From:
The Handbook ofEvolutionay Psycholoy
Edited by David Buss
Jolm Wiley and Sons, Hoboken, NJ, 2005
CHAPTER
32
Evolutionary Psychology
and Mental Health
RANDOLPH 1. NESSE
N EVOLUTJONi\RY PERSPECTIVE revolutionized our understanding of be­
havior over a generation Jgo, b u t most tnental health clinicians and
researchers stil l view evolution as an interesting or even thr�atcning al­
ternative, instead of recognizing it as an essential basic science for understanding
mental di sorders. v1any factors explain this lag in incorporating new knowledge,
but the n1ost important 1nay be the clinician's pragn1atic focus on finding ways to
help people nmv. Evolutionary researchers have not found a new treatment for a
single mental disorder, so why should n1ental health clinicians and researchers
care about evolutionary psychology (EP)? This chapter attempts to answer that
question. The greatest value of an evolutionary approach is not some specific find­
ing or ne\v therapy, but is in stead the framework it provides for uniting a l l JSPL'cts
of a biopsychosocial model. Perhaps equa l ly valuable is the deeper empathy fos­
tered by an evolutionary perspective on l ifl•'s vicissitudes. An evolutionary per­
spective does not con1pctc with other theories that try to explain why some people
have ment.1l di�orders and others do not. Instead, i L a�ks a fundamental ly d i ffer­
ent question: Why has natural selection left a l l hun1ans so vulnerable to 1nental
d isorders? At first, the question seems senseless. Natural selection shapes mecha­
n isn1s that \vork, so how can it help us understand why the mind fails? It is also
d i fficult to sec how i t is useful to know vvhy we are vulnerable. Who cares why a l l
humans are vulnerable t o depression, when the goal i s t o help the individual who
is depressed here and now? Surmounting these conceptual hurdles is a challenge
that requires time and effort. Researchers and cl inicians w i l l n1ake the effort when
they know what evolution offers to the understanding of mental disorders.
A
WHAT EVOL U T IO N O F F E RS
v1any ha\'C contributed to the grmv th of evolutionary psychiatry, but the contri­
butions are in d iverse sources and not ahvays consistent. Early applications of
903
904
EVOLUIONJZINC TRADITIONAL DISCIPL I NES OF PSYCHOLOGY
Table 32.1
Eight Fundamental Contributions
An evolutionary perspective on mental disorders:
1. Asks new questions about why natural selection has left us all vulnerable to mental
disorders, questions with six kinds of possible answers,
2. Offers the beginnings of the kind of functional understanding for mental health professions that physiology provides for the rest of medicine,
3. Provides a framework for a deeper and more empathic understanding of individuals,
4. Explains how relationships work,
5. Provides a way to think clearly about development and the ways that early experiences influence later characteristics,
6. Provides a foundation for understanding emotions and their regulation,
7. Provides a foundation for a scientific diagnostic system,
8. Provides a framework for incorporating multiple causal factors that explain why some
people get mental disorders while others do not.
ethology to mental disorders (McGuire & Fairbanks, 1977; White, 1 174) gave rise
to mort> specific and comprehensive evolutionary approaches (McCuin· & Troisi,
1998; Pitchford, 2001; Stevens & Price, 1996; Wcncgrat, 1990). Several books cover
specific conditions (Baron-Cohen, 1 99�. 1 997; Cilbert, 1 992; Wcn<'grat, 1995).
while others take a more anthropological approach (Fabrcga, 2002). Many articles
address specific mt'ntal disorders, and some provide a new found<.llion for defin­
ing the categories that describe disordc'rs (Cosmidcs & Tooby, 1 YY9; Wakefidd,
1992). Mony chapters in this Handbook ,md many ,;eneral books about El' tackle
one or another mental disorder (Badcock, 2000; Barkow, Cosmidcs, & Tooby, 1992;
Barrett, Dunbor, & Lycctt, 2002; Buss, 1994, 1 995, 2003, 2004; Crow ford, Smith, &
Krebs, 1 987; Caulin & McBurney, 20ll1 ; Wright, 1 994). The ideas in these sources
are too 1nany and too diverse to even list, but many can be summ.1rizcd in a list of
eight fundamental contributions that an evolutionary pcrspectiH' offers to psy­
chiatry and clinical psychology (Table 32.1 ) A brid summary uf c-.1ch sl'ls the
stage for considL·ring specific disorders.
.
EXPLAJNJNG VUL..'EHABl!JTY TO M t·: N TAL O!�ORDERS
The task of explaining why \Ve are vulnerable to mental disorders is no different
from that of explaining why we arc vulnerable to physical diseases. Tht' tendency
in both cases l1as been to oversimplify the problc1n by attributing v ulnerability to
the limited powers of natural selection. ThesE' limits are important expl1n,1tions
for some disl'ases, but there arc five other posslblc reasons thut tlw body and
mind are not better designed, starting with the mismatch bchvccn our bodies ,1nd
our environments (Nessc & WilliJms, 1 994; Willia1ns & Ncsse, 1991).
Mismatch Most common chronic diseases arc caused by novel cnvironn1cntcd
factors. For instance, atherosclerosis and breast cancer arc prcv<1knt now be­
cause our bod ics are not \veil dcsign(•d for life in <l xnodcrn en\' ironnwnt (Eaton
et al., 2002). Whether rates of mental disorders are also increasing remains un­
certain. An internationzd effort to gather prevalt'llet' data on mental disorders
frmn 72,000 interviews in 1l countrh�s (Kessler & Ustun, 2000) uses urban or
Evolutionary Pst;clzologt; and Mental Health
905
rural agricultural sites. No con1parable effort is estilnating d isorder rates i n
hunter-gatherer populations. This i s unfortunate because such studies m a y not
be possible in the next generation, but understandable because o f the method­
ological obstacles.
Mental d i�orders are often blamed on the modern environment. When reading
and writing vverc first -spreading, Burton at tributed n1clancholy to excessive
study and "too little Venus" ( Burton, 16241911 ) . Much more recentlv, retrospec­
tive data seemed to suggest th,lt depression rates were increasing r,1pidly with
each generation (Cross-Na tional Collaborah\re Croup, 1 992). l--f-wever, data gath­
ered using consistent questions in the same population over n'cent decades
showl'd no such increase (J. M. vfurphy, Laird, fvlonsun, Sobol, & Leightun, 2000).
For drug 1nd a l cohol problems, the story is more clL'ar-cut. The rapid spread o f
i!cohol-making technology ch,1nged our \Vorld i n \vays o u r species has n o t yet
adapted to (Institute of Medicine, 1987), although selection n1ay have increased
the frequency of a defective aldehyde dehydrogenase gene Lhat may protect Asian
populations from alcoholism (M. Smith, 1986).
Infections persist because our every evolutionary nd­
vance to escape bacteria and viruses is mJtched by their n faster evolution
(A . S. Brown ct a l . , 2004; Ewald, 1 994). Furthermore, the ddcnses that protect
us, espt' c i a l l y in1mune responses, tend to cause problen1s t hen1sclves. Some
men t a l d isorders mi!y resu t from arms races .vith pathogens and their <Juto­
i nnTune :-;equelae. For instance, some cases of obsessive-compulsive disorder
n1ay result fn}m streptococcal-induced autoimmune dan1agc to t11e caudate nu­
cleus (S\vcdo, l.eonard, & Kie�sling, Fl94). Prena tal exposure to infection n1ay
pred i-;pose to schizophrenia (lxdgL•rwood, Ewald, & Cochran, 200:1) cls sug­
gested by inc re<lsed rates of schizophrenio in babies born during influenza epi­
delnics ( Kunugi e t a l., 1995) 1nd a sevenfold risk increase for babies born to
motl1ers who had influenza during tlw first trinwstcr (A. S. Brown ct al., 2004).
