Emerging Trends in The Social and Behavioral Sciences · An Evolutionary Perspective on Developmental Plasticity

An Evolutionary Perspective on Developmental Plasticity

Media

Part of An Evolutionary Perspective on Developmental Plasticity

Title: An Evolutionary Perspective on Developmental Plasticity
extracted text: An Evolutionary Perspective on
Developmental Plasticity
SARAH HARTMAN and JAY BELSKY

Abstract
In this essay, we advance the argument that variations in developmental plasticity
should be treated as an individual-difference construct in research on environmental influences on human development. As guided by the diathesis-stress framework,
past research has focused mainly on the development of dysfunction and negative
outcomes in “vulnerable” individuals and the absence of such effects in “resilient”
ones in response to adverse developmental experiences and environmental exposures. An evolutionary perspective challenges this traditional and prevailing framework for understanding person-X-environment interaction, leading to the view that
there are individual differences in developmental plasticity, with those individuals
most susceptible to the negative effects of adverse experiences also most likely to
benefit from positive ones. Evidence consistent with this view is summarized and
directions for future research are outlined.

INTRODUCTION
It has long been appreciated that Homo sapiens are a developmentally plastic
species whose growth and functioning are affected by environmental experiences and exposures encountered while growing up. Such sensitivity to the
environment is presumed to enable the individual to prepare for the future
and manage its resources effectively, thereby promoting reproductive fitness,
that is, the passing on of genes to future generations.
Insufficiently appreciated by many developmental scholars, however, is
that plasticity is not an unmitigated good, carrying just benefits (Sih, 2011).
One potential cost derives from a “mismatch” between the early environment
that a person develops in and adjusts to and the one the person encounters
later in life. As a dramatic example, consider the cost incurred by Cambodian children (and their genetic relatives) who followed parental entreaties
to study hard and do well in school, only to find when they grew up that they
were the first to be murdered by the Khmer Rouge who distrusted the educated classes! As another example, consider a child who becomes (wisely?)
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.

1

2

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

hostile, aggressive, and excessively alert to threats to his or her well-being
as a result of being abused at home, but then ends up in a school that is safe
and fair-minded, expecting nevertheless that others will take advantage of
him or her? Developmental plasticity may also carry costs associated with
the greater complexity required of an organism capable of developing in a
variety of ways depending on its early life experiences, given that a more
complex system has more ways to go awry than a less complex one.
No matter what the benefits of plasticity, then, these observations suggest
that natural selection should have “hedged its bets,” with some individuals
being more and others less—or hardly at all—developmentally plastic. This
analysis implies that developmental plasticity should be regarded as a phenotype or individual-difference construct in its own right (Belsky & Pluess,
2013a).
As it turns out, appreciation of individual differences in sensitivity to
the environment have been well recognized—at least in research on and
thinking about contextual risk and developmental resilience. After all, some
individuals have long been regarded as more likely to succumb to adversity
(i.e., the “vulnerable”) than others (the “resilient”) as a function of their
temperament, physiology, and/or genetic makeup (Luthar, Cicchetti, &
Becker, 2000). Such “diathesis-stress” thinking says nothing about variation
in response to environmental support or enrichment, however. Moreover,
it remains unclear why natural selection would craft the development of
some organisms to go awry in the face of contextual risk, as this predominant perspective on person-X-environment interaction seems to presume
would be the case. Recently, an alternative to the prevailing diathesis-stress
framework has been advanced.
DIFFERENTIAL SUSCEPTIBILITY
A perspective emphasizing differential susceptibility to environmental
influence is built on evolutionary theory and acknowledges both the costs
and benefits of plasticity (for extensive treatment, see Belsky & Pluess,
2009a; Ellis, Boyce, Belsky, Bakermans-Kranenburg, & Van IJzendoorn,
2011). It differs from the traditional diathesis-stress framework by treating
plasticity as a phenotype and highlighting the fact that evidence for what
appears to be a disproportionate vulnerability of some to adversity may,
in fact, reflect a more general susceptibility to both positive and negative
environmental influences. This may have gone unnoticed owing to the
absence of evolutionary thinking in so much developmental and psychiatric
research and the fact that so much of this work has focused principally if
not exclusively on contextual adversity and developmental dysfunction

An Evolutionary Perspective on Developmental Plasticity

3

instead of the full range of environmental exposures—from positive to
negative—and their effects, again from positive to negative.
As a result, “vulnerable” individuals have been viewed as solely susceptible to the negative effects of adversity instead of being recognized as disproportionately susceptible to both positive and negative influences, that
is, “for better and for worse” (Belsky, Bakermans-Kranenburg, & Van IJzendoorn, 2007). By the same token, individuals regarded as resilient in the face
of adversity may also be unlikely to benefit from environmental support and
enrichment. The latter clearly implies that resilience stemming from characteristics of the individual and so heralded in the developmental and psychiatric literature may not be the unmitigated good it is typically regarded
as. Evidence consistent with the differential-susceptibility view that is extensively reviewed by Belsky and Pluess (2009a, 2013a) highlights temperamental, physiological, and genetic plasticity factors distinguishing those more
and less susceptible to both positive and negative environmental effects.
NEGATIVE EMOTIONALITY
The first evidence for differential susceptibility indicated that it was infants,
toddlers, and children with difficult or negatively emotional temperaments
who developed especially poorly in the face of contextual adversity (e.g.,
poverty, and maternal depression), but proved most likely to benefit from
supportive experiences (for review, see Belsky, 2005). Further evidence to
this effect comes from work linking maternal empathy (Pitzer et al., 2011)
and anger (Poehlmann et al., 2012) with externalizing problems; mutual
responsiveness observed in mother-child dyads with effortful control (Kim
& Kochanska, 2012); intrusive maternal behavior (Conway & Stifter, 2012)
and poverty (Raver, Blair, & Willoughby, 2012) with executive functioning;
and sensitive parenting with social, emotional, and cognitive-academic
development (Roisman et al., 2012). One issue that merits additional empirical attention concerns the plasticity marker, negative emotionality, given
that it has been operationalized in diverse ways across studies, including
fear, inhibition, difficult temperament, and negative affect.
PHYSIOLOGICAL REACTIVITY
A claim central to Boyce and Ellis’ (2005) biological-sensitivity-to-context
(BSC) model of differential susceptibility is that physiological reactivity is
a plasticity factor regulated by environmental experience, with heightened
physiological reactivity in children being the mechanism responsible for
greater environmentally sensitivity—in a for-better-and-for-worse manner. This has been shown in research on effects of actual marital conflict

