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152 The APA Publishing Textbook of Mood Disorders, Second Edition
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oblique drawing up of the eyebrows, the puckering of their inner ends, and the formation of rectangular furrows on the middle of the forehead” as a species-typical expression of this kind of low mood (Darwin 1872, p. 192).
Clinicians will immediately notice the similarities of the behavioral correlates of
protest and despair to signs and symptoms of agitated (protest) and retarded (de
spair) depression, respectively. In that attachment styles are “transposed” over the
lifespan to important relationships other than the primary caregiver (Bowlby 1969),
separation or loss can trigger low mood and depressive responses by activating evo
lutionarily and developmentally “primitive” mechanisms that originally evolved as
coping strategies for impending or real abandonment. Depression in response to social
losses is more likely to occur in individuals who as children were exposed to neglectful
or inconsistent parenting and hence developed insecure attachment. Arguably, attachment insecurity results in individuals having greater difficulties in eliciting social support, while their mistrustful inner working models promote the subjective experience
of social isolation and emotional distance from others (Gilbert 2006), potentially creat
ing a vicious circle from which there is no escape without therapeutic support. This
interpretation is compatible with ethological work showing that poor maternal care
predicts an unfavorable subsequent course of depression (Geerts et al. 2009). Bereavement is another typical response associated with low mood in reaction to the loss of
an important attachment figure; it is not to be pathologized and mistaken for depres
sion (Nesse 2005). Aside from attachment issues, however, mood extremes of depression or mania can emerge from other potential social hazards, such as ones relating to
social hierarchy.
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Social Competition
Interpersonal tension is another common source of low mood and depression,
whereas ingratiation and dominance are drivers of high mood and mania. In social
animals, conflict can arise over any one of the above-described biosocial goals. Indeed, disputes over access to mates, social status, and reciprocal relationships occur
in every primate society, including human social groups (de Waal 1989). Succinctly
put, competition for mates, resources, and status is so inevitably linked to human so
cial life that everybody is exposed to it at some point (Wilson 1998). Accordingly,
there are several evolutionary theories about the role of social competition in relation
to excessive mood states (Price et al. 1994). These theories differ in nuances—that is,
whether the focus is on the chosen strategy to negotiate social hierarchy (escalating
vs. deescalating social conflict) (Gardner 1982), the role of defeat (Price 1967), or in
voluntary subordination in relation to social rank (Gilbert 1992), which includes the
expression of arrested anger (Gilbert et al. 2004), entrapment in situations where submission is ineffective (Gilbert 1992; Price and Wilson 2011), or the reduction of social
risk (Allen and Badcock 2003), including the functional role of ruminative thinking
(Watson and Andrews 2002). For its part, mania can be seen as an unconstrained acquisitive drive (Wilson 1998).
In a now-classic contribution, Price (1967) was the first to highlight similarities in
behavior between nonhuman primates negotiating social rank and the signs and
symptoms of human depression. He argued that dominant individuals display aggression overtly or more subtly to subordinates in response to challenges to, or to sim-
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ply maintain, their social rank. Submissive behavior and defeat, in contrast, are typical
behavioral responses by the subordinate to deescalate social conflict (i.e., signal ap
peasement) (Price et al. 2007). Changes in rank usually cause elation when climbing
up the social ladder, or depression when slipping (Sloman et al. 2011). The former is
an equivalent to (hypo)mania, which can also include challenging behavior (Sloman
et al. 2011). The latter is protective because it prevents subordinates from fighting back
(although irritable mood may be redirected against “inferior” subjects) (Price 1967). In
human depression, as Price and colleagues subsequently argued, not only do individ
uals signal social defeat by withdrawing from the social arena, but they also actively
deescalate conflict through manifest submission, such as hunched body posture, gaze
aversion, and avoidance of movements that could be interpreted as competitive (re
viewed in Hagen 2011). In addition, loss of appetite and libido indicate abstention
from competition for resources or mates. Internal signals or subjective appraisals of
defeat comprise feelings of inferiority, shame or guilt, loss of self-esteem, self-criti
cism, and powerlessness, altogether contributing to low mood (Carvalho et al. 2013;
Gilbert 2006). This is entirely consistent with ethological work on nonverbal behavior
showing that depressed individuals avoid eye-to-eye contact, manifest reduced facial
expressivity and speech production, and frequently make use of species-specific child
behaviors (traditionally labeled “regression”), thus reducing the risk of being attacked
(Geerts and Brüne 2009). Conversely, mania is associated with the activation of evolutionarily ancient systems involved in the regulation of arousal and ambition (Wilson 1998).