Infectious causes h ;we been proposed for a wide range o f nwntal disordt'rs, es­
p ec i a l l y a f fe c tive disorders (Ewilld, 2000).
A mort' insid ious resul t of rapid coevolution arises fron1 con1petition within
our species that induces more and mon' >xtreme traits, especially thosl' th<1t lead
to winning social con1pcti tions (A l'x,1ndcr, 197-; Humphrey, 1 976; Whiten &
Byne, 1 997). I f sexual select ion has shaped mental traits ( M i ller, 2000), this could
account for vulnerabil i t y to certain disorders, espl'cia l l y thuse associated with
creativity ( R ich8rds, Kinner, Lunde, & Bt'net, 19S8; ShanL'r, M i ller, & Mintz,
2004). Even aside from cmnpcting for p1rtncrs, competing for status absorbs vast
human energy ( Bj]rkow, 1989; Veblen, N9) and gives rise to much suffL-ring from
cn.Ty and the ncgntlve emotions associ;1ted with f<1ilures (Gilbert, Price, & /\Ilen,
1995). Such emotional tendt'ncies might well resut from arms races that often
l cmTe us in zero-sum competitions ( Fr(]nk, lJ99).
Infection and Coevolution
Tmde-0}�s Design tr1de-offs makL' pcrft•ction in1possible for any trajt, natural or
hun1an n1ade. A car tha t gets 60 m i les pt'r ga l lon w i l l not get to hO mi lt's per hour
in 6 seconds. Wt' humans could run faster i f our legs were longt>r, but our bones
vvould be Inon• fr<1gile. \Ve could han:' lt•ss anx iety, but only a t the cost of being
more l ikt'l.Y to be injured or killed.
906
EvoLuT rONIZJNG TRADITIONAL DrsC!PUNES oF PsvcHoLocv
Constraints Systen1s shaped by natural selection are subject to several special
constraints, especially path dependence. For instance, we are stuck with eyes
'rhose vessels and nerves run between the light and the retina. Fu r thern1ore, in
contrast to consciously created designs, biological designs are products of selec­
tion that involve lilnited options, random effects, inaccu rate tran smission of the
DNA code, and the vagaries of intPraction effpcts with diff>rent environments.
Far from a.1suming that everything i'i adaptive, an evolutionary approach cal ls at­
ten tion to defective and substandard designs that result from multiple trade-offs,
constraints, and errors.
SelccUon Is for Reproductive Success, Not Health Many imagine that selection
shapes bodies zmd minds that arc heathy, long-lived, and coopcratiVl'. I t does,
wl1E'n those traits increase reproductive SUCCC'SS (RS). HowenT, cl gene that de­
creases health, longevity, or coopl'rativeness \vill nonetheless spread if it in­
creases RS. Such genes are likely responsible for many of ou r least valued
characteristics, such as bitter competition, envy/ greed, and unqut·nchable sexual
desire and jealousy ( Buss, 2000). The djfferl'nces between the seAL'S arise largely
because different reproductive stratE'gics shape different physic1l and n1cntal
traits, even at the expense of longevity and individual wel l-being: (C ronin, 199 1 ;
Daly & Wilson, 1 983; Geary, 1 998; Kruger & Ncsse, 2004).
Pain, cough, fever, and other protective responses are unpleasant but
useful responses that protect us from dangl'r and loss. The prevalent tendency to
confuse these defenses with disease's <Jnd defects has been caled "The Clinician's
ll lusion" ( Ncsse & Williams, J994). Most physicians knmv that cough and infldm­
mation are adaptations, but the utility of fl'\rcr, diarrhea, and anxiety is less widely
rcconized. A naYve view sues our vulnerJbility to neg;1tive emotions as examples
of poor design. But notural selection does not care 1 fig for our happiness; it just
mindkssly shapes whatever emotional tcndenciL'S incrc'ase RS ( Nessc, 1 991n;
Tooby & Cosmides, 1990). While positive emotions are useful in situations whefl'
energy and risk-taking pay off ( Fredrickson, 1 998), they ciln be fataJ in dangerous
situations ( N cssc, 2004).
Dcfcn;cs
Summing Up Six Causes Smne evolutionary approaches to mental disorders em­
phasize one of the preceding six possible explan<ltions. For instance, some au­
thors attribute much psychopathology to living in a modern environment (Clantz
& Pearce, 1989); others e mphasize infection (Ewald, 2000), constraints, tradc-offs,
or poth dependencies (Crow, 1997; Horrobin, 199K). Others propose thot mental
disordL'rs persist because of fitness benefits, even for conditions such as schizo­
phrenia (J. S. A l len & Sarich, 1988; Shaner et o l., 2004), bipolar disorder (Wilson,
1998), and suicide (dcCatanzaro, 1900). The resulting confusion is substantial for
those in the field and overwhelming for others.
Vhik the hu m;:m mind prefers monoc<�us;:d explanntions, a full evolutionary
explanation for onl' disorder may include scL'ral different factors. For l'xamplc,
vuhwrabiity to depression may CJrisc from novel aspects of modern life, fron1 in­
fection, from constraints and trade-offs/ zmd because lcnv n1ood may be a defense
that can increase RS at the expense of }Wrsonal happiness. Par frnm offering a
Evolutionary Psychology and Mental Health
907
silnplistic approach to the causes of mental disorders, an evolutionary perspective
provides a framework for organizing the genuine complexity into a biopsychoso­
cial perspective (Weiner, 1998).
AN EVOLUTIONARY FRAMEWORK FOR UNDERSTANDING HUMAN
BEHAVIOR AND EMOTIONS
When a patient comes to the gl'neral 1nedical clinic with cough or kidney failure,
the physician knows that cough is a protective response and that the kidney fil­
ters out toxins and rq;ulates salt and \Vater babncc. By contr,lst, when a p<ltient
comes to a mental health clinic with a phobia, the utility of anxiety may never be
considl'rcd. VVhen someone conws with jealousy, consideration of its normal func­
tions is unlikdy. Mental health profession<Jls l<1ck <1 body of knowledge about nor­
mal emotional functions comparable to the understanding physiology offers to
general medicine. EF is beginning to provide this missing body of knowlcdgC', as
shmvn by tlw chapters in this 1-landbook, and by evolutionary perspectives on mo­
tivation (French, Kamil, & Leger, 2000), emotion (Plutchik, 2003), and specific
topics such as grid (Archer, 19Y9).
U NLJEHSTAND!NC IiDIV!UUAL L Jv J:s
EP can bring information about an individual's idiosyncratic values, goals, and
life situations into a scientific framework. Consider John, a d>pressed 20-year-old
man \Vho \vorks two jobs in local stores to support his disabled metlwr.-Whcn he
vvc1s 14, his dying father made him promise to t1kc care of his mother always. He
has been doing th<Jt ever since, but with increasing resentment and depression.
These three sentt>nces give more insight into his depre'ision than a dozen deno­
gr<lphic variables and a brain scan. An evolutionary understanding of motivation
can begin to bring such inform<ltion into a nomothetic fraJnC'work based on bc­
haviural ecology categories of life history effort. Tw tradc-offs among these catc­
gorh.'s are as universal as tlwy arc problL'mc1tic (Krebs & Davies, 1984; Stearns,
1992). No solution can be perfect, and tht' conflicts account for much human suf­
fering (Chisholm, 1999; Low, 2000; E. A. Smith & Wintcrhalder, 1992; Sterelny &
Griffiths, 1999). UndL'rstanding these tradc-offs fosters realistic clinical thinking
<1nd enhances empathy for the vicissitudes of people's lives.
REL;\TJC)NS!-!JPS
EP's greatest contribution may be a deeper understanding of rebtionships.