4

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

(Obradovic, Bush, & Boyce, 2011) and simulated interparental aggression
(Davies, Sturge-Apple, & Cicchetti, 2011) on externalizing problems; family
adversity on school achievement (Obradovic, Bush, Stamperdahl, Adler,
& Boyce, 2010); and teacher-child conflict on change in symptom severity
(Essex, Armstrong, Burk, Goldsmith, & Boyce, 2011). What remains unclear
is the stability of physiological reactivity across childhood and into adulthood and thus whether those who are highly reactive early in life but are
exposed to nurturing experiences that promote well-being remain highly
physiologically reactive—and thus highly susceptible (for better and for
worse)—as they develop. After all, it could be that supportive rearing down
regulates reactivity, thereby reducing environmental susceptibility.
GENETIC POLYMORPHISMS
Like other polymorphisms, the serotonin transporter gene, 5-HTTLPR, and
the dopamine receptor gene, DRD4, have been regarded by psychiatric
geneticists as “vulnerability genes” predisposing carriers of particular
alleles to depression, and ADHD, respectively, in the face of adversity.
Ever more evidence indicates, however, that they be regarded as “plasticity
genes” (Belsky & Pluess, 2009b), making carriers of the putative risk alleles
especially susceptible to environmental influences—for better and for worse.
Regarding 5-HTTLPR, individuals carrying one or more short alleles
show greater “for-better-or-for-worse” plasticity when the rearing predictor and child outcome are, respectively, maternal responsiveness and
moral internalization (Kochanska, Kim, Barry, & Philibert, 2011), child
maltreatment and antisocial behavior (Cicchetti, Rogosch, & Thibodeau,
2012), and supportive parenting and positive affect (Hankin et al., 2011).
Differential-susceptibility-related findings also emerge (among male
African-American adolescents) when perceived racial discrimination is
used to predict conduct problems (Brody et al., 2011); when life events are
used to predict neuroticism (Pluess, Belsky, Way, & Taylor, 2010) and life
satisfaction of young adults (Kuepper et al., 2012); and when retrospectively
reported childhood adversity is used to explain aspects of impulsivity
among college students (e.g., pervasive influence of feelings, and feelings
trigger action) (Carver, Johnson, Joormann, Kim, & Nam, 2011). Nevertheless, other work makes clear that 5-HTTLPR operates in a manner consistent
with diathesis-stress thinking (e.g., Bakermans-Kranenburg, Dobrova-Krol,
& van IJzendoorn, 2012; Brody et al., 2012). This underscores the need
to determine when one process or the other proves operative. A recent
meta-analysis reveals that in the case of Caucasian children under 18 years
of age, short-allele carriers are more susceptible than long-allele carriers

An Evolutionary Perspective on Developmental Plasticity

5

to both positive and negative developmental experiences (van IJzendoorn,
Belsky, & Bakermans-Kranenburg, 2012).
Regarding DRD4, heightened if not exclusive susceptibility emerged for
individuals who carry the 7-repeat allele in contexts where the environmental predictor and developmental outcome were, respectively, maternal
positivity and pro-social behavior (Knafo, Israel, & Ebstein, 2011); early
nonfamilial childcare and social competence (Belsky & Pluess, 2013b);
contextual stress and support and adolescent negative arousal (Beach et al.,
2012); childhood adversity and young-adult persistent alcohol dependence
(Park, Sher, Todorov, & Heath, 2011); and newborn risk status (i.e., gestational age, birth weight for gestational age, length of stay in the hospital)
and observed maternal sensitivity (Fortuna et al., 2011). Notable also is
that a meta-analysis of G×E research involving dopamine-related genes
revealed that children of 8 years and younger respond to positive and
negative experiences in a manner consistent with differential susceptibility
(Bakermans-Kranenburg & van IJzendoorn, 2011).
In addition to the two polymorphisms just highlighted, there is evidence
that others may operate as plasticity factors, making some individuals more
susceptible to environmental influences—for better and for worse. Especially
important to appreciate is that most polymorphisms that have emerged as
potential plasticity factors derived from psychiatric-genetic studies guided
by diathesis-stress thinking. Researchers should expand their list of candidate genes beyond polymorphisms associated with disturbed functioning to
incorporate a biologically driven inquiry of physiological processes affecting
plasticity. A recent example of such an effort yielding evidence of differential
susceptibility focused on the CHRNA4 genotype because of its role in acetylcholine production, a component strongly related to plasticity and learning
(Grazioplene, DeYoung, Rogosch, & Cicchetti, 2013).
FUTURE RESEARCH DIRECTIONS
However much progress has been made in chronicling differentialsusceptibility to environmental influences, many issues remain to be
explored or illuminated.
POLYGENETIC PLASTICITY
Rather than regarding some individuals as plastic or malleable and others
as not, it probably makes more sense to think of a gradient, with some being
especially malleable, some reasonably malleable, some less so, and some not
at all. Certainly that is suggested by work using multiple plasticity genes, as
it reveals a dose–response relation between the number of plasticity genes

6

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

and the extent to which individuals are affected for better and for worse (e.g.,
Belsky & Beaver, 2011; Conner, Hellemann, Ritchie, & Noble, 2010). Future
work of this kind should be guided by a “system-level genetic approach”
involving the composting of putative plasticity genes on an a priori basis
guided by knowledge of a particular biological process or pathway, such
as the dopaminergic or serotonergic system, or neurological morphology.
Even further insight may be gained through analysis of subsystems, including those involved with synthesis, degradation/transport, receptor and
modulation (Chen et al., 2011).
REPEATED MEASURES
A key assumption underlying the notion of differential susceptibility is that
if those who prove vulnerable to adversity or who benefit the most from
support found themselves growing up under opposite conditions that they
would develop in a manner opposite to that which they do. For example,
children, carrying the 7-repeat allele of the DRD4 gene who show high levels of externalizing problems when their parents are unskilled would show
especially low levels of problems—and perhaps greater competence than
others—if raised with more skilled parents. It is difficult to evaluate this proposal owing to ethical issues; one cannot create a bad rearing milieu for a
child who has a good one.
Researchers may overcome this limitation by experimentally manipulating
environments in a repeated-measures design. Consider as an example work
by Roiser et al. (2006) on decision making during a gambling game in which
individuals in one condition had good chances of winning and in the other
poor chances. Results revealed that individuals with more 5-HTTLPR short
alleles took the most risk (i.e., placed a bet) when chances of winning were
good yet these same individuals engaged in the least gambling risk-taking
when chances of winning were poor. Another repeated-measures study took
advantage of a natural experiment, discovering that short allele carriers experienced the most stress, tension, and negative mood on exam days but the
least on nonexam days (Verschoor & Markus, 2011).
EXPERIMENTAL TESTING OF PLASTICITY FACTORS
Most differential-susceptibility-related research has been observational in
nature. This can challenge interpretation because environmental experiences
may be selected rather than randomly assigned, creating the possibility
that gene–environment correlation masquerades as gene–environment
interaction. One solution to this problem involves conducting intervention
experiments with random assignment of participants to experimental or

