explanations.
I have argued that the mismatch model as a specific
application of evolutionary theory to depression does shed
light on particular aspects of depression and might create a
preliminary platform that has the potential to integrate what
seem as disparate aspects. But overall, if it is to provide a
credible alternative, the mismatch model needs to provide
more convincing answers: it needs to show why more
individuals are not afflicted by the condition, and it needs to
the assumption that it can identify something like a static,
ideal moment in human evolution. In the second part of the
paper, I have dealt more extensively with the persistence
account. In my attempt to follow a bifocal approach, I have
provided a philosophical elaboration of some of the underlying assumptions. My conclusion was that the persistence
account fails to show that depressive rumination actually
deals with problems, that complex social problems are to be
dealt with in an analytical, calculative manner, and that
depression promotes productive analysis that helps people
solve underlying problems. While these points seriously
challenge the account, additional doubt was shed on the
persistence approach by drawing on an established body of
research. Overall, it seems highly unlikely that depression
really does have the kind of adaptive capacity that the
proponents of the persistence account claim.
However, the failure of the assessed evolutionary theories of depression does not lead to the conclusion that we
should generally reject all attempts to apply evolutionary
theory to depression. Our understanding of depression is
still rudimentary, and there is no general reason why the
fact that mental capacities evolved should not be considered as a significant source of knowledge. Indeed, the
evolutionary theories of depression have provided perspectives that might not have been raised without an evolutionary perspective on human social behaviors. Also, the
heuristic value of evolutionary hypotheses in the development of testable assumptions should not be overlooked,
especially given the link between mind, behavior, and
society that such hypotheses provide. However, having said
this, I found that the mismatch and persistence theories of
depression could not be defended convincingly.
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S. Varga
Acknowledgments I wish to thank Laurence J. Kirmayer and Jennifer Radden for helpful comments and suggestions.
Conflict of interest
There are no conflicts of interest.
References
Acheson, O. 1998. Independent inquiry into inequalities in health.
London: HMSO.
Andrews, P.W.J., and A. Thomson Jr. 2009. The bright side of being
blue: depression as an adaptation for analyzing complex
problems. Psychological Review 116(3): 620–654.
Baptista, T., E. Aldana, F. Angeles, and S. Beaulieu. 2008. Evolution
theory: An overview of its applications in psychiatry. Psychopathology 41: 17–27.
Bebbington, P., J. Hurry, C. Tennant, E. Sturt, and J.K. Wing. 1981.
Epidemiology of mental disorders in Camberwell. Psychological
Medicine 11: 561–579.
Beck and Alford. 2009. Depression. Causes and treatment. Philadelphia, PA: University of Pennsylvania Press.
Cosmides, L., and J. Tooby. 1987. From evolution to behavior:
evolutionary psychology as the missing link. In The latest on the
best. Essays on evolution and optimality, ed. J. Dupre, 277–306.
Cambridge, MA: MIT Press.
Cosmides, L., and J. Tooby. 1994. Origins of domain specificity. In
Domain specificity in cognition and culture, ed. L. Hirschfeld
and G. Susan. Cambridge: Cambridge University Press.
Cosmides, L., and J. Tooby. 1999. Toward an evolutionary taxonomy
of treatable conditions. Journal of Abnormal Psychology 108:
453–464.
Cosmides, L., and J. Tooby. 2000. Consider the source: The evolution
of adaptations for decoupling and metarepresentation’. In
Metarepresentations, ed. D. Sperber. Oxford: Oxford University
Press.
Darwin, C. 1859. The origin of species by means of natural selection
or the preservation of favoured races in the struggle for life.
Random House, New York: The Modern Library.
Davis, D.R. 1970. Depression as adaptation to crisis. British Journal
of Medical Psychology 43: 109–116.
Dennett, D.C. 1978. Brainstorms: Philosophical essays on mind and
psychology. Cambridge, MA: Bradford Books.
Donaldson, C., and D. Lam. 2004. Rumination, mood and social
problem-solving in major depression. Psychological Medicine
34: 1309–1318.