For instance, Bmvlby's (1969) insights about the evolutionary functions of attach­
ment have been extended by suggestions that apparently "abnormal" kinds of at­
tachnwnt may represent alternativL' strategies for infants to get resources fron1
mothL'rs in difficult circumstances (Belsky, ]999; Chisholm, 1Y96) and a deeper
understanding of women's n'productive stratt.�gies in gerwral (Hrdy, 1999).
Analysis of mutually beneficial re-ciprocal exchanges has led to extensive studit>s
of econmnic games (Fchr & Fischbaclwr, 2003) that illuminate the origins of
the social en1otions (Fessler, in press; Fiske, 1992; Henrich & Cil-Whitc, 2001).
Hmve\'tT, interpreting all human relationships as calcubtc•d exchanges ignores
908
EvotunoNJZING TRADITIONAL DiSCIPLINES oF PsYCHOLOGY
aspects of human behavior that are essential to understanding n1ental disorders,
such as our capacities for moral action and the emotions of pride and guilt (Katz,
2000). Selection n1ay have shaped capacities for connitment that are superior to
rational calculation (Frank, 1988; Gintis, 2000; Nesse, 2001a).
Freud's theories are ridiculed because some are wrong and be­
cause psychoanalysis is not reliably effective. However, the reality of repression is
a profound fact of human nature that needs an evolutionary explanation (Bad­
cock, 1988; Sulloway, 1985), along with phenomena such as the Oedipus complex
!Ericson, 1993). Trivers and Alexander separately suggested that self-deception is
a strategy for deceiving others (Alexander, 1975; Trivers, 1976, 2000), but people
also may repress the sins of others to preserve valuable r'Iationships (Nesse,
1990b). Closely related is Trivers's (1974) insight that regression may be an effec­
tive strategy used by offspring to manipulate their parents into providing re­
sources that would be appropriate only if they were younger or sick. His more
general theory of parent-offspring conflict is the neglected foundation for under­
standing many childhood disorders. Attempts to provide an evolutionary founda­
tion for psychodynamics are developing (Badcock, 1988; Slavin & Kriegman, 1992;
Sulloway, 1985) but remain relatively unappreciated by psychoanalysts, perhaps
because an evolutionary view fosters skepticisn1 that undermining repression
will be helpful routinely (Slavin & Kriegman, 1990).
Psychodynamics
Development Developmental psychology now offers sophisticated assessments of
extensive data about what children do at different stages of life and how these
phenon1ena vary across cultures. It increasingly takes evolution into account
(Bateson & Martin, 2000; Geary & Bjorklund , 2000; Rutter & Rutter, 1993). In the
midst of a burst of interest in facultative developmental mechanisn1s and their
role in evolution (Hall, 1998; West-Eberhard, 2003), evolutionary psychologists
have begun looking for mechanistns that use environment inputs to adjust devel­
opmental pathways. An obvious facultative adaptation is the regulation of female
reproductive onset by fat stores (Surbey, 1987). Less well supported are proposals
that early father absence induces early reproduction (Belsky, Steinberg, & Draper,
1991; Draper & Harpending, 1982; Surbey, 1990). A possible adaptation with par­
ticular relevance for mental disorders is the adjustment of the gain in the hypo­
thalamic pituitary axis system in response to early stress and the transmission of
this sensitivity across the generations by maternal influences on fetal brain de­
velopment (Essex, Klein, Eunsuk, & Kalin, 2002; Teicher et a!., 2003).
EMOTIONS A ND T H E EVIOTIONAL D ISORDERS
Most mental disorders are emotional disorders. People come for treatment be­
cause they experience anxiety, deprl'Ssion, anger, or jealousy. Many assume that
such negative emotions are abnormal, but they are usefut at least for our genes.
People with depression and anxiety are so obviously impaired that it is difficult
to see how such emotions could be useful. However, selection has shaped emo­
tion regulation mechanisms that often give rise to normal but useless suffering
(Nesse, 2004, 2005). An evolutionary foundation for studies of emotions is now
routine (Ekman, 1992; Nesse, 1990a; Plutchik, 2003; Tooby & Cosmides, 1990) and
Evolutionary Psychology and Mental Health
909
recognition is growing that en1otions are special states shaped by selection to
give advantages in fitness-significant situations that have recurred over evolu­
tionary tilne.
OJ\CNOSIS
When is an e1notion abnonnal? The criteria for psychiatric diagnoses are based on
intensity, dur.:Jtion, and associated disability (American Psychiatric Association,
]994). The extremes are abnormal, but without knmving the functions of emo­
tions, the line between normal and abnormal re1nains subjective (D. Murphy &
Stich, 2000; Ncsse, 2001b; Troisi & McGuire, 2002; Wakefield, 1992). The lack of an
evolutionary foundation fosters serious errors including describing continuous
emotions as categories and neglecting abnormal conditions characterized by ex­
cess positive or deficient neg<ltive enwtions. Jn addition, diagnostic criteria do not
consider the appropriateness of an emotion to the situation. If general nwdicinc
n1ade diagnoses according to the strategy used in psychiatry, it would diagnose
abnormal cough disorder based on cough frequency and severity without consid­
ering \Vhcther the cough \va; a norma] response in certain situations. Far from
genuine] y atlworetical, the Diag1wstic and Stati�tical Mmwal (�f Mental Disorders sys­
tL'l11 (DS\1; A1nerican Psychi,1tric Association, J994) fosters a crudt' biological
view (Horwitz, 2002).
Many agree that the DSM system inhibits understanding (Phillips, First, & Pin­
cus, 2003), and several authors have suggested hmv evolutionary principles can help
to m,1kc diagnosPs more scientific. D. Murphy and Stich (2000) take}he DSM to task
for its atheoretical approach and suggest distinguishing disorders that arise from
brain abnormalities from those that arise from normal brains exposed to novd 'nvi­
ronmcnts. Tlwy propose categories based on the presumed modularity of cognitive
design. VVakefield (1992) offers a strong critique of the DSM, using tlw concept of
"harmful dysfunction" to clarify what is and is not a disorder. This sophisticatL·d
evolutionary analysis of psychiatric diagnosis argues that it is essenti.l for mental as
well as physical disorders to separate normcll from abnormal phenomena based on
whether thl'y arc h<umful and whether tlwy arise from a dysfunction. This sophisti­
cated understanding of evolutionary function is the scientific foundation for future
psychi<1tric diagnostic systems (Wakefield, this volume).
An C\'olution,uy view highlights the central flJw in the DSM criteria; they do
not rcfll'ct the most basic distinction in medical diagnosis: that between diseases
and symptoms of diseases. Negative emotions such as anxiety and sadness cue
useful ciJpacitics shaped by natural selection. Determining \Vhen they are abnor­
mal requirL'S undt>rstanding when <1nd hmv they are u�eful.
An approach based on Darwinian medicine, following Wakefield, suggests
global cakgories of mental problems based on ansv�T·rs to three questions: ( 1 ) Are
cognitive and brain mc'chanisn1s normal or defective? (2) Do the symptoms arise
frmn non'I aspects of the environment, <lnd (3) Are the symptmns in the interests
of the individual, his or her genes, or neither? The rC'sulting categories are:
1 . Emotional, cognitive, or behavioral responses that arise from normal systl'lns:
a. Useful responses that miJy be a\'ersivc (ordinary anxiety and anger).
b. Normal responses that b'ncfit the indiv idual's gcnl's, at the expense of
the individual's interests.
910
EvoLUlONIZING TRADJTTONAL D rscrrLTNES oF PsYCHOLOGY
c. Responses that arise from norn1al system b u t that are not useful in the
particular instance.
d . Nonnal responses that are useless or harmful now but would not have
been in the ancestral environment.
e. Normal responses that do not harm the individua I b u t that are defined as
abnormal by a group or culture.