An Evolutionary Perspective on Developmental Plasticity

7

control conditions, work that is just beginning (Bakersman-Kranenburg, van
IJzendoorn, Mesman, Alink, & Jeffer, 2008; Scott & O’Connor, 2012). Because
of the previously mentioned ethical considerations, this approach has only
been used to detect plasticity factors affecting response to interventions
promoting positive functioning. Even though this design is limited to
examining just the “for-better” side of plasticity, it still enables evaluation
of whether those found to be most vulnerable to adversity in other research
actually do benefit disproportionately from intervention efforts to promote
positive functioning, whereas those regarded as resilient in the face of
adversity turn out to be unaffected by the intervention.
DOMAIN SPECIFIC OR DOMAIN GENERAL?
Reflection on this observation raises a related issue about whether plasticity
is domain general or domain specific. That is, are more malleable individuals
especially responsive to and influenced by a wide variety of environmental
conditions and developmental exposures and other not particularly influenced by the same large set of experiences? Alternatively, are individuals
mostly “mosaics” of plasticity, being highly sensitive to some contextual
conditions but not others and/or with respect to some developmental
outcomes but not others?
However surprising it might seem, there is some evidence for the
domain-general view. Consider the results of two interventions that used
strikingly dissimilar methods to promote different aspects of development.
In one case the intervention sought to promote sensitive parenting in order
to reduce toddler’s externalizing behavior (Bakersman-Kranenburg, van
IJzendoorn, Pijlman, Mesman, & Juffer, 2008) and cortisol-related stress
reactivity (Bakersman-Kranenburg, van IJzendoorn, Mesman, et al., 2008),
whereas in the other a computerized instructional program was employed
to foster preschooler’s phonemic awareness and, thereby, early literacy
(Kegel, Bus, & van IJzendoorn, 2011). Despite the dramatic differences in the
interventions and in the features of development being studied, it was children carrying 7-repeat DRD4 allele who benefited disproportionately, if not
exclusively, from both! Before it can be concluded, however, that plasticity
is more domain general than domain specific, far more work is required. We
suspect that some individuals will be on the extremes of plasticity—highly
responsive or virtually unaffected by almost all contextual conditions—but
that most might fall somewhere between these extremes.
ENVIRONMENTAL CUE RELIABILITY
There is likely a variation in the reliability of environmental cues that children receive in developmental contexts. For instance, harsh environments

8

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

can be characterized as consistently and thus predictably high in conflict or
episodically but not as predictably high in conflict. Frankenhuis and Panchanathan (2011) propose that highly plastic individuals growing up in these
differing environments could vary in the timing of their “commitment” to a
developmental strategy. A person developing in a highly predictable harsh
environment may “commit” early, having high confidence in the state of the
environment, whereas someone in an erratic environment may delay commitment to allow more time for a better estimation of the current—and thus
future environment. Future work should seek to illuminate this issue.
TIMING OF SUSCEPTIBILITY
It is widely assumed that environmental exposures and developmental experiences exert their greatest influence early in life when biological systems are
forming. Even if this may generally be true, it is still possible that some individuals could be more plastic later rather than earlier in life. All it would have
taken for this to be so is for later plasticity to have paid off more than earlier
plasticity some time in our ancestral past and for natural selection to thus
have preserved genes responsible for such deferred developmental plasticity. This raises the possibility that some individuals may be highly responsive
to environmental influences—in a for-better-and-for-worse manner—across
the life course, others never, some especially early and some especially later.
CONCLUSION
From an evolutionary perspective, we have outlined the need to move
beyond considering only the benefits of plasticity—as is typically done
when comparing our species to that of others—to an evolutionary-inspired
theoretical framework that acknowledges both the costs and benefits of
developmental plasticity. Moreover, rather than presuming that some
individuals are simply more susceptible to the negative developmental
effects of contextual adversity, as the prevailing person-X-environment,
diathesis-stress framework does, differential-susceptibility thinking presumes that there are (i) individual differences in developmental plasticity;
(ii) such that those most susceptible to adversity are also especially likely
to benefit from environmental support and enrichment; and (iii) thus that
developmental plasticity should be treated as an individual-difference
construct. Evidence highlighting diverse plasticity factors proves consistent
with this claim, though many questions remain to be addressed. Perhaps a
major contribution of the differential-susceptibility perspective is to underscore the theoretical and empirical risks of focusing disproportionately on

An Evolutionary Perspective on Developmental Plasticity

9

contextual risk, dysfunctional development and vulnerability and benefits
of viewing developmental from an evolutionary perspective.
REFERENCES
Bakermans-Kranenburg, M. J., Dobrova-Krol, N. A., & van IJzendoorn, M. H. (2012).
Impact of institutional care on attachment disorganization and insecurity of
Ukrainian pre-schoolers: Protective effect of the long variant of the serotonin transporter gene (5HTT). International Journal of Behavioral Development, 36(1), 11–18.
Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2011). Differential susceptibility to rearing environment depending on dopamine-related genes: New
evidence and a meta-analysis. Development and Psychopathology, 23(1), 39–52.
doi:10.1017/s0954579410000635
Bakermans-Kranenburg, M. J., van IJzendoorn, M. H., Mesman, J., Alink, L. R.,
& Juffer, F. (2008). Effects of an attachment-based intervention on daily cortisol moderated by dopamine receptor D4: A randomized control trial on 1- to
3-year-olds screened for externalizing behavior. Development and Psychopathology,
20(3), 805–820.
Bakermans-Kranenburg, M. J., van IJzendoorn, M. H., Pijlman, F. T., Mesman, J., &
Juffer, F. (2008). Experimental evidence for differential susceptibility: Dopamine
D4 receptor polymorphism (DRD4 VNTR) moderates intervention effects on toddlers’ externalizing behavior in a randomized controlled trial. Developmental Psychology, 44(1), 293–300.
Beach, S. R. H., Lei, M. K., Brody, G. H., Simons, R. L., Cutrona, C., & Philibert,
R. A. (2012). Genetic moderation of contextual effects on negative arousal and
parenting in African-American parents. Journal of Family Psychology, 26(1), 46–55.
doi:10.1037/a0026236
Belsky, J. (2005). Differential susceptibility to rearing influences: An evolutionary
hypothesis and some evidence. In B. Ellis & D. Bjorklund (Eds.), Origins of the
social mind: Evolutionary psychology and child development (pp. 139–163). New York,
NY: Guildford.
Belsky, J., & Pluess, M. (2013a). Beyond risk, resilience and dysregulation: Phenotypic plasticity and human development. Development and Psychopathology,
25(4pt2), 1243–1261.
Belsky, J., & Pluess, M. (2013b). Genetic moderation of early child care effects on
behavior problems and social competence across childhood: A developmental
analysis. Child Development, 84(4), 1209–1225.
Belsky, J., Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). For better and for worse: Differential susceptibility to environmental influences. Current
Directions in Psychological Science, 16(6), 300–304.
Belsky, J., & Beaver, K. M. (2011). Cumulative-genetic plasticity, parenting and adolescent self-control/regulation. Journal of Child Psychology and Psychiatry, 52(5),
619–626.
Belsky, J., & Pluess, M. (2009a). Beyond diathesis-stress: Differential susceptibility to
environmental influences. Psychological Bulletin, 135(6), 885–908.