Drummond, J.M., F.A. Issa, C.-K. Song, J. Heberholz, S.-R. Yeh, and
D.H. Edwards. 2002. Neural mechanisms of dominance hierarchies in crayfish. In The crustacean nervous system, ed. K. Wiese,
124–135. Berlin: Springer.
Eachus, J., M. Williams, P. Chan, et al. 1996. Deprivation and cause
specific morbidity: Evidence from the Somerset and Avon
survey of health. British Medical Journal 312: 287–292.
Fodor, J. 1983. The modularity of mind: An essay in faculty
psychology. Cambridge: The MIT Press.
Fodor, J. 2000. The mind doesn’t work that way. Cambridge MA:
MIT Press.
Frankfurt, H. 1988. The importance of what we care about.
Philosophical essays. Cambridge: Cambridge University Press.
Gerrans, P. (2002) The theory of mind module in evolutionary
psychology Biology and Philosophy 17: 305–321.
Gilbert, P., and S. Allan. 1998. The role of defeat and entrapment
(arrested flight) in depression: Exploring an evolutionary view.
Psychological Medicine 28: 585–598.
Evolutionary psychiatry and depression
Gilbert, P. 1992. Depression: The evolution of powerlessness.
London: Lawrence Erlbaum Associates.
Gilbert, P. 2006. Emotion and depression: Issues and implications.
Psychological Medicine 36: 287–297.
Glantz, K., and J. Pearce. 1989. Exiles from Eden: Psychotherapy
from an evolutionary perspective. New York: Norton.
Grant, K.A., C.A. Shively, M.S. Nader, R.L. Ehrenkaufer, S.W. Line,
T.E. Morton, H.D. Gage, and R.H. Mach. 1998. Effects of social
status on striatal dopamine D2 receptor binding characteristics in
cynomologus monkeys assessed with positron emission tomogrphy. Synapse 29: 80–83.
Hadley, C., and C.L. Patil. 2008. Seasonal changes in household food
insecurity and symptoms of anxiety and depression. American
Journal of Physical Anthropology 135: 225–232.
Hagen, E.H. 1999. The functions of postpartum depression. Evolution
of Human Behaviour 20: 325–359.
Hamburg, D.A. 1974. Coping behaviour in life-threatening circumstances. Psychotherapy and Psychosomatics 23, 13–25: 240.
Hamilton, W.D. 1964. The genetical evolution of social behaviour II.
Journal of Theoretical Biology 7: 17–32.
Hammen, C. 1992. Life events and depression: The plot thickens.
American Journal of Community Psychology 20: 179–193.
Hasday, J.D., K.D. Fairchild, and C. Shanholtz. 2000. The role of
fever in the infected host. Microbes and Infection 2: 1891–1904.
Hayes, A.M., C.G. Beevers, G.C. Feldman, J.P. Laurenceau, and C.
Perlman. 2005. Avoidance and processing as predictors of
symptom change and positive growth in an integrative therapy
for depression. International Journal of Behavioral Medicine 12:
111–122.
Hertel, G., J. Neuhof, T. Theuer, and N.L. Kerr. 2000. Mood effects
on cooperation in small groups: Does positive mood simply lead
to more cooperation? Cognition & Emotion 14: 441–472.
Horwitz, A.V., and J.C. Wakefield. 2007. The loss of sadness: How
psychiatry transformed normal sorrow into depressive disorder.
New York: Oxford University Press.
Just, N., and L.B. Alloy. 1997. The response styles theory of
depression: Tests and an extension of the theory. Journal of
Abnormal Psychology 106: 221–229.
Kessler, R.C., K.A. McGonagle, S. Zhao, et al. 1994. Lifetime and
12-month prevalence of DSM-III-R psychiatric disorders in the
United States. Archives of General Psychiatry 51: 8–19.
Kohrt, B.A., R.D. Kunz, J.L. Baldwin, N.R. Koirala, V.D. Sharma,
and M.K. Nepal. 2005. ‘‘Somatization’’ and ‘‘comorbidity’’: A
study of jhum-jhum and depression in rural Nepal. Ethos 33:
125–147.
Kravitz, E.A. 2000. Serotonin and aggression: Insights gained from a
lobster model system and speculations on the role of amine
neurons in a complex behavior. Journal of Comparative
Physiology 186: 221–238.
Kuehner, C., and I. Weber. 1999. Responses to depression in unipolar
depressed patients: An investigation of Nolen-Hoeksema’s
response styles theory. Psychological Medicine 29: 1323–1333.
Leahy, R.L. 2000. Sunk costs and resistance to change. Journal of
Cognitive Psychotherapy: An International Quarterly 14:
355–371.
LeDoux, J. 1996. The emotional brain: The mysterious underpinnings
of emotional life. New York: Simon & Schuster.
Lonnqvist, J.K. 2009. Suicide. In New oxford textbook of psychiatry,
2nd ed, ed. M.N. Gelder, Lopez-Ibor J. Andreasen, and J.
Geddes, 951–957. Oxford: Oxford University Press.
Lyubomirsky, S., and S. Nolen-Hoeksema. 1993. Self-perpetuating
properties of dysphoric rumination. Journal of Personality and
Social Psychology 65: 339–349.
Lyubomirsky, S., K.L. Tucker, N.D. Caldwell, and K. Berg. 1999.
Why ruminators are poor problem solvers: Clues from the
51
phenomenology of dysphoric rumination. Journal of Personality
and Social Psychology 77: 1041–1060.
MacLean, P.D. 1985. Evolutionary psychiatry and the triune brain.
Psychological Medicine 15: 219–221.
McGuire, M.T., and A. Troisi. 1987. Physiological regulation deregulation and psychiatric disorders. Ethology & Sociobiology 8:
9S–12S.
McGuire, M., and A. Troisi. 1998. Darwinian psychiatry. Press, New
York: Oxford University.
Meltzer, H., B. Gill, M. Petticrew, et al. 1995. The prevalence of
psychiatric morbidity among adults living in private households.
OPCS surveys of psychiatric morbidity in Great Britain. Report
I. London: HMSO.
Meyer, J.H., S. McMain, S.H. Kennedy, L. Korman, G.M. Brown,
J.N. DaSilva, A.A. Wilson, T. Blak, R. Eynan-Harvey, V.S.
Goulding, S. Houle, and P. Links. 2003. Dysfunctional attitudes
and 5-HT2 receptors during depression and self-harm. American
Journal of Psychiatry 160: 90–99.
Murphy, D. 2005. Can evolution explain insanity? Biology and
Philosophy 20(4(22)): 745–766.
Murphy, D., and S. Stich. 2000. Darwin in the madhouse: Evolutionary psychology and the classification of mental disorders. In
Evolution and the human mind, ed. P. Carruthers and
A. Chamberlain, 62–92. Cambridge: Cambridge University Press.
Nesse, R.M. 1984. An evolutionary perspective on psychiatry.
Comparative Psychiatry 25: 575–580.
Nesse, R.M. 1999. Testing evolutionary hypotheses about mental
disorders. In Evolution in health and disease, ed. S.C. Stearns,
261–266. New York: Oxford University Press.
Nesse, R.M. 2000. Is depression an adaptation? Archives of General
Psychiatry 57: 14–20.
Nesse, R.M., and G.C. Williams. 1995. Why we get sick. New York:
Times Books.
Nettle, D. 2004. Evolutionary origins of depression: A review and
reformulation. Journal of Affective Disorders 81: 91–102.
Nolan, S.A., J.E. Roberts, and I.H. Gotlib. 1998. Neuroticism and
ruminative response style as predictors of change in depressive
symptomatology. Cognitive Therapy and Research 22: 445–455.
Nolen-Hoeksema, S. 1991. Responses to depression and their effects
on the duration of depressive episodes. Journal of Abnormal
Psychology 100: 569–582.
Nolen-Hoeksema, S. 2000. The role of rumination in depressive
disorders and mixed anxiety/depressive symptoms. Journal of
Abnormal Psychology 109: 504–511.
Nolen-Hoeksema, S., and C.G. Davis. 1999. ‘‘Thanks for sharing
that’’: Ruminators and their social support networks. Journal of
Personality and Social Psychology 77: 801–814.
Nolen-Hoeksema, Wisco, and S. Lyubomirsky. 2005. Rethinking
rumination. Perspectives on Psychological Science 3: 400–424.
Patel, V. 2001. Cultural factors and international epidemiology.
British Medical Bulletin 57: 33–45.
Patil, C., and C. Hadley. 2008. Symptoms of anxiety and depression
and mother’s marital status: An exploratory analysis of polygyny
and psychosocial stress. American Journal of Human Biology 20:
475–477.
Pinker, S. 1997. How the mind works. New York: W.W. Norton &
Company.
Price, J.S. 1972. Genetic and phylogenetic aspects of mood variations.
International Journal of Mental Health 1: 124–144.
Price, J.S., and L. Sloman. 1987. Depression as yielding behaviour:
An animal model based on Schjelderup-Ebb’s pecking order.
Ethology and Sociobiology 8: 85–98.
Price, J.S., L. Sloman, R. Gardner, P. Gilbert, and P. Rohde. 1994.
The social competition hypothesis of depression. British Journal
of Psychiatry 164: 309–315.
123
52
Randolph, M., and M.D. Nesse. 2000. Is depression an adaptation?
Archives of Gen Psychiatry 57: 14–20.
Schmale, A. 1973. The adaptive role of depression in health and
disease. In Separation and depression, ed. J.P. Scott and F.C.
Senay, 187. Baltimore, MD: King.
Segrin, C., and J.P. Dillard. 1992. The interactional theory of
depression: A meta-analysis of the research literature. Journal of
Social and Clinical Psychology 11: 43–70.
Shively, C. A. 1999. Social subordination stress, behavior, and central
monoaminergic function in cynomolgus monkeys. Biological
Psychiatry 44: 882–891.
Sloman, L., P. Gilbert, and G. Hasey. 2003. Evolved mechanisms in
depression: The role and interaction of attachment and social
rank in depression. Journal of Affective Disorders 74(2):
107–121.
Stansfeld, S.A., and M.G. Marmot. 1992. Social class and minor
psychiatric disorder in British civil servants: A validated
screening survey using the General Health Questionnaire.
Psychological Medicine 22: 739–749.
Stansfeld, S.A., J. Head, and M.G. Marmot. 1998. Explaining social
class differences in depression and well being. Social Psychiatry
and Psychiatric Epidemiology 33: 1–9.
123
S. Varga
Stevens, A., and J. Price. 1996. Evolutionary psychiatry: A new
beginning. London: Routledge.
Thornicroft, G., O. Margolius, and D. Jones. 1992. The TAPS Project.
6: New long-stay psychiatric patients and social deprivation.
British Journal of Psychiatry 161: 621–624.
Tooby, J., and L. Cosmides, 1995. Foreword. In Baron-Cohen (1995),
xi–xviii.
Treynor, W., R. Gonzalez, and S. Nolen-Hoeksema. 2003. Rumination reconsidered: A psychometric analysis. Cognitive Therapy
and Research 27: 247–259.
Wallace, A.R. 1875. Natural selection. London: Macmillan.
Watson, P.J., and P.W. Andrews. 2002. Towards a revised evolutionary adaptationist analysis of depression: The social navigation hypothesis. Journal of Affective Disorders 72: 1–14.
Weissman, M.M. 1987. Epidemiology of depression: Frequency, risk
groups, and risk factors. In Perspectives on depressive disorders:
A review of recent research, 1–22, Rockville, MD: National
Institute of Mental Health
Wenzlaff, R.M., and D.D. Luxton. 2003. The role of thought
suppression in depressive rumination. Cognitive Therapy and
Research 27: 293–308.
Wilson, E.O. 1975. Sociobiology. Boston: Belknap Press.