2. Sy1nptoms arising from abnormal regulation of a normal emotion or cap<Kity.
a . Specific defects, genetic or acquired, account for the dysrcguL1tion (cau­
sation from below, hardware problems).
b . Dysregulation arising from soci;1l dilemmas or complexities (c<1tJSiltion
from abovL', software problems).
c. E x tremes of a trait d i stribution that increJse vulnerability.
3. Abnormalities of behavior, cognition, and emotion that arisL' from funda­
nlental brain or cognitive abnormalities not pri1narily involved vvith systems
that regulate e motion and behavior (e.g., lead poisoning).
INDIVIDUAL DrFFERFNC'ES
Most psychiatric research attcn1pts to explain individual differences. Despite
growing agreement on the importance of gene-environment intcroctions (Kendlcr,
Kuhn, & Prescott, 2004; Ridky, 2003; Rutter & Rutter, 1993), m<>jor disagreenwnls
persist about why some people get i l l and others do not. D ifferent authorities L'm­
phasize different causal factors (gem,tic, developmental, situational, t•tc.). Far
from emphasizing genetic differences, an evolutionary view provides a framl'\Vork
that highlights the relationships among a l l fJctors and levels. 1 t also contributes
strategies for avoiding some s i mple n1istakes.
Much misunderstanding arises from confusing attempts to expla i n the exis­
tence of a trait with attempts to explzli n variations in a trait. It is scnsclt•ss to ask
whetlwr a rectangle is caused 1norc by its length or its w i d th. However, rect,1n­
gles can vary in area only if thei r width or length (or both) chrmges. Likcw isL>,
variutions among individuals can result only from diff'rc•ncf's in gl�IWS, differ­
ences in environments, and the interactions between thcn1. The proportion of
variance <1ttributablc to each component is not fixed, but varies dl'pL'nding on tlw
particular environment and the range of genotypes. Preoccupation wdh n<lture
versus nurture has distracted atkntion from the tnany different routes to < J dis­
order. An evolutionary approach fosters s imultaneous cont>idt•ration of the m,1ny
fc1ctors that may explain i ndividual variation in a trait, some of which <lrc listed in
Table 32.2.
The task of accounting for individual differences should not bL' reduced to <tr­
guing about the relative importanc' of one factor compared tu another. It is,
instead, the challenge of explicating how each contributes to individual diffl'r­
e ncl's in a particular trait and how their contributions to a particuLn trait m;1y
be different not only between families, populations, or cultures, b u t even be­
'\Vel'n indiv iduals. The responsible factors may be mainly genetic in one i ndi­
vidual and tnainly environmental in another. This has practical implic,ltions for
mentol health research. For instance, we need to take SL'riously the possibility
that 1nany different genes contribute to depression v u l nerability by many d_if­
ferent routes.
Evolutionary Psychology and Mental Health
911
Table 32.2
Twelve Sources of Individual Differences
1. Additive genetic differences among individuals that result in phenotypic differences
(in this environment)
2. Variation resulting from Gene x Environment interactions
3. Variation resulting from Gene x Gene interactions
4. Assortative mating-nonrandom mating increases or decreases trait variance
5. Random factors in development, such as the stochastic paths of neuron migration
6. Effects of cues that influence development via facultative mechanisms to a trajec­
tory suited to the particular environment, such as early heat exposure influencing
the number of adult sweat glands
7. Effects of trauma, toxins, and other environmental exposures outside the range of
normal that damage the organism or distort its development
8. Effects of environmental factors that influence the organism "top�down" via percep�
tual experience without resulting in damage or acting via a specific facultative
mechanism
9. Effects of environmental factors that influence the organism from the "bottom-up"
that are neither damaging nor mediated via facultative adaptations
10. Effects of individual learning that facilitate flexible coping with current aspects of
the environment
11.
Experiences shared within a culture that are incorporated into values and emotional
proclivities that may be difficult to change later (such as values or sexual attitudes)
12. Experiences shared within a culture whose effects account for variation that
changes readily when conditions change
SPECIFIC DISORDERS
An evolutionary perspective calls attention to a distinction that is fundamental
and well recognized in 1nost of medicine, but unaccountably neglected in psychi�
atry. Son1e 1nedical conditions, such as cancer and epilepsy, are diseases that arise
from some abnormality in the body's mechanisms, while others, such as pain and
cough, are protective responses. Some mental disorders, such as schizophrenia
and autism, are allnost certainly specific diseases or clusters of diseases, while
others, such as depression and panic disorder are fundamentally different in that
they are useful protective mechanisn1s, albeit ones that readily go awry. Not all
mental disorders are c1notional disorders, but n1any are, and they deserve consid­
eration together.
EMOTIONAL D ISORDERS
Most mental disorders are emotional disorders, but they are not yet based on
knowledge about the origins and functions of emotions. Instead, intense or pro­
longed negative emotions are said to be abnormal, irrespective of the situation,
while deficits in negative emotions and excesses of positive emotions are rarely rec­
ognized as disorders. An evolutionary perspective provides a n1ore balanced view.
Although anxiety can be usefut a dry mouth and tre1nor
when standing before a large group seem worse than ust:'1ess. Likewise, the
symptoms of panic may help escape fron1 a lion, but they are unhelpful in a gro­
cery store. We nov have a vast amount of knowledge about the responsible brain
Anxiety Disorders
912
EvoLUTIONlZ!NG TRADITIONAL DJSCJPLTNES or PsYCHOLOGY
n1echanisms, but no comparable body of knowledge about the evolutionary ori­
gins and utility of social anxiety or panic (Nesse, 1987). Similarly, hundreds of
studies document every aspect of excessive anxiety states, but only a handful
look for states of deficient anxiety, the hypophobias (Marks & Nesse, 1994). One
study tried to confirm that fear of heigbts often results from severe falls early in
life. It found adult f'ar of heights in 18) of the control group but only 3% of the
group that had experiL'nced a fall early in life. Those \>'ith hypophobia early in
life still had deficient anxiety decades later (Poulton, Davies, Menzies, Langley, &
Siha, 1998).
Anxiety illustrc1tes the diversity of the body's regulation mechanisn1s (Barlow,
, 1 9H8; Marks, 1987; Poulton & Menzies, 2002; Stein & Bouwer, 1997). For instance,
rigid defensive responses to fixed cues, such as chicks hiding from hawk-shaped
shadows, are useful when a correct response to the first encounter is esscntiat
but they n:sult in many false alarms and do not protect against novel dangers.
Fll'xible learning mechanisms protect against novel cbngcrs but may fail during a
crucial initial exposure, and they are prone to result in phobias. Social l'arning is
another solution. Infzmt rhesus monkeys show no innate fear of snakes; hmvever,
a single observation of another monkey displaying fear of snakes induces long­
lasting <woicbncl'. Wutching another monkey display fear of a fluwer induces no
such fc,ar (Mineka, K'ir, & !'rice, 1980).
Exposu rl: treatment is effective for phobias, but the fear rcsponst' is not un­
leam'd (Borlow, 19k8; Foa, Stekl'lce, & Ozarow, 1905; Marks & Tobena, 1990). In­
stead, a new cortical process suppresses the fear response (Quirk, 2002). Exposure
to dmger disrupts this suppression. Thus, the great flood in Moscow caused the
reemergence of previously extinguished fears in Pavlov's dogs. This rnay rdlcct a
constraint in a path-dependent mechanism; simple• unlearning apparently may be
in1possiblc•.