10

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Belsky, J., & Pluess, M. (2009b). The nature (and nurture?) of plasticity in early human
development. Perspectives on Psychological Science, 4(4), 345–351.
Boyce, W. T., & Ellis, B. J. (2005). Biological sensitivity to context: I. An
evolutionary-developmental theory of the origins and functions of stress reactivity. Development and Psychopathology, 17(2), 271–301.
Brody, G. H., Beach, S. R. H., Chen, Y.-F., Obasi, E., Philibert, R. A., Kogan, S. M., &
Simons, R. L. (2011). Perceived discrimination, serotonin transporter linked polymorphic region status, and the development of conduct problems. Development
and Psychopathology, 23(2), 617–627. doi:10.1017/s0954579411000046
Brody, G. H., Yu, T., Chen, Y. F., Kogan, S. M., Evans, G. W., Windle, M., … Philibert, R. A. (2012). Supportive family environments, genes that confer sensitivity,
and allostatic load among rural African American emerging adults: A prospective
analysis. Journal of Family Psychology. doi:10.1037/a0027829
Carver, C. S., Johnson, S. L., Joormann, J., Kim, Y., & Nam, J. Y. (2011). Serotonin
transporter polymorphism interacts with childhood adversity to predict aspects
of impulsivity. Psychological Science, 22(5), 589–595. doi:10.1177/0956797611404085
Chen, C., Moyzis, R., Stern, H., He, Q., Li, H., Li, J., … Dong, Q. (2011). Contributions of dopamine-related genes and environmental factors to highly sensitive
personality: A multi-step neuronal system-level approach. PLoS One, 6(7), e21636.
doi:10.1371/journal.pone.0021636
Cicchetti, D., Rogosch, F. A., & Thibodeau, E. L. (2012). The effects of child maltreatment on early signs of antisocial behavior: Genetic moderation by tryptophan
hydroxylase, serotonin transporter, and monoamine oxidase A genes. Development
and Psychopathology, 24(3), 907–928.
Conner, B. T., Hellemann, G. S., Ritchie, T. L., & Noble, E. P. (2010). Genetic, personality, and environmental predictors of drug use in adolescents. Journal of Substance
Abuse Treatment, 38(2), 178–190. doi:10.1016/j.jsat.2009.07.004
Conway, A., & Stifter, C. A. (2012). Longitudinal antecedents of executive function in preschoolers. Child Development, 83(3), 1022–1036. doi:10.1111/j.14678624.2012.01756.x
Davies, P. T., Sturge-Apple, M. L., & Cicchetti, D. (2011). Interparental aggression and children’s adrenocortical reactivity: Testing an evolutionary model
of allostatic load. Development and Psychopathology, 23(3), 801–814. doi:10.1017/
s0954579411000319
Ellis, B. J., Boyce, W. T., Belsky, J., Bakermans-Kranenburg, M. J., & van IJzendoorn,
M. H. (2011). Differential susceptibility to the environment: An evolutionary—
neurodevelopmental theory. Development and Psychopathology, 23(1), 7–28.
doi:10.1017/s0954579410000611
Essex, M. J., Armstrong, J. M., Burk, L. R., Goldsmith, H. H., & Boyce, W. T. (2011).
Biological sensitivity to context moderates the effects of the early teacher-child
relationship on the development of mental health by adolescence. Development and
Psychopathology, 23(1), 149–161. doi:10.1017/s0954579410000702
Fortuna, K., van IJzendoorn, M. H., Mankuta, D., Kaitz, M., Avinun, R., Ebstein,
R. P., & Knafo, A. (2011). Differential genetic susceptibility to child risk at birth

An Evolutionary Perspective on Developmental Plasticity

11

in predicting observed maternal behavior. PLoS One, 6(5). doi:10.1371/journal.
pone.0019765
Frankenhuis, W. E., & Panchanathan, K. (2011). Individual differences in developmental plasticity may result from stochastic sampling. Perspectives on Psychological
Science, 6(4), 336–347. doi:10.1177/1745691611412602
Grazioplene, R. G., DeYoung, C. G., Rogosch, F. A., & Cicchetti, D. (2013). A novel
differential susceptibility gene: CHRNA4 and moderation of the effect of maltreatment on child personality. Journal of Child Psychology and Psychiatry, 54(8), 872–880.
Hankin, B. L., Nederhof, E., Oppenheimer, C. W., Jenness, J., Young, J. F., Abela, J. R.
Z., … Oldehinkel, A. J. (2011). Differential susceptibility in youth: Evidence that
5-HTTLPR x positive parenting is associated with positive affect ‘for better and
worse’. Translational Psychiatry, 1, e44. doi:10.1038/tp.2011.44
Kegel, C. A. T., Bus, A. G., & van IJzendoorn, M. H. (2011). Differential susceptibility in early literacy instruction through computer games: The role of the
dopamine D4 receptor gene (DRD4). Mind, Brain, and Education, 5(2), 71–78.
doi:10.1111/j.1751-228X.2011.01112.x
Kim, S., & Kochanska, G. (2012). Child temperament moderates effects of parent–
child mutuality on self-regulation: A relationship-based path for emotionally negative infants. Child Development, 83(4), 1275–1289. doi:10.1111/j.1467-8624.2012.
01778.x
Knafo, A., Israel, S., & Ebstein, R. P. (2011). Heritability of children’s prosocial
behavior and differential susceptibility to parenting by variation in the dopamine
receptor D4 gene. Development and Psychopathology, 23(1), 53–67. doi:10.1017/
s0954579410000647
Kochanska, G., Kim, S., Barry, R. A., & Philibert, R. A. (2011). Children’s genotypes interact with maternal responsive care in predicting children’s competence:
Diathesis-stress or differential susceptibility? Development and Psychopathology, 23,
605–616.
Kuepper, Y., Wielpuetz, C., Alexander, N., Mueller, E., Grant, P., & Hennig, J. (2012).
5-HTTLPR S-Allele: A genetic plasticity factor regarding the effects of life events
on personality? Genes, Brain, and Behavior. doi:10.1111/j.1601-183X.2012.00783.x
Luthar, S. S., Cicchetti, D., & Becker, B. (2000). The construct of resilience: a critical
evaluation and guidelines for future work. Child Development, 71(3), 543–562.
Obradovi´c, J., Bush, N. R., & Boyce, W. T. (2011). The interactive effect of marital
conflict and stress reactivity on externalizing and internalizing symptoms: The
role of laboratory stressors. Development and Psychopathology, 23(01), 101–114.
Obradovi´c, J., Bush, N. R., Stamperdahl, J., Adler, N. E., & Boyce, W. T. (2010). Biological sensitivity to context: The interactive effects of stress reactivity and family
adversity on socio-emotional behavior and school readiness. Child Development,
81(1), 270–289.
Park, A., Sher, K. J., Todorov, A. A., & Heath, A. C. (2011). Interaction between the
DRD4 VNTR polymorphism and proximal and distal environments in alcohol
dependence during emerging and young adulthood. Journal of Abnormal Psychology, 120(3), 585–595. doi:10.1037/a0022648

