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CHAPTER
32
Evolutionary Psychology
and Mental Health
RANDOLPH 1\1. NESSE
WHAT EVOL U T IO N O F F E RS
l'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
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902
Szasz, T. S. (1974). Tfu: myth ofmenlnl illness: Foundations ofa theory of persona! conduct (Revised cdi
tionr New York: Harper & Row.
Tinbergcn, N. (1963). On aims and methods of ethology. Zl'ifschrift fiir Ticrpsychofogic, 20, 410-433.
Wakefield,]. C. (1992a). The concept of mental disorder: On the boundary between biological facts
and social values. American Psychologist, 47, 373-388.
Wakefield, J. C. (1992b). Disorder as harmful dysfunction: A conceptual critique of DSM-III-R's
definition of mental disorder. Psychological Rct'icw, 99, 232-247.
Wakefield, J. C. (1997). Di01gnosing OSM: Pt. 1. DSM and the concept of m.ental disorder. Bcluwior
Research and Thcmpy, 35, 633-650.
Wakefield, J. C. (1999a). Disorder as a black box essentiolist concept. journal of Al111ormal Psyclwlogy,
lUS, 465-472.
Wakefield, J. C. (1999b). Evolutionary versus prototype analyses of the concept of di sorder. jou rnal
of Abnormal Psychology, 108, 374-399.
Wakefield, J. C. (2000). Spimdrels, vestigia! organs, and such: Reply to Murphy and Woolfolk's
"The harmful dysfunction analysis of mental disorder." Philosophy, Psycltinfry, and Psyclwlogy, 7,
253-270.
Wakefield, J. C. (2004). The myth of open concepts: Meehl's analysis of construct meaning versus
black box essenti illism. Applied and Preventive Psychology, 11, 77-82.
Wakefield, J. C., & First, M . (2003). Clarifying the distinction between disorder and non-disorder:
Confronting the overdiagnosis ("false positives") problem i n DSM-V. In K. A. Phillips, M . B.
First, & H. A. Pincus (Eds.), Advancing DSM: Dilemmas in psychiatric diaguosis. Washington, DC:
American Psychiatric Press.
Wakefield, J. C., Pottick, K. ]., & Kirk, S. A. (2002). Should the DSM-lV diagnostic criteria for con
duct disorder consider social context? American journal of Psycltiatry, 159, 380-386.
Wil liams, G. C. (1966). Adaptation and natural selection. Princeton, NJ: Princeton University Press.
Willi ams, G. C. (1992). Natural selection: Domains, fn,cls, and challenges. New York: Oxford University
Press.
Wright, L. (1973). Functions. Philosophicnl Review, 82, 139-168.
Wright, L. (1976). Tcleologicnl explanations. Berkeley, CA: University of California Press.
904
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 considLring specific disorders.
.
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 expl.1n,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 & Willi<Jms, 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 1-l countrhs (Kessler & Ustun, 2000) uses urban or
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906
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 called "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
rccoh:rnized. 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
907
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 I0.iDIV!UUAL L Jv J:s
908
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
909
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 Statitical Mmwal (f Mental Disorders sys
tL'l11 (DSi\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 C'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 sophisticatLd
evolutionary analysis of psychiatric diagnosis argues that it is essentiJ.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 ueful.
An approach based on Darwinian medicine, following Wakefield, suggests
global cakgories of mental problems based on ansvTrs 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 bl'ncfit the indiv idual's gcnl's, at the expense of
the individual's interests.
910
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
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 "topdown" 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
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 novv have a vast amount of knowledge about the responsible brain
Anxiety Disorders
912
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 CI 953) long ago suggeste-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
aggrct-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 essentict!, 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, 1991). 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, l:--Iarris, & Hepworth, 1995; Kendlcr, Hcttema, ButL'ra, Gardner, &
Prescott, 2ClrJJ ) . Also related is the suggestion that sex diffL'fl'l1Cl'S in ckpn:ssinn
may Jrisc from the male tendency to strive for position i.lnd resources, lc<1ving
many women vulnerable to depression because they huve fewer options (Gilbert,
1992; WL'ncgrat, 1Sl9S).