Otlwr fears cannot bv Pxtinguished. For instilncc, posttraumatic stress disorder
(PTSD) illustrates Olw-time Jparning of the strongest sort. A single !ifc-thn'<ltcning
experience induces a subsequent terror response to any cue that sugg'sts a
recurrence of the dangerous situ<ltion (Breslau, Davis, & Andreski, 1995). Proxi­
Inate science is steadily honing in on the mechanisms that account for this syn­
drome (Pitman, 1989; Yehuda, Halligan, Colit>r, Grossman, & Bierer, 2004), but it
has lwen morL' difficult to find ways to diffen•ntiate altf'rnative evolution1ry hy­
potlwses. PTSD could result from damage to JncchanisJns not desiplC'd to copl'
\vith such extreme situations. Howe\'er, nearly dying is so important to fitness
that t might well havL' sharwd a one-time learning mcchunism th<lt gives rise to
the symptoms of postiT<lUHlatic stress that might Iwlp prevent a recurrence.
Fear has distinct subtypes that S.'l'II to have been partially differentioted from
generic clnxi'ty to cope with domain-specific challenges (M,1rks & Nessc, 1994).
For instance, p<lnic flight is just the ticket to l'Scupc from a prcdutor, but frozen
immobility is superior wh'n teetpring on a cliff. Soci,ll anxiety is present in most
peopk (Cilbcrt, 2001; Leary & Kowalski, !99i), and pcopk wbo l<Kk it are often
insuffl'rabk', even if tlwy do not qualify for a psychiatric diilgnosis. WL' wonder
how they would ha\'e fared in small hunkr-gath..'rer groups. The char<lct'ristics
of subtypes of c1l1Xi'ty m.1p vvcll onto the challenges posed by diffen'nt threats.
The smoke dl:tl'ctor principlL' helps to explain sonw apparent pcculiaritiL'S of
the nwch<tnisms that regulatl' anxiety and other defL•nses (Nesse, .005; Stein &
Buuv·er, 1997). Because nwst ,1nxiety rcsponsL'S arL' incxpensi\·e and protect
Evolutionary Psychology and Mental Health
913
against huge potential harms, an optimal system will express many alarms that
are unnecessary in the particular instance, but nonetheless perfectly norn1al.
This suggests that using drugs to block defenses may be safe in most instances
but that in some situations blocking a defense may be fatal.
Mood Disorders The utility of sachwss and depression is less obvious than for
anxiety, but Bib ring I 953) long ago suggest-d that depression signaled the need
to detach when libido persists in a connection to an unre\varding object. Ham­
burg, Hamburg, and Barchas ( 1975) and Klinger ( 1 975) described how L'motions
regulate goal pursuit more generally, with inability to reach a goal first arousing
aggrc-Jsive attempts to overcoml' an obstacle, then low mood motivating disen­
gagement. If the person docs not give up, the m'gative affect escalates into de­
pression. This principle, nmv confirmed by much research ( Brickmtm, '19H7;
Carver & Scheier, 1990, 1998; Emmons & King, 1988; Janoff-BulmcH1 & Brickman,
1982; Little, 1999; Wrosch, Scheier, & Miller, 2003), provides the foundation for a
1nore general approach to n1ood as a mechanism that allocates effort proportionzll
to propitiousness (Ncsse, 1991b, 2000). When payoffs are high, positive mood in­
creases initiative and risk-taking. \Vhcn risks are substantial or effort is likely to
be vvastcct lovv n1ood blocks in\'estments. In this perspective, ordiniJry episodes
of sadness and low mood motivate ch,1nging behavioral strategies (Watson & An­
drews, 2002). If no alternative is found 1nd the goal is essentic!, persistenn� may
result in depression (Klinger, 1975; Wrosch, Scheier, & Carver, 2003).
Observations of chickens and monkeys \vho lost their positions in the hicr<trchy
have suggested a view of depression as "involuntary yielding" thilt protects against
continuing attack (Cilbert 1992; Sloman, Price, Gilbert, & Gardner, 199·1). This is
consistent with dcltZl shovving that stressful events cause dL'pression mainly if they
are char,lCtcrizcd by humiliation and/or being trapped in an impossible quest
(G. W. Brmvn, -Iarris, & Hepworth, 1995; Kendlcr, Hcttema, ButL'ra, Gardner, &
Prescott, 2JJ) . Also related is the suggestion that sex diffL'fl'l1Cl'S in ckpn:ssinn
may Jrisc from the male tendency to strive for position ilnd resources, lc1ving
many women vulnerable to depression because they huve fewer options (Gilbert,
1992; WL'ncgrat, 1l9S).
Depr'ssion has also been vie\.ved as a social m:mipulation (HagL'n, 2002; VVatson
& Andrews, 2002). Hagen sees postpartum depression as a " blackmail threat" to
abandon the infant, but otlwr theories can ;·dso l'xplain thL' association of postpar­
tu_m depression \Vith poor resourres and relationships. fn a n'lated but more gen­
eral view, Watson <llld /\ndrews (2002) suggest that depression facilitates "socicd
naYig<ltion" by signaling that current strategies are failing <Jnd nevv' directions arc
needed. This approach echoes psychoanalyst Emmy Cut's (1 9H9) work on produc­
tive and unproductive eL-pression. Nettle (2004) notes inadequacies of the social
navigation hypotlwsis and emphasizes the possible adaptive value of neuroticism.
DL'Catanzaro (1 9SO) proposed that suicide can bt� adaptive if an individu.l has
no chance for rq;roduction but can increils: future reproduction of kin by ceasing
to use resources that they could usc instead. DJta showing that suicides are more
conunon in old <llld sick pl'ople are consistent; hmvever, alternative' explanations
are m·ailabh:, separation from kin docs not protect against suicide, and there are
no animal examples. In a rt'\'crsc twist on lhis perspective', the benefits of social
support result more from h'lp given than help received. lndi\·iduals who provide
help to others have higher mood ;1nd incrL'ascd longc•vity (R. Brmvn, Dahll'n,
914
EVOLUTJONIZING TRADITIONAL DJSCIPUNES OF PSYCHOLOCY
Mills, Rick, & Biblarz, 1999; S. L. Brown,Nessc, V inokr, & Smith, 2003). The role
of the group is also central toN. B. Allen and Badcock's (2003) model, in which
people carefully monitor what they can contribute to a group. People who realize
they can contribute little retreat into depression that is hypothesized to prevent
active expulsion frmn the group.
These approaches are guitC' different from the prevalent view that depression is
a brain disorder (Andreasen, 1984; Valenstein, 1998; Wolpert, 1999). The brain
mechanisms that mediate 1nood certainly can go awry, but two questions ne'd
consideration. First, is low mood a useful response like cough or ,111 abnormality
unrelated to defenses like epileptic seizures? Second, do individual differences in
vulnerability to depression arise n1ainly fronl primary brain differences or from
brain changes mediated by social experience (C. W. Brown & Harris, 1978; Mon·
roe & Sin1ons, 1991)? These are not mutually exclusive alternatives, and most de­
pression i s best understood as the outcome of gene x environnwnt interactions
(Caspi ct a!., 2003). Also, there arc different routes to depression, some of which
progress irrespective of environment, others of which arise from life circum­
stances, perhaps especially those invoh'ing pursuit of unreachable goals.
Anxiety and dE'pn•ssion get all the atl'ntion, but every
emotion is subject to at least two kinds of disorckr: excesses or deficits. For in­
stance, pathological jealousy is common, but few clinicians know why jealcmsy
exists (Buss, Larsen, Westen, & Semml'lro1h, 1992). Jealousy may arise for good
reasons (Buss et al., 1999) or from delusions. Feelings of inadequacy make son1e
men think that their partners might \veil prefer someone else <lnd then that they
do prefer someone else. Depression treatml'nt often relieves pathological jealousy
(Stein, Hollander, & Josephson, 1994). The syndrome of pathological lack of jeal­
ousy has yet to be described.