12

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Pitzer, M., Jennen-Steinmetz, C., Esser, G., Schmidt, M. H., & Laucht, M. (2011). Differential susceptibility to environmental influences: The role of early temperament
and parenting in the development of externalizing problems. Comprehensive Psychiatry, 52(6), 650–658. doi:10.1016/j.comppsych.2010.10.017
Pluess, M., Belsky, J., Way, B. M., & Taylor, S. E. (2010). 5-HTTLPR moderates effects
of life events on neuroticism: Differential susceptibility to environmental influences. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 34, 1070–1074.
Poehlmann, J., Hane, A., Burnson, C., Maleck, S., Hamburger, E., & Shah, P. E. (2012).
Preterm infants who are prone to distress: Differential effects of parenting on
36-month behavioral and cognitive outcomes. Journal of Child Psychology and Psychiatry, and Allied Disciplines. doi:10.1111/j.1469-7610.2012.02564.x
Raver, C. C., Blair, C., & Willoughby, M. (2012). Poverty as a predictor of 4-year-olds’
executive function: New perspectives on models of differential susceptibility.
Developmental Psychology. doi:10.1037/a0028343
Roiser, J. P., Rogers, R. D., Cook, L. J., & Sahakian, B. J. (2006). The effect of polymorphism at the serotonin transporter gene on decision-making, memory and executive function in ecstasy users and controls. Psychopharmacology, 188(2), 213–227.
doi:10.1007/s00213-006-0495-z
Roisman, G. I., Newman, D. A., Fraley, R. C., Haltigan, J. D., Groh, A. M., & Haydon,
K. C. (2012). Distinguishing differential susceptibility from diathesis-stress: Recommendations for evaluating interaction effects. Development and Psychopathology,
24(2), 389–409. doi:10.1017/S0954579412000065
Scott, S., & O’Connor, T. G. (2012). An experimental test of differential susceptibility to parenting among emotionally-dysregulated children in a randomized controlled trial for oppositional behavior. Journal of Child Psychology and Psychiatry,
and Allied Disciplines. doi:10.1111/j.1469-7610.2012.02586.x
Sih, A. (2011). Effects of early stress on behavioral syndromes: An integrated
adaptive perspective. Neuroscience and Biobehavioral Reviews, 35(7), 1452–1465.
doi:10.1016/j.neubiorev.2011.03.015
van IJzendoorn, M. H., Belsky, J., & Bakermans-Kranenburg, M. J. (2012). Serotonin transporter genotype 5HTTLPR as a marker of differential susceptibility? A
meta-analysis of child and adolescent gene-by-environment studies. Translational
Psychiatry.
Verschoor, E., & Markus, C. R. (2011). Affective and neuroendocrine stress reactivity
to an academic examination: Influence of the 5-HTTLPR genotype and trait neuroticism. Biological Psychology, 87(3), 439–449. doi:10.1016/j.biopsycho.2011.06.001

SARAH HARTMAN SHORT BIOGRAPHY
Sarah Hartman received her BS degree in psychology with an emphasis
in biology from University of California, Davis, in 2009. During 2012, she
received her MA degree in psychology from CSU Stanislaus with distinction.
She is currently a PhD student at University of California, Davis working
under the supervision of Professor Jay Belsky.

An Evolutionary Perspective on Developmental Plasticity

13

JAY BELSKY SHORT BIOGRAPHY
Jay Belsky is the Robert M. and Natalie Reid Dorn Professor of Human
Development at the University of California, Davis. He is an internationally
recognized expert in the field of child development and family studies.
His areas of special expertise include the effects of day care, parent–child
relations during the infancy and early childhood years, the transition to
parenthood, the etiology of child maltreatment, and the evolutionary basis of
parent and child functioning. He obtained his PhD in 1978 in Human Development and Family Studies from Cornell University. From 1999 to 2010, he
served as founding Director of the Institute for the Study of Children, Families and Social Issues and Professor of Psychology at Birkbeck University of
London. Before that, he served on the faculty at Penn State University for 21
years, rising to the rank of Distinguished Professor of Human Development.
In 1983, he won the Boyd McCandless Award for Distinguished Early
Contribution from the Developmental Psychology Division of the American
Psychological Association. In 2002, the Institute of Scientific Information,
Philadelphia, PA granted him the Highly-Cited-Researcher designation. In
2007, he was awarded the American Psychological Association Urie Bronfenbrenner Award for Lifetime Contribution to Developmental Psychology
in the Service of Science and Society. In 2010, he was made a member of the
Academy of Europe.
Webpage: http://hcd.ucdavis.edu/faculty/webpages/jbelsky/

RELATED ESSAYS
Economics of Early Education (Economics), W. Steven Barnett
Kin-Directed Behavior in Primates (Anthropology), Carol M. Berman
Neighborhoods and Cognitive Development (Psychology), Jondou Chen and
Jeanne Brooks-Gunn
Genetics and the Life Course (Sociology), Evan Charney
Cognitive Processes Involved in Stereotyping (Psychology), Susan T. Fiske
and Cydney H. Dupree
Social Class and Parental Investment in Children (Sociology), Anne H.
Gauthier
Changing Family Patterns (Sociology), Kathleen Gerson and Stacy Torres
Language and Thought (Psychology), Susan Goldin-Meadow
Family Relationships and Development (Psychology), Joan E. Grusec
Genetics and Social Behavior (Anthropology), Henry Harpending and Gregory Cochran
Grandmothers and the Evolution of Human Sociality (Anthropology), Kristen
Hawkes and James Coxworth

14

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Childhood (Anthropology), Karen L. Kramer
Two-Systems View of Children’s Theory-of-Mind Understanding (Psychology), Jason Low
Evolutionary Perspectives on Animal and Human Personality (Anthropology), Joseph H. Manson and Lynn A. Fairbanks
Neural and Cognitive Plasticity (Psychology), Eduardo Mercado III
A Bio-Social-Cultural Approach to Early Cognitive Development: Entering
the Community of Minds (Psychology), Katherine Nelson
The Intrinsic Dynamics of Development (Psychology), Paul van Geert and
Marijn van Dijk
How Form Constrains Function in the Human Brain (Psychology), Timothy
D. Verstynen
Theory of Mind (Psychology), Henry Wellman
Behavioral Heterochrony (Anthropology), Victoria Wobber and Brian Hare; An Evolutionary Perspective on
Developmental Plasticity
SARAH HARTMAN and JAY BELSKY

Abstract
In this essay, we advance the argument that variations in developmental plasticity
should be treated as an individual-difference construct in research on environmental influences on human development. As guided by the diathesis-stress framework,
past research has focused mainly on the development of dysfunction and negative
outcomes in “vulnerable” individuals and the absence of such effects in “resilient”
ones in response to adverse developmental experiences and environmental exposures. An evolutionary perspective challenges this traditional and prevailing framework for understanding person-X-environment interaction, leading to the view that
there are individual differences in developmental plasticity, with those individuals
most susceptible to the negative effects of adverse experiences also most likely to
benefit from positive ones. Evidence consistent with this view is summarized and
directions for future research are outlined.

INTRODUCTION
It has long been appreciated that Homo sapiens are a developmentally plastic
species whose growth and functioning are affected by environmental experiences and exposures encountered while growing up. Such sensitivity to the
environment is presumed to enable the individual to prepare for the future
and manage its resources effectively, thereby promoting reproductive fitness,
that is, the passing on of genes to future generations.
Insufficiently appreciated by many developmental scholars, however, is
that plasticity is not an unmitigated good, carrying just benefits (Sih, 2011).
One potential cost derives from a “mismatch” between the early environment
that a person develops in and adjusts to and the one the person encounters
later in life. As a dramatic example, consider the cost incurred by Cambodian children (and their genetic relatives) who followed parental entreaties
to study hard and do well in school, only to find when they grew up that they
were the first to be murdered by the Khmer Rouge who distrusted the educated classes! As another example, consider a child who becomes (wisely?)
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.