Deprt'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 elL-pression. Nettle (2004) notes inadequacies of the social
navigation hypotlwsis and emphasizes the possible adaptive value of neuroticism.
DL'Catanzaro (1 9.SO) proposed that suicide can bt adaptive if an individuJ.l has
no chance for rq;roduction but can increilst: future reproduction of kin by ceasing
to use resources that they could usc instead. DiJta showing that suicides are more
conunon in old <llld sick pl'ople are consistent; hmvever, alternative' explanations
are mailabh:, 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 hl'lp given than help received. lndi\iduals who provide
help to others have higher mood ;:1nd incrL'ascd longcvity (R. Brmvn, Dahll'n,
914
Mills, Rick, & Biblarz, 1999; S. L. Brown,Nessc, V inokur, & 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 neC'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'pnssion get all the atlt'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 C'n1otion. People arc t<lkcn over by
envy, love, suspicion, anger, awe, or rapture. Whether it is normal or abnormnl
depends on the situation. I<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
BEI-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 e<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
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.
VuLnl'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
stancL' dbuse is a universal human vulnerabillty to drugs that hijack reward
mech,ln isms.
VVhy peoplL differ in vulnerability is a fundamentally different question.
Those \-vho find it difficult to quit have different gcnl'S and more psychiatric
syn1ptoms (Ponwrleau, FN7). 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'\Vt"lnt thus possibly t'xplaining why poor people 1non.' often plaY the lottery.
Gambling is a bigger problem for men than 1-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
cvoJvcd bch,wior regulation mechanisms lead to n1uch other nonadaptive behav
ior in modern environments such as watching pornography, going to prostitutes,
habitu<ll web brovvsing, reading cheap novels, and engaging in private rituals,
such <lS organizing and reorganizing a collection of stamps or coins.
916
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. i\..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 hmc' 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 lm.ver
than average RS: .3 of avLrage for m,1les and .5 for femtdcs { AviLl, Thaker, &
Adami, 2()(Jl ; Pulver l't aL, 2004). The same data show no incrcacd fitness of their
close rt'lativcs, arguing against any st'lective benefit manifest in otl;s'r individu
als. It ha.s lwen suggeshd th;1t schizophrenia nli.lY persist " because it is the unat
tractivl', low-fitness cxtnnw 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 alnady, infection has been implicated as an ex
planation for some cases of schizophrenia.
Tradc-uffs Jnd the limits of natural selection mJy be import.1nt. Schizophrenia
is not a uni\'t: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
gemtic 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 substi.lntial
variation, leaving some individual:-; 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
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 seven_' mental diseases th at a l so
have a n i n cidence of tlbout 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 rt.1 m,1 tical ly for childn'n
who \..VL'n: conceivLd \Vhen their fathers vverc over 10 ( Byrnc, Ag<.:'rbo, E1.va ld, Ec1ton,
& Mortl'nsen, 2003; M,1laspina el al., 2002). Cencs transmitted by the mother have
divided only 24 t iml'S pl'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 gl't good genes.
Obse;;sivc-COJilp 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 rq_tctitive bt>h,wiors and fears that sonw small O\'l'rsight w i l l lc,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, Lctmard, Gan'l'y, & M i ttleman, 1996). It rcn1,1ins
uncl'rLlin if OCD is dysrcgulation of useful nwchanisn1s or i f it is something en
tirely separate (Rapoport & Fiske, 1998).
ATITNTION D JSOJ.;:DERS
919
RELAT!ONSHIP DIFF!CULTIES
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 Z! 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 vvhy natural selection
has not e l i m i n a ted the genl'tic \,1riatinns that result i n d isease for so1ne. Its most
920
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