Comparable pathologies exist for every 'n1otion. People arc t<lkcn over by
envy, love, suspicion, anger, awe, or rapture. Whether it is normal or abnormnl
depends on the situation. <ecognizing the evolutionary origins and functions of
emotions provides a framework for describing their disorders and the long­
sought scientific basis for distinguishing emotional disorders from emotions
that are si1nply unwanted.
Other Emotional Disorders
BE-IAVJORAI_, DISORDERS
Other disorders involve inability to control behavior. Most obvious arc the add ic­
tions and other habits, but other proble1ns of behavioral control range from e<Jting
disorders to violence.
The human toll taken by addictions is magnified bec;-mse their effects
harm others as well as the addict. A whole iss1w of Addiction \Nas devoted to l'\'olu­
tionary approachE'S (Hill & Newlin, 2002), with suggestions about the adaptive
significance of oddiction (Sul!iv,ln & Hagen, 2002), life· history thc,,rv (Hill &
Chow, 2002), and the significance of fermentation (Dudley, 2002), among others.
One of the most important evolutionary insights is simplt>, hmve\'L'f. Learning is
chemically mediated, so exogenous subst.1nccs m din'ctly stimulate rl'-vard
n1echanisms (Nesse, 1994; Nesse & Berridge, 1997). The subjective sensations arc
pleasurable, and the associated reinfurcemcnt incn.·a.vs the frequency of drug-
Addictions
Evolutionary Psychology and Mental Health
915
taking behavior. Aversive withdrawal sympton1s become cues that stimulate fur­
ther drug taking. Over time, the subjective pleasurable " liking" wanes, the with­
dravval effects become more severe, and the habit strength of "wanting" increases,
trapping the addict in a vicious cycle that may offer little pleasure, even as it con­
sumes most of what is valuable in life.
VuLn'rability to substance abuse results from our novel environn1cnt. The
aY,lilahility of pure chen1icals and clever routes of achninistration increase the
ratL' of drug taking. Tobacco administered via the technological advance of ciga­
rettes is the must widespread and harmful addiction, vvith alcohol a close sec­
ond. The so-c1lll'd bard drugs of abuse, such as amphetamine and cocaine, act
even more directly on ascending dopamine tracts to establish addiction. Sub­
stanc' dbuse is a universal human vulnerabillty to drugs that hijack reward
mech,ln isms.
Vhy peoplL� differ in vulnerability is a fundamentally different question.
Those \vho find it difficult to quit have different gcnl'S and more psychiatric
syn1ptoms (Powrleau, N7). The responsible genes arc not "defective" ; they
GlUSL'd no harm until the modern t'nvironment. Other vulnerability factors arise
from cnvironnwntal exposures, such as adverse circumstances that arouse aver­
sive emotions that increase the reinforcing properties of drugs.
Ha[;if; Vulnerabilities to otlwr habits have related evolutionary explanations.
Carnbling dot'S not directly influence brain chemicals, but it is as potent for son1e
people clS heroin. Men without other options may take big risks to get a possible
big rt'\Vtlnt thus possibly t'xplaining why poor people 1non.' often plaY the lottery.
Gambling is a bigger problem for men than -vomen, probably because over evolu­
tionary history substantial resources brought increased mating success for men
n1on' than women. The tendency to persist in games of chance with known long­
tcrn1 negative payoffs, such as slot machines, reflects the distortions built into
human decision making (Kahnen1an, Slavic, & Tversky, 1 982). Similarly, our
cvoJ·vcd bch,wior regulation mechanisms lead to n1uch other nonadaptive behav­
ior in modern environments such as watching pornography, going to prostitutes,
habitu<ll web brovsing, reading cheap novels, and engaging in private rituals,
such <lS organizing and reorganizing a collection of stamps or coins.
Half of iunC'ricans are now overwc•ight, and a third arc clinically
obe�t:. They spc'nd billions on books and treatment, but nothing works very well.
Vast amounts of research have tried to understand what is wrong with the heavy
half. An evolutionary appro,1ch suggests a different question: Why are we all vul­
nerable to obesity? A silnpk answer is that our behavior regulation mechanisms
wcrl' �hapcd in the very different environment of the African savannah where the
penalt}· for eating too little was swift and f_tal. Even when food was plentiful,
obesity' remained rare bt•cause choices were li1nitcd and getting food involved
burning as many calories per day as a modern aerobics instructor (Eaton, Shostak,
& Konrwr, 19HH).
Attempts to control \veight by willpowL'r leod to the other eating disorders,
anorexia llLT\'OS<l and bulin1ia. Adaptive explanations for anorexia as a \·ariant mat­
ing str<1tegy h,wc been suggested (Surbey, 1987; Voland & Voland, 1989). Hmvevcr, a
simpln .:L1rting place is the nhs0rv<1tion that these disorders usually hegln with
strenuous diets. Such diets cause episodes of gorging, a hallmark of bulimiJ, but
Entinx Oi,<ordcrs
�
916
EvOLUTJONIZfNG TRADITIONAL DrscrPLJNES OF PsYCHOLOGY
life-saving during famine. G orging precipitates shame, feelings of lack of control,
more intense fear of obesity, and new resolutions in a vicious cycle of escalating
anorexia and bulimia. Eating disorders are also fostered by the intense mating
c ompetition in large social groups, augmented by media images that make real
bodies seem inadequate. In light of the pervasiveness of mating competition, this
makes perfect sense (Buss, 1988, 1994). As \vith other syndromes, vulnerability
varies for many reasons.
C ivcn its in1portancc, you might think selection would have
n1ade sex foolproof. Instead, it exe1nplifies tl1e vulnerabilities of :1 trait shaped by
..ntultiple strong forces of .election (Troisi, 2003). For instance, men compbin
about premature orgus1n while \Vonen cmnplain about lack of orgasm. . Why? Sex
differences in br<.lin nwchanisn1s and differences in anatomic proximity to stimu­
lation, yes, but these are proxi1n<1tc explanations. VVhy is the syskm so poorly de­
signed for mutul l satisfJction? Because selection docs not shape mechanisms for
n1utual sJtisfaction. Women who had orgasms very quickly might well have had
fewer children, as might men \Vho dallied too long when intcrruptiun is likely.
This is c onsistent ·with the observation th:1t premature ejaculation is <l probl>1n
mainly for men \Vho an• young or fearful.
Another dram,ltic sex difference is .vhat it takes to initiate <HOUS<ll. For many
men, the answer is almost any sexual cue, anytinw, any\vlwre (Symons, 1 979).
Pornography is a male pursuit; even magazines th1t display male bodies Jre bought
mainly by men. Then there is the related problematic issue of why such a wide
range of stimuli arouses men. We might suppose that sdectiun would ensure th;1t
men want only potcntia.tly fertile partners, and most do. However, about 2qi�) ,1tT l'X­
clusively homosexual, others are preoccupied \Vith immature girls, and many hdvc
fantasy lives that involve domin;1tion or a fetish objt>c t. One explanation may be ,1n
error managpmcnt theory for why men so systemltically and optimistically distort
the intentions of wonwn (Hasdton & Buss, 2000). As for why so many indJ,·iduals
an.' exclusively hon1osexual, this remains unanswered, but not for want of tlwurics
(Ruse, 19R8).
Sexual Disordrs
BRAIN DIS( lRln-:.s
Public relations campais'11s, many supportt.• d by pharmaceutical companies, pro­
mote the view that n1ental disordt.'rs ;uc brain disorckrs. This is necessarily true in
the sense that brain changes medi,1tc zdl emotion 1nd behavior. However, slogans
such as "depression is a brain disease" leave the mistaken impression that brain
abnormaities arc always the primary causes and that drugs are the only appropri­
ate trt.'atm�.:nt. For son1e disorders such as schizophrenia, bipobr disorder, and
autism, brain abnormalities are indeed i hc primary and usually sufficient cause.