1

2

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

hostile, aggressive, and excessively alert to threats to his or her well-being
as a result of being abused at home, but then ends up in a school that is safe
and fair-minded, expecting nevertheless that others will take advantage of
him or her? Developmental plasticity may also carry costs associated with
the greater complexity required of an organism capable of developing in a
variety of ways depending on its early life experiences, given that a more
complex system has more ways to go awry than a less complex one.
No matter what the benefits of plasticity, then, these observations suggest
that natural selection should have “hedged its bets,” with some individuals
being more and others less—or hardly at all—developmentally plastic. This
analysis implies that developmental plasticity should be regarded as a phenotype or individual-difference construct in its own right (Belsky & Pluess,
2013a).
As it turns out, appreciation of individual differences in sensitivity to
the environment have been well recognized—at least in research on and
thinking about contextual risk and developmental resilience. After all, some
individuals have long been regarded as more likely to succumb to adversity
(i.e., the “vulnerable”) than others (the “resilient”) as a function of their
temperament, physiology, and/or genetic makeup (Luthar, Cicchetti, &
Becker, 2000). Such “diathesis-stress” thinking says nothing about variation
in response to environmental support or enrichment, however. Moreover,
it remains unclear why natural selection would craft the development of
some organisms to go awry in the face of contextual risk, as this predominant perspective on person-X-environment interaction seems to presume
would be the case. Recently, an alternative to the prevailing diathesis-stress
framework has been advanced.
DIFFERENTIAL SUSCEPTIBILITY
A perspective emphasizing differential susceptibility to environmental
influence is built on evolutionary theory and acknowledges both the costs
and benefits of plasticity (for extensive treatment, see Belsky & Pluess,
2009a; Ellis, Boyce, Belsky, Bakermans-Kranenburg, & Van IJzendoorn,
2011). It differs from the traditional diathesis-stress framework by treating
plasticity as a phenotype and highlighting the fact that evidence for what
appears to be a disproportionate vulnerability of some to adversity may,
in fact, reflect a more general susceptibility to both positive and negative
environmental influences. This may have gone unnoticed owing to the
absence of evolutionary thinking in so much developmental and psychiatric
research and the fact that so much of this work has focused principally if
not exclusively on contextual adversity and developmental dysfunction

An Evolutionary Perspective on Developmental Plasticity

3

instead of the full range of environmental exposures—from positive to
negative—and their effects, again from positive to negative.
As a result, “vulnerable” individuals have been viewed as solely susceptible to the negative effects of adversity instead of being recognized as disproportionately susceptible to both positive and negative influences, that
is, “for better and for worse” (Belsky, Bakermans-Kranenburg, & Van IJzendoorn, 2007). By the same token, individuals regarded as resilient in the face
of adversity may also be unlikely to benefit from environmental support and
enrichment. The latter clearly implies that resilience stemming from characteristics of the individual and so heralded in the developmental and psychiatric literature may not be the unmitigated good it is typically regarded
as. Evidence consistent with the differential-susceptibility view that is extensively reviewed by Belsky and Pluess (2009a, 2013a) highlights temperamental, physiological, and genetic plasticity factors distinguishing those more
and less susceptible to both positive and negative environmental effects.
NEGATIVE EMOTIONALITY
The first evidence for differential susceptibility indicated that it was infants,
toddlers, and children with difficult or negatively emotional temperaments
who developed especially poorly in the face of contextual adversity (e.g.,
poverty, and maternal depression), but proved most likely to benefit from
supportive experiences (for review, see Belsky, 2005). Further evidence to
this effect comes from work linking maternal empathy (Pitzer et al., 2011)
and anger (Poehlmann et al., 2012) with externalizing problems; mutual
responsiveness observed in mother-child dyads with effortful control (Kim
& Kochanska, 2012); intrusive maternal behavior (Conway & Stifter, 2012)
and poverty (Raver, Blair, & Willoughby, 2012) with executive functioning;
and sensitive parenting with social, emotional, and cognitive-academic
development (Roisman et al., 2012). One issue that merits additional empirical attention concerns the plasticity marker, negative emotionality, given
that it has been operationalized in diverse ways across studies, including
fear, inhibition, difficult temperament, and negative affect.
PHYSIOLOGICAL REACTIVITY
A claim central to Boyce and Ellis’ (2005) biological-sensitivity-to-context
(BSC) model of differential susceptibility is that physiological reactivity is
a plasticity factor regulated by environmental experience, with heightened
physiological reactivity in children being the mechanism responsible for
greater environmentally sensitivity—in a for-better-and-for-worse manner. This has been shown in research on effects of actual marital conflict

4

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

(Obradovic, Bush, & Boyce, 2011) and simulated interparental aggression
(Davies, Sturge-Apple, & Cicchetti, 2011) on externalizing problems; family
adversity on school achievement (Obradovic, Bush, Stamperdahl, Adler,
& Boyce, 2010); and teacher-child conflict on change in symptom severity
(Essex, Armstrong, Burk, Goldsmith, & Boyce, 2011). What remains unclear
is the stability of physiological reactivity across childhood and into adulthood and thus whether those who are highly reactive early in life but are
exposed to nurturing experiences that promote well-being remain highly
physiologically reactive—and thus highly susceptible (for better and for
worse)—as they develop. After all, it could be that supportive rearing down
regulates reactivity, thereby reducing environmental susceptibility.
GENETIC POLYMORPHISMS
Like other polymorphisms, the serotonin transporter gene, 5-HTTLPR, and
the dopamine receptor gene, DRD4, have been regarded by psychiatric
geneticists as “vulnerability genes” predisposing carriers of particular
alleles to depression, and ADHD, respectively, in the face of adversity.
Ever more evidence indicates, however, that they be regarded as “plasticity
genes” (Belsky & Pluess, 2009b), making carriers of the putative risk alleles
especially susceptible to environmental influences—for better and for worse.
Regarding 5-HTTLPR, individuals carrying one or more short alleles
show greater “for-better-or-for-worse” plasticity when the rearing predictor and child outcome are, respectively, maternal responsiveness and
moral internalization (Kochanska, Kim, Barry, & Philibert, 2011), child
maltreatment and antisocial behavior (Cicchetti, Rogosch, & Thibodeau,
2012), and supportive parenting and positive affect (Hankin et al., 2011).
Differential-susceptibility-related findings also emerge (among male
African-American adolescents) when perceived racial discrimination is
used to predict conduct problems (Brody et al., 2011); when life events are
used to predict neuroticism (Pluess, Belsky, Way, & Taylor, 2010) and life
satisfaction of young adults (Kuepper et al., 2012); and when retrospectively
reported childhood adversity is used to explain aspects of impulsivity
among college students (e.g., pervasive influence of feelings, and feelings
trigger action) (Carver, Johnson, Joormann, Kim, & Nam, 2011). Nevertheless, other work makes clear that 5-HTTLPR operates in a manner consistent
with diathesis-stress thinking (e.g., Bakermans-Kranenburg, Dobrova-Krol,
& van IJzendoorn, 2012; Brody et al., 2012). This underscores the need
to determine when one process or the other proves operative. A recent
meta-analysis reveals that in the case of Caucasian children under 18 years
of age, short-allele carriers are more susceptible than long-allele carriers