In an extension to the social rank theory of depression, Gilbert et al. (2002) have
pointed out that in situations in which signaling defeat is ineffective, social support
is lacking, or control over social resources is poor, feelings of entrapment and arrested
anger may occur, and are associated with persistent high arousal. In such circumstances, feelings of inferiority necessitate holding upward aggression against dominant individuals in check (Carvalho et al. 2013). Behaviorally, conflicting motivation
involving fight-or-flight responses is expressed through so-called displacement activ
ities, such as self-grooming, locomotor activity, or “nervousness,” any of which may
present in what is clinically called “agitated depression” (Troisi 2002). As Gilbert and
Allan (1998) have noted, subjective feelings of entrapment can be amplified by internal processes such as intrusive thoughts and ruminations. For example, continuous
rumination about one’s inferiority may enhance perceptions that there is no escape
from the situation, which may ultimately lead to suicidal ideation or actions. In contrast, Andrews and Thomson (2009) ascribe to rumination associated with low mood
a functional role, which helps direct one’s attention away from distracting and unattainable goals and reallocate energy to solving problems entailed in the precipitation
of the current situation (Durisko et al. 2015).
The social competition hypothesis is in full accord with the broader concept of low
mood and depression as a risk-averse strategy for co pin g wit h social thre at ( Alle n an d
Badcock 2003). This version of the same theme emphasizes that whereas people with
a functional social network can engage in some risk-taking activities, individuals
with less supportive social relationships are reluctant to take social risks. Thus, this
view emphasizes the role of social adversity in depression, implying that subjects
who are risk a verse are also more vigilant toward social threats and avoidance of their
own failure.
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In essence, the multiple versions of the social competition hypothesis are by no
means mutually exclusive. Moreover, the attachment perspective and the social com
petition approach converge on findings that the association between insecure attachment and depression is mediated by one’s perceived social rank, which is not the case
for individuals with secure attachment patterns, even though the picture is less clear
for people with bipolar disorder (Gilbert et al. 2007). On the other hand, Keller and
Nesse (2005) noted some interesting differences in symptomatology between depressed subjects who experienced loss and depressed subjects who failed to achieve
important biosocial goals. Indeed, the former more often display crying and sadness
(akin to Bowlby’s [1969] protest-despair stages following loss or abandonment),
whereas the latter more frequently experience subjective feelings of pessimism and fatigue. Low mood in response to social losses or thwarted biosocial goals can serve as
an honest signal to elicit help from one’s social environment, but also can express a
(nonconscious) dishonest strategy of extracting “unearned” resources from others, especially when disguised as “learned helplessness” (Watson and Andrews 2002). This
interpretation is consistent with ethological research analyzing nonverbal behavior of
depressed patients and their interlocutors during clinical interviews, in which high
levels of nonverbal support-seeking on the part of the depressed patient and high lev
els of received nonverbal support from the interviewer were found to be associated
with an unfavorable prognosis. Indeed, Segrin (2000) found that even mild symptoms
of depression can induce rejection responses in other people, particularly if the depressive symptomatology persists over extended periods of time. Thus, ethological perspectives on depression suggest that depression can also be the consequence of malfunctioning interpersonal processes, rather than a strategy to ameliorate interpersonal
social stress (Geerts and Brüne 2009). It is something of a paradox that members of an
altruistic and empathic species like ours sometimes reject those who need help.