Other disorders, however, c<Jn ocn1r in a brain that is perfectly normal or a br<lin
that was nonnal until it experienced unnatural stimuli such ,1s psychological
tr<�uma, drugs of abuse, severe dieting, or trying to work in a hostile bureaucracy.
As noted alre ady, an evolutionary pt.'rspectivc fosters a sophisticated .1sscssnwnt
of the many bctors that explain individual differences. Snnw mental disordL'rs are
normal aversive emotions, others are dysrcgulated emotion:;, <Jnd some ;:uisL' from
Evolutionary Psyclzology and Mental Hmltlz
917
factors only distantly related to the normal regulation of en1otions, cognition, and
behavior (Nesse, 1984). We turn to this last group to see what an evolutionary
view can offer.
Schjzophrenia is the most serious comn1on mental disorder. The
symptoms have little to do \Vith a "split n1ind" but instead H'flcct a systematic
breakdown of perception, cognition, and emotion (Jablcnsky, Satorius, & Ern berg,
1 992). W hile precursor syn1ptoms can usually be detected, fulJ-flcdgL'd psychosis
most often begins just as the individual is trying to establish an individual iden­
tity in a social group. ..1any patil' nts first feel excluded, then suspicious, then
frankly paranoid with delusions that others arc trying to harm them. Datil shm.v­
ing strong i nfluences of genetic factors Jnd brain changes hm·c' convinced most
researchers that the schizophrenias (there an' multiple disordL'rs) JIT best under­
stood as the manifestations of hr,1in abnorn1alities. Some have suggestl'd Jdaptivc
functions for symptmns of schizophrenia (J. S. Allen & Sarich, 1 98H; Feicrman,
19H2; jarvik & Chadw ick, 1972), but little evidence supports this idc,l.
Delusions and hallucinations <lrC not part of the routine experience of most hu­
mans. They are more like sei7lllTS ,1 nd quite unlike <tdaptivc defenses such as
fever, cough, or anxiety. Schizophrcni;1 prevalence Lltes <.Hc consistent at about
1 % across cuHures (J,1blcnsky ct al. , 1992), undermining the idL'a th<lt novelty ex­
plains psychosis. There is zdso strong cvidenct> that schizophrenics hJvc lver
than average RS: .3 of avL�rage for m,1les and .5 for femtdcs { AviLl, Thaker, &
Adami, 2()(l ; Pulver t aL, 2004). The same data show no incrca�cd fitness of their
close rt'lativcs, arguing against any st'lective benefit manifest in otl;s'r individu­
als. It ha.s lwen suggesh�d th;1t schizophrenia nlilY persist " because it is the unat­
tractivl', low-fitness cxtn•nw of a highly variable InenLll trait that evolved ,ls a
fitness ('good gpnes') indicator through mutual mate choice" (Shil ncr, Mil ler, &
Mintz, 2004). Also, as mentioned aln·ady, infection has been implicated as an ex­
planation for some cases of schizophrenia.
Tradc-uffs Jnd the limits of natural selection mJy be impor.1nt. Schizophrenia
is not a uni\':rsal human trait like the appendix; it is a rare syndrome. The evolu­
tionary question is why natural scledion has not elin1in<1ted such fitness-reducing
gem·tic variations. There art' many possibilities. Selection might not be pcnvcrful
enough to purg" rccurrL'nt deleterious mutations from the gene pool. This is un­
Jikl'ly bl'causc the uniformity of incidence across cultures argul'S against a muLl­
tion occurring in the past 1 00,000 years, long enough to purge most seriously
deleterious mutL1 tions. Another possibility is that so 1nany genes are involved
that sclccti,)n can act on them only weakly. A n'Llted perspccti\'l' is that normal­
izing selection can never shape a desib'll parameter to an extremel y narrow zone
(Keller, in press). Even traits coded for by only ,1 few genes are products of inkr­
aclions \Vith other gcnl'S ,1nd environmental factors that introduce substilntial
variation, leaving some individua:-; Jt maladaptive c'xtreincs.
A phylogcrwtic perspectivl' ofkrs rl'latcd explanations. Human c<1pacities for
language and social cognition have ndvanced at a lightning p<tcc in the past
100,000 .v c,us, almost certainly bccausL' thL'Y offer major fitness ,1 dvantages
(Humphrey, "1976). Such strong selection has costs that might \">'ell predispose to
serious problctns (Crow, 1 997). Schizophrenia genes might also spread if tlwy are
linked to �trongly beneficial genes l Burns, in press), but pll\iotrupic effects arc
Schizophrcni11
918
EvoLUTIONIZJNC TRADITIONAL DISCIPLINES O F PsvcHOLOCY
more important. Cliff-edge effects offer a related possibility. For instance, race­
horse breeding has resulted i n longer and t h i n ner leg bones that increase speed
but are increasingly prone to fracture. I f son1e mental characteristic gives increas­
ing fitness up to a point where catastrophic fa ilure becomes a problem, such cliff­
edge effects could account for the genetic patterns seen i n schizophrenia and
n1anic-deprcssive i l l ne:;s (Ncsse, 2005) .
The sa m e l i nes of reasoning apply also to other seve_' mental diseases th at a l so
have a n i n cidence of lbout 1 in l OO·� autism in particular. Baron-Cohen (2002) has
suggested that the manifestations of autism arc examples of a pathological ex­
treme of cogn itive styles that ore typically male. Thb would help to explain the
·� predom i n ance of males who get the disorder.
Otlwr hypotheses also tksen:c con sideL1tiun. For inst,1ncc, it bas bc'L'n con­
firm,:d rl'ccntly that tlw rates of schizophrenia increase d r.1 m,1 tical ly for childn'n
who \..VL'n: conceivL·d \Vhen their fathers vverc over ·10 ( By·rnc, Ag<.:'rbo, E.va ld, Ec1ton,
& Mortl'nsen, 2003; M,1laspina el al., 2002). Cencs transmitted by the mother have
divided only 24 t iml'S p'f generation, com}hlH'd to SOU cell divisions for the DNA
i n sperm of older L1tlwrs, suggesting thilt many cases of schizophrenia arisl' from
recurring Ill'W mutations. Among other implications, this falsifies the idea that
.VOnwn chooSl' older men to g't good genes.
Obse;sivc-CJilp iil;itll' Disorder ()bsessivc-cmnpulsive d isordl;r (()CD) also shows
subsL.l ntial heritab ility and ,1 l 'X1 incidence. Tlw condition is characterized by rit­
u a l i s tic rqtctitive bt>h,wiors and fears that sonw small O\'l'rsight w i l l l,ad to d i s­
aster. People 1vith OCD tend to have <l smaller than normal e<1udate nucleus in the
pons, and as already nott.' d , some cases result from an autoilnmune reaction to
streptococcal infection (Swedo, Lc•tmard, Gan'l'y, & M i ttleman, 1996). It rcn1,1ins
unc'rLlin if OCD is dysrcgulation of useful nwchanisn1s or i f it is something en­
tirely separate (Rapoport & Fiske, 1998).
ATITNTION D JSOJ:DERS
The cvolution,ny origins of attention deficit hyperactivity disorder (ADHD ) have
been the focus for several articles suggesting possible functions ( Baird, Stevenson,
& Williams, 2000; Brody, 2l01; jensen et a!., 1997; Shcll<•y-Trcmblay & Rosen, 1996)
or th,1t i t is a facultative adaptation to certain environments (Jensen et al., 1997).