An Evolutionary Perspective on Developmental Plasticity

5

to both positive and negative developmental experiences (van IJzendoorn,
Belsky, & Bakermans-Kranenburg, 2012).
Regarding DRD4, heightened if not exclusive susceptibility emerged for
individuals who carry the 7-repeat allele in contexts where the environmental predictor and developmental outcome were, respectively, maternal
positivity and pro-social behavior (Knafo, Israel, & Ebstein, 2011); early
nonfamilial childcare and social competence (Belsky & Pluess, 2013b);
contextual stress and support and adolescent negative arousal (Beach et al.,
2012); childhood adversity and young-adult persistent alcohol dependence
(Park, Sher, Todorov, & Heath, 2011); and newborn risk status (i.e., gestational age, birth weight for gestational age, length of stay in the hospital)
and observed maternal sensitivity (Fortuna et al., 2011). Notable also is
that a meta-analysis of G×E research involving dopamine-related genes
revealed that children of 8 years and younger respond to positive and
negative experiences in a manner consistent with differential susceptibility
(Bakermans-Kranenburg & van IJzendoorn, 2011).
In addition to the two polymorphisms just highlighted, there is evidence
that others may operate as plasticity factors, making some individuals more
susceptible to environmental influences—for better and for worse. Especially
important to appreciate is that most polymorphisms that have emerged as
potential plasticity factors derived from psychiatric-genetic studies guided
by diathesis-stress thinking. Researchers should expand their list of candidate genes beyond polymorphisms associated with disturbed functioning to
incorporate a biologically driven inquiry of physiological processes affecting
plasticity. A recent example of such an effort yielding evidence of differential
susceptibility focused on the CHRNA4 genotype because of its role in acetylcholine production, a component strongly related to plasticity and learning
(Grazioplene, DeYoung, Rogosch, & Cicchetti, 2013).
FUTURE RESEARCH DIRECTIONS
However much progress has been made in chronicling differentialsusceptibility to environmental influences, many issues remain to be
explored or illuminated.
POLYGENETIC PLASTICITY
Rather than regarding some individuals as plastic or malleable and others
as not, it probably makes more sense to think of a gradient, with some being
especially malleable, some reasonably malleable, some less so, and some not
at all. Certainly that is suggested by work using multiple plasticity genes, as
it reveals a dose–response relation between the number of plasticity genes

6

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

and the extent to which individuals are affected for better and for worse (e.g.,
Belsky & Beaver, 2011; Conner, Hellemann, Ritchie, & Noble, 2010). Future
work of this kind should be guided by a “system-level genetic approach”
involving the composting of putative plasticity genes on an a priori basis
guided by knowledge of a particular biological process or pathway, such
as the dopaminergic or serotonergic system, or neurological morphology.
Even further insight may be gained through analysis of subsystems, including those involved with synthesis, degradation/transport, receptor and
modulation (Chen et al., 2011).
REPEATED MEASURES
A key assumption underlying the notion of differential susceptibility is that
if those who prove vulnerable to adversity or who benefit the most from
support found themselves growing up under opposite conditions that they
would develop in a manner opposite to that which they do. For example,
children, carrying the 7-repeat allele of the DRD4 gene who show high levels of externalizing problems when their parents are unskilled would show
especially low levels of problems—and perhaps greater competence than
others—if raised with more skilled parents. It is difficult to evaluate this proposal owing to ethical issues; one cannot create a bad rearing milieu for a
child who has a good one.
Researchers may overcome this limitation by experimentally manipulating
environments in a repeated-measures design. Consider as an example work
by Roiser et al. (2006) on decision making during a gambling game in which
individuals in one condition had good chances of winning and in the other
poor chances. Results revealed that individuals with more 5-HTTLPR short
alleles took the most risk (i.e., placed a bet) when chances of winning were
good yet these same individuals engaged in the least gambling risk-taking
when chances of winning were poor. Another repeated-measures study took
advantage of a natural experiment, discovering that short allele carriers experienced the most stress, tension, and negative mood on exam days but the
least on nonexam days (Verschoor & Markus, 2011).
EXPERIMENTAL TESTING OF PLASTICITY FACTORS
Most differential-susceptibility-related research has been observational in
nature. This can challenge interpretation because environmental experiences
may be selected rather than randomly assigned, creating the possibility
that gene–environment correlation masquerades as gene–environment
interaction. One solution to this problem involves conducting intervention
experiments with random assignment of participants to experimental or

An Evolutionary Perspective on Developmental Plasticity

7

control conditions, work that is just beginning (Bakersman-Kranenburg, van
IJzendoorn, Mesman, Alink, & Jeffer, 2008; Scott & O’Connor, 2012). Because
of the previously mentioned ethical considerations, this approach has only
been used to detect plasticity factors affecting response to interventions
promoting positive functioning. Even though this design is limited to
examining just the “for-better” side of plasticity, it still enables evaluation
of whether those found to be most vulnerable to adversity in other research
actually do benefit disproportionately from intervention efforts to promote
positive functioning, whereas those regarded as resilient in the face of
adversity turn out to be unaffected by the intervention.
DOMAIN SPECIFIC OR DOMAIN GENERAL?
Reflection on this observation raises a related issue about whether plasticity
is domain general or domain specific. That is, are more malleable individuals
especially responsive to and influenced by a wide variety of environmental
conditions and developmental exposures and other not particularly influenced by the same large set of experiences? Alternatively, are individuals
mostly “mosaics” of plasticity, being highly sensitive to some contextual
conditions but not others and/or with respect to some developmental
outcomes but not others?
However surprising it might seem, there is some evidence for the
domain-general view. Consider the results of two interventions that used
strikingly dissimilar methods to promote different aspects of development.
In one case the intervention sought to promote sensitive parenting in order
to reduce toddler’s externalizing behavior (Bakersman-Kranenburg, van
IJzendoorn, Pijlman, Mesman, & Juffer, 2008) and cortisol-related stress
reactivity (Bakersman-Kranenburg, van IJzendoorn, Mesman, et al., 2008),
whereas in the other a computerized instructional program was employed
to foster preschooler’s phonemic awareness and, thereby, early literacy
(Kegel, Bus, & van IJzendoorn, 2011). Despite the dramatic differences in the
interventions and in the features of development being studied, it was children carrying 7-repeat DRD4 allele who benefited disproportionately, if not
exclusively, from both! Before it can be concluded, however, that plasticity
is more domain general than domain specific, far more work is required. We
suspect that some individuals will be on the extremes of plasticity—highly
responsive or virtually unaffected by almost all contextual conditions—but
that most might fall somewhere between these extremes.
ENVIRONMENTAL CUE RELIABILITY
There is likely a variation in the reliability of environmental cues that children receive in developmental contexts. For instance, harsh environments