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Sickness Behavior, the Immune System, and Depression
Natural selection has endowed all living creatures with defense mechanisms against
pathogenic agents. Higher vertebrates possess an innate and adaptive immune sys
tem that activates when the body is attacked by viruses, bacteria, fungi, or prions.
Proinflammatory states are associated with a behavioral response, known as “sick
ness behavior.” Sickness behavior is characterized by lethargy, fatigue, loss of appetite, psychomotor retardation, and social withdrawal. This evolutionarily conserved
defense reaction to infection is adaptive, because it helps the organism recuperate by
saving energy and by reducing the risk of being attacked in times of enhanced vulnerability (Eisenberger et al. 2017; Raison and Miller 2017). In fact, in gregarious species, sick individuals not only are at risk of predation but also are susceptible to decline in social rank, and to suffering a reduction in reproductive success, as their sexual attractiveness decreases (Schaller 2011). Thus, sickness behavior is also associated
with heightened vigilance toward social threats (Eisenberger et al. 2017). In addition,
kin selection theory (Hamilton 1964) suggests that social withdrawal may reduce the
risk of infection for genetically related individuals, even though the costly side of social avoidance may be the loss of provisionary care (Schaller 2011). Interestingly, animals, including humans, are well able to recognize even subtle signs of sickness in
others, which activates an immune response in the observer, and often fosters rejec-
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tion and avoidance of the sick individual (Schaller 2011). In humans, however, sickness behavior is usually associated with approaching close others and avoiding
contact with strangers (Eisenberger et al. 2017).
Because sickness behavior is associated with low mood and anhedonia, depression
can be seen as an evolved state of “pathogen defense readiness” (Raison and Miller
2017). Aside from the behavioral similarities between sickness behavior and depres
sion, abundant evidence from immunological research supports the idea that depression can be associated with a proinflammatory state (Dantzer and Kelley 2007; see also
Chapter 7, “Role of the Immune System in Mood Disorders,”
precipitating conditions of low mood and depression, including parental separation,
loss, childhood trauma, intense social competition, loneliness, or social disconnected
ness, are accompanied by increased immune activation. In other words, evolved environmental contingencies identified as potentially dangerous for survival and reproduction—for example, loss of important attachment figures or thwarted biosocial
goals—cause the organism to take preparatory action by activating the immune sys
tem. Notably, in terms of causality, proinflammatory states, such as ones induced by
the experimental application of lipopolysaccharide, a bacterial agent that triggers an
inflammatory response, induce not only low mood and anhedonia but also feelings
of social disconnectedness, loneliness, and desire for closeness to familiar others, as
well as greater vigilance toward social threat (Eisenberger et al. 2017).
Together, the evidence strongly suggests that evolution by natural selection has
produced powerful mechanisms that protect organisms against a broad variety of
threats, including infectious and social ones. Immunological response patterns seem
to be designed in ways that bodies do not discriminate between different causes of
threats, but instead uniformly react with proinflammatory states. With regard to de
pression, it has been debated as to whether the increase in prevalence, particularly in
urban areas of developed countries, could be related to alterations of the immune sys
tem caused by a diminished exposure to pathogens early in life. According to the “old
friends” hypothesis, exposure to some pathogenic agents early in life is necessary for
normal development of immunoregulation. In the absence of the acquisition of normal
immunocompetence, a person’s risk for chronic proinflammatory states increases, as
well as risk for autoimmune disease. Due to space limitations, this perspective on epi
demiological aspects of depression cannot be dealt with in greater detail here (for further discussion, see Rook and Lowry 2009, as well as Chapter 7 in this text). It is
noteworthy, however, that recent research indicates that the picture is even more complex, with both elevated pro- and anti-inflammatory markers in treatment-naïve patients with major depressive disorder (Syed et al. 2018). Interestingly, lack of response
to treatment was associated with a pervasive upregulation of proinflammatory cytokines, suggesting that a downregulation of defense mechanisms at both somatic and
psychological levels is vital for the improvement of depressed mood states.
in this text). In addition,
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Evolutionary Genetics, Depression, and Mania
Excessive mood states of depression and mania are so common across the globe that
it is implausible to assume that genes associated with the condition are wholly disadvantageous in terms of survival and reproduction, or even selectively neutral. The
156 The APA Publishing Textbook of Mood Disorders, Second Edition
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crucial question is why genes conferring risk for depression and mania have been
preserved in the human gene pool (Wilson 1998). A meta-analysis in about 250,000 in
dividuals with depression and 560,000 control subjects revealed 102 independently
segregating genes and another 269 genes associated with depression (Howard et al.