The stiking male bias o f the sex ratio, over 5 to 1, gives hints that ADHD 1nay sim­
ply be the extreme end of a continuum on which males tend to be higher than fe­
males, much a k i n to a reet:nt suggestion about <mtism ( Ba ron-Cohen, 2002). I n the
ancestral en\·irunnwnt, a tendency to move quickly to a new activity when current
efforts ,1re unproductive' is a foraging strategy that may pay off 1nnre for hunting
males than gatlwring females. As for the capacity to sit in one place indoors for
hours under L'nforced contact \Vitll a boring book, that i s iO far frmn anything the
natural l'nvironment ever required, it is astounding that any of us can do it. The
heritability of ADHD is high, and associations with candidate genes, notably
DRDl, offer promising leads (Biederman & Spencer, 19Y9). Because the 71\ a l lele is
common and in ,trong l inkage disequilibrium, it mJy ho\'e experienced recent pos­
itive seiL•ction (Crady ct al., 2003).
Evolutionary Psychology and Mcnlnf Hcnlth
919
RELAT!ONSHIP DIFF!CULTIES
The enormous importance of relationships in causing (and occasionally curing)
n1en t a l disorders i s so obvious that it i s easy to neglect its significance. Mental
heath professionals often bclit'Ve thot normal relationsh ip s are worm, loving, and
ba�cd. on moral and emotional cmnn1itnents. VVould that it were �o. By contrast,
an evolubonary view of reL1 tionships emphasiZl'S the costs and pzyoffs of d i ffer­
ent social strategies in Lcrn1s of resources, reciprocal hdp, or i nclusive fitness that
can explain most tendencies to <1Hruism (Fiske, 1992; l-l i n dc', 1979; Hofer, 1984;
Kirkpatrick, 1998). Evol utionary approaclll's hmie aLso emphasized the prevalence
of deceptive strategies and self-deception ( Krebs & Dawk i ns, 1 9H4; Lnckard &
Paulhu�, "1988; I\ue, \ 994; Slav i n & Kriegman, 1 992; Trivcrs, 20UO), thus opening a
l i ttk-trav'lcd avenul' betwet>n EP ,1nd psychoanalysis. Other ch<lpters i n this
Handl100k shmv how selection shapL'd the lllL'Chtmisms that nwdiatc rcL1tionships,
k n ovvledgt' crucial to understanding ho· relationships go vvTong.
Scxu,1 l relationships and strategies have been a focus for EP, and the results of
that research arc ripe for application to clin ical situations ( Buss, 1 994; Buss &
M a l a mulh , 1996). For species \\'i th mating systems s i milar to those of hunt.:ms,
careful choice nf partners benefits females more th<ln males, und efforts to get
milny matings lwnefit females n1on: than mah•s. As a result, sexual jL',l lousy i s
morL' intense for n1ah•s, ,1 nd opposition to maks g i v i ng resources to others tl'nds
to bP greater for women ( Buss & Schmitt, 199]). Moreover, as every grandmother
k nlH·V S, the facts of pr:;nancy and mz dc' jealousy makL! short-term nwtings less
costly and predictably more common i n malt•s.
Cltild Abuse C h i ld abuse h a s been a major focus for mental lwalth preVL·ntion
and trcatmL'nt. Understa n ding the l'\'olutionary origins and functions of attach­
ment has helped to explain why most parents do not abusL' their children despite
provocations ( Bowl by, 1984). \n evolutionary perspective n1otivated two bch<Jv­
ior'-1 1 ecologists to ask the now-obYious question: b child abuse mort' common i n
f<l m i l ies with a stepparent? Their a�tounding result i s that death <1 t t-he hands of
parents i s SO t i mes more common if there is a sh•pparcnt i n the hcmsL' ( Daly &
W ilson, 1 9?\H). T h is f i n di ng i s comrnnnly presented in a context franwd by the tc'n­
dency of m<.1 lcs i n many species to k i l l a l l unwca1wd i n hn ts shortly ,1 ftcr they
take oVL'r a fem;:1 lc mating group (I rely, ] 977). I lowcver, tlw mat i ng pattL•rn of hu­
mans docs not routinely involH' males fighting to take ovt•r a harem \V ith multi­
ple fcrna [es who clTL' nursing i nf.lnts, S O tJW lna Jogy i s incorrL'Ct. l nst>ad, thL'
mt'cha nisms that protect babies i n fam i liL'S w i th two related parents seem more
prone to fai l in n•const ituted fa m i l ies (GC'llcs & Lancastc'r, 1 987).
CONCLUSIONS
A l l i t \'Otlld take i s d iscovery of a single cure. Even d i scovery of the def i n i t i ve
caust' for a single illness would do. If EP let1ds d irectly to such a treatment or dis­
covery, it w i l l g rovv quickly. Is this ! legiti mate hope? Superficial ly, the a nsvvcr is
no. I nstead of explanations for why some i nd ividuals gd sick c1nct others do noC
EP explains wl1y mechanisms a rc the vvay they ne and vhy natural selection
has not e l i m i n a ted the gen'tic \·,1riatinns that result i n d isease for so1ne. Its most
920
EVOLUTIONIZING TRADITJON\L DISCIPLINES or PSYCJ-IOLOCY
profound contribution i s a solid framework for understanding hov behaviors are
regulated to accomplish the many con f l ic ting tasks of life, from getting food and
surviving, to finding mates an d protecting children. Instead of vic,wing one
kind of life as normal and others as deviations, it sees the inherent conflicts i n
relationships, the struggles that go on i n groups, and the dilemiI<lS every person
faces to allocate efforts among a host of competing needs. Far from providing a
rigid and cold perspective, :m evolu tion<1ry v ievv fosters deepl'r e1npathy for the
challenges we all face and deeper amazement that so many people arc able to
f i nd loving relationships, meaningful \.Vork, and a \Vay to juggle a bevy o f re­
sponsibi l i t ie s w i t h good humor and even joy.
Does this presage a new kind of psychotherapy? There certainly are major iin­
plications for how to do psychotherapy (Cilbert & Bailey, 2000) and psychoanaly­
sis (Slavin & Krieg1nan, 1992), but they do not constitute a new kind of therapy
competing with hundreds of others. Every kind of therapy should n1ake use of
evolutionary principles. The juggernaut now is psychopharmacology, soon to be
united with genetics to yield nt:w methods for tnanipulahng c_motions and be­
havior that we cannot yet imagine. I n the near futu re, they should yield more ef­
fective treJtments for schizophrenia <lnd manic-depressive i l l ness. Evolu t ionary
investigations can assist in these quests by defining phcnotypt's and identifying
evol ved behavior regulation tnechanisms. These same gt·nctic ,1nd pha.rmat:ologic
technologies will make it easier to 1nanipulate normal <lS \vi l as abnorm<ll l'tno­
tions. Tlwir focus exclusively on prox i mate perspectives holds tlw risk t h a t we
will block negative emotions and promote positive ones cYen before \VC grasp
why they exist 11t all. Cautionary tales ;1bound. For instance, vv·hen cortisol was
first discovered, it was used to rel ieve the symptcnns of � 1 1 k i n d s of inf L:1mn11t i on.
I t worked like a miracle and patients felt better, so why not? J n a few years, how­
ever, the serious consequences of blocking these normJ.l reactions became clt,ar.
An evolutionary view of 1nental disorders docs not nwan acn·pting the pains
a n d difficulties of the humJn condition. Many Cln be prcventc>d or eli minated
s afely, but only when we better understand the functions of nl'gative emotions.
Furthermore, a signal detection analysis of their regulation suggests that in many
s i tuations they are about as useful as pain after surgery. I t i s l'ven cmKeivdbJe
that the personality tendencies that foster envy and bitter competition, to say
nothing of violence, m i gl1t we'll be n1odifiahle. None of this \Vi l l be simph', how­
ever. Moreover, every such new major capacity for intervention \vi l l be far safer
and more sensible i f developed in a sophisticated evol ution<uy context.
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