8

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

can be characterized as consistently and thus predictably high in conflict or
episodically but not as predictably high in conflict. Frankenhuis and Panchanathan (2011) propose that highly plastic individuals growing up in these
differing environments could vary in the timing of their “commitment” to a
developmental strategy. A person developing in a highly predictable harsh
environment may “commit” early, having high confidence in the state of the
environment, whereas someone in an erratic environment may delay commitment to allow more time for a better estimation of the current—and thus
future environment. Future work should seek to illuminate this issue.
TIMING OF SUSCEPTIBILITY
It is widely assumed that environmental exposures and developmental experiences exert their greatest influence early in life when biological systems are
forming. Even if this may generally be true, it is still possible that some individuals could be more plastic later rather than earlier in life. All it would have
taken for this to be so is for later plasticity to have paid off more than earlier
plasticity some time in our ancestral past and for natural selection to thus
have preserved genes responsible for such deferred developmental plasticity. This raises the possibility that some individuals may be highly responsive
to environmental influences—in a for-better-and-for-worse manner—across
the life course, others never, some especially early and some especially later.
CONCLUSION
From an evolutionary perspective, we have outlined the need to move
beyond considering only the benefits of plasticity—as is typically done
when comparing our species to that of others—to an evolutionary-inspired
theoretical framework that acknowledges both the costs and benefits of
developmental plasticity. Moreover, rather than presuming that some
individuals are simply more susceptible to the negative developmental
effects of contextual adversity, as the prevailing person-X-environment,
diathesis-stress framework does, differential-susceptibility thinking presumes that there are (i) individual differences in developmental plasticity;
(ii) such that those most susceptible to adversity are also especially likely
to benefit from environmental support and enrichment; and (iii) thus that
developmental plasticity should be treated as an individual-difference
construct. Evidence highlighting diverse plasticity factors proves consistent
with this claim, though many questions remain to be addressed. Perhaps a
major contribution of the differential-susceptibility perspective is to underscore the theoretical and empirical risks of focusing disproportionately on

An Evolutionary Perspective on Developmental Plasticity

9

contextual risk, dysfunctional development and vulnerability and benefits
of viewing developmental from an evolutionary perspective.
REFERENCES
Bakermans-Kranenburg, M. J., Dobrova-Krol, N. A., & van IJzendoorn, M. H. (2012).
Impact of institutional care on attachment disorganization and insecurity of
Ukrainian pre-schoolers: Protective effect of the long variant of the serotonin transporter gene (5HTT). International Journal of Behavioral Development, 36(1), 11–18.
Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2011). Differential susceptibility to rearing environment depending on dopamine-related genes: New
evidence and a meta-analysis. Development and Psychopathology, 23(1), 39–52.
doi:10.1017/s0954579410000635
Bakermans-Kranenburg, M. J., van IJzendoorn, M. H., Mesman, J., Alink, L. R.,
& Juffer, F. (2008). Effects of an attachment-based intervention on daily cortisol moderated by dopamine receptor D4: A randomized control trial on 1- to
3-year-olds screened for externalizing behavior. Development and Psychopathology,
20(3), 805–820.
Bakermans-Kranenburg, M. J., van IJzendoorn, M. H., Pijlman, F. T., Mesman, J., &
Juffer, F. (2008). Experimental evidence for differential susceptibility: Dopamine
D4 receptor polymorphism (DRD4 VNTR) moderates intervention effects on toddlers’ externalizing behavior in a randomized controlled trial. Developmental Psychology, 44(1), 293–300.
Beach, S. R. H., Lei, M. K., Brody, G. H., Simons, R. L., Cutrona, C., & Philibert,
R. A. (2012). Genetic moderation of contextual effects on negative arousal and
parenting in African-American parents. Journal of Family Psychology, 26(1), 46–55.
doi:10.1037/a0026236
Belsky, J. (2005). Differential susceptibility to rearing influences: An evolutionary
hypothesis and some evidence. In B. Ellis & D. Bjorklund (Eds.), Origins of the
social mind: Evolutionary psychology and child development (pp. 139–163). New York,
NY: Guildford.
Belsky, J., & Pluess, M. (2013a). Beyond risk, resilience and dysregulation: Phenotypic plasticity and human development. Development and Psychopathology,
25(4pt2), 1243–1261.
Belsky, J., & Pluess, M. (2013b). Genetic moderation of early child care effects on
behavior problems and social competence across childhood: A developmental
analysis. Child Development, 84(4), 1209–1225.
Belsky, J., Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). For better and for worse: Differential susceptibility to environmental influences. Current
Directions in Psychological Science, 16(6), 300–304.
Belsky, J., & Beaver, K. M. (2011). Cumulative-genetic plasticity, parenting and adolescent self-control/regulation. Journal of Child Psychology and Psychiatry, 52(5),
619–626.
Belsky, J., & Pluess, M. (2009a). Beyond diathesis-stress: Differential susceptibility to
environmental influences. Psychological Bulletin, 135(6), 885–908.

10

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Belsky, J., & Pluess, M. (2009b). The nature (and nurture?) of plasticity in early human
development. Perspectives on Psychological Science, 4(4), 345–351.
Boyce, W. T., & Ellis, B. J. (2005). Biological sensitivity to context: I. An
evolutionary-developmental theory of the origins and functions of stress reactivity. Development and Psychopathology, 17(2), 271–301.
Brody, G. H., Beach, S. R. H., Chen, Y.-F., Obasi, E., Philibert, R. A., Kogan, S. M., &
Simons, R. L. (2011). Perceived discrimination, serotonin transporter linked polymorphic region status, and the development of conduct problems. Development
and Psychopathology, 23(2), 617–627. doi:10.1017/s0954579411000046
Brody, G. H., Yu, T., Chen, Y. F., Kogan, S. M., Evans, G. W., Windle, M., … Philibert, R. A. (2012). Supportive family environments, genes that confer sensitivity,
and allostatic load among rural African American emerging adults: A prospective
analysis. Journal of Family Psychology. doi:10.1037/a0027829
Carver, C. S., Johnson, S. L., Joormann, J., Kim, Y., & Nam, J. Y. (2011). Serotonin
transporter polymorphism interacts with childhood adversity to predict aspects
of impulsivity. Psychological Science, 22(5), 589–595. doi:10.1177/0956797611404085
Chen, C., Moyzis, R., Stern, H., He, Q., Li, H., Li, J., … Dong, Q. (2011). Contributions of dopamine-related genes and environmental factors to highly sensitive
personality: A multi-step neuronal system-level approach. PLoS One, 6(7), e21636.
doi:10.1371/journal.pone.0021636
Cicchetti, D., Rogosch, F. A., & Thibodeau, E. L. (2012). The effects of child maltreatment on early signs of antisocial behavior: Genetic moderation by tryptophan
hydroxylase, serotonin transporter, and monoamine oxidase A genes. Development
and Psychopathology, 24(3), 907–928.
Conner, B. T., Hellemann, G. S., Ritchie, T. L., & Noble, E. P. (2010). Genetic, personality, and environmental predictors of drug use in adolescents. Journal of Substance
Abuse Treatment, 38(2), 178–190. doi:10.1016/j.jsat.2009.07.004
Conway, A., & Stifter, C. A. (2012). Longitudinal antecedents of executive function in preschoolers. Child Development, 83(3), 1022–1036. doi:10.1111/j.14678624.2012.01756.x
Davies, P. T., Sturge-Apple, M. L., & Cicchetti, D. (2011). Interparental aggression and children’s adrenocortical reactivity: Testing an evolutionary model
of allostatic load. Development and Psychopathology, 23(3), 801–814. doi:10.1017/
s0954579411000319
Ellis, B. J., Boyce, W. T., Belsky, J., Bakermans-Kranenburg, M. J., & van IJzendoorn,
M. H. (2011). Differential susceptibility to the environment: An evolutionary—
neurodevelopmental theory. Development and Psychopathology, 23(1), 7–28