2019); however, even though the analysis indicated some interesting inverse correla
tions of depression with age of menarche and menopause, it failed to examine potential evolutionary implications of these findings. As with many other genetic studies,
the basic misconception is that genes associated with disorder are maladaptive (Wil
son 1998). The prevailing view on gene-environment interaction concerning psychopathological conditions (also known as the “diathesis-stress model,” per Monroe and
Simons 1991) suggests that individuals carrying certain genetic variants who are ex
posed to negative life events are vulnerable to developing clinically relevant signs
and symptoms. In contrast, individuals not possessing the “risk allele” are genetically
protected or resilient (Feder et al. 2009). For example, the short (S) allele of the serotonin transporter gene predisposes to depression if accompanied by stressful life
events (Caspi et al. 2003); however, variation at the corticotropin-releasing hormone
receptor may prevent depression even in the presence of childhood maltreatment
(Polanczyk et al. 2009).
A pervasive theoretical problem associated with the diathesis-stress model concerns the observation that many of the supposed “vulnerability genes” have undergone positive selection in human evolution. It is simply implausible to assume that
natural selection has favored the preservation of alleles in the human gene pool that
increase vulnerability to adversity, particularly when considering that the environment of evolutionary adaptedness was probably fraught with negative life events
occurring throughout the entire life span. Instead, positive selection of such alleles
strongly suggests that these genes exert hitherto undetected or overlooked beneficial
effects on reproductive fitness (which is not the same as being “good for health”) (Ellis et al. 2011). For example, the S allele of the serotonin transporter gene predisposes
to depression if associated with adverse life events, but it is also linked to cognitive
performance and social conformity, which may compensate for its disadvantageous
effect on mood in a “balanced polymorphism” fashion (Homberg and Lesch 2011).
Along similar lines, there is evidence to suggest that genes predisposing to depres
sion and mania may play an important role in immune function, potentially being involved in the defense against pathogens that were more prevalent in our evolutionary
past (Raison and Miller 2017). Such a proposition would be compatible with seasonal
peaks of depression during winter and spring, when exposure to pathogens is high
(Anders et al. 2013).
In addition, a given genetic variation that predisposes to psychopathology if associated with adverse life events can have beneficial effects when environmental contingencies are developmentally more supportive; this variability is known as “differential
susceptibility” or “phenotypic plasticity.” Put another way, the idea that genes confer
responsivity to both positive and negative conditions can explain why they persist in
human gene pools (Boyce and Ellis 2005). Consistent with this conceptualization, the
S allele of the serotonin transporter gene confers a lower risk for depression in individuals who grow up in favorable early environments (Taylor et al. 2006).
In any event, because the search for so-called risk alleles for psychopathological
conditions has been criticized for methodological reasons, and especially because the
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role of the serotonin transporter gene in depression has come under attack, with
meta-analyses both in favor of and against its involvement (e.g., Clarke et al. 2010;
Culverhouse et al. 2018), we need to emphasize that the heritability of mood disor
ders is polygenic, with individual candidate genes contributing only small effects to
the phenotypic expression (Howard et al. 2019). It may nevertheless be fruitful to reframe research into the relevance of gene-environment interaction for mood disor
ders in a broader Darwinian perspective.
Conclusion
In this chapter, we set out to explore the evolutionary or “ultimate” dimensions of
mood and mood disorders, while leaving aside the “proximate” factors, including the
neurophysiological and endocrinological foundations of mood disorders, which are
discussed in other chapters of this text (see Chapter 5, “Neurochemistry of Mood Disorders”; and Chapter 6, “Psychoneuroendocrinology of Mood Disorders”). We also
skipped the increasing evidence for a role of epigenetic changes in mood disorders
(see
Chapter 13, “Epigenetics of Mood Disorders”) and shed only a sketchy light on
immunological and genetic aspects of mood disorders (see
mune System in Mood Disorders”; and Chapter 12, “Genetics of Mood Disorders”
well as the impact of coevolutionary processes of the human microbiota on brain func
tion (Cryan and Dinan 2012). Instead, we have focused on the role of low mood as a
defense mechanism against abandonment and social threats, and on its protective
role for organisms in times of increased vulnerability, in contrast to high mood, which
is a mechanism for resource and/or social attainment.
At a general level, symptoms associated with clinical depression such as avolition
and anergia can be understood as imbalances between active and passive responses
to threat (LeDoux and Daw 2018). However, it is a common misconception to believe
that positive mood states are superior to low mood states simply because the latter are
associated with potentially disadvantageous situations and subjectively bad feelings.
Even suicidal behavior may be interpreted, under specific circumstances, as biologically advantageous (in the evolutionary sense). For example, “perceived burdensomeness” toward kin may undermine self-preservation motives, such that sacrificing
one’s own life may eventually foster survival of one’s genes (Joiner et al. 2002). From
an evolutionary point of view, killing oneself is, however, such a tremendously costly
behavior (aside from being a personal tragedy, of course) that eusocial motives or entrapment can certainly not fully account for such a multifaceted phenomenon that is
putatively human specific (even though self-sacrificial behavior is widespread in eusocial animals) (Chiurliza et al. 2018). Although an evolutionary analysis of suicidality
is beyond the scope of this chapter, we assert that severe clinical depression does not
serve adaptive purposes. However, the boundaries between adaptive low or high
mood and maladaptive depression or mania may wax and wane with individual ecological contingencies and have likely become more prominent as the modern environment differs from the environment of evolutionary adaptedness, and hence are
difficult to determine (Wilson 1998). Recent calculations suggest that the global prevalence of unipolar depression is about 8 times that of bipolar disorder, 14 times that
of schizophrenia, and 34 times that of autism spectrum disorder, and therefore is too
Chapter 7, “Role of the Im
), as
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frequent to conclude that it is always associated with biological malfunction. Moreover, mood disorders may be the only major psychiatric condition to be associated
with increased biological fitness (i.e., fecundity), especially in women (Durisko et al.
2015). This idea is consistent with evolutionary explanations for sex differences in
prevalence of depression as well as hypersexuality in mania. Women are twice as vulnerable to developing depression as men, which could relate to the biological fact that
they invest much more in offspring and thus are more dependent on support from
their mates and close kin (Troisi 2001). Therefore, the risk of losing important social
connections when engaging in conflict-escalating strategies may be more relevant for
women than men, even though this is not reflected in differences in the prevalence of
bipolar disorder. In contrast, the preservation of genes predisposing to (hypo)mania
may, in part, relate to the enhanced creativity, charisma, and leadership found in firstdegree relatives of patients with bipolar disorder, all of which likely serve as proxies
for reproductive success (Wilson 1998).
Understanding mood and mood disorders in an evolutionary perspective can also
be informative with regard to therapy. One conclusion could be that it might not al
ways be useful to suppress low mood, just as it is not always helpful to block cough,
fever, or pain. Instead, it might be more appropriate to analyze individual needs in
terms of mood regulation systems, including motivation, affiliation, and safeness, as
conceptualized in compassion-focused therapy (Gilbert 2014).
Evolutionary accounts of psychopathology, including this abbreviated consideration of mood and mood disorders, have limitations and certainly many critics. Nevertheless, because nothing in biology really makes sense except from an evolutionary
perspective, additional research on the evolved bases of mood and its disorders will
surely make further and significant contributions (Dobzhansky 1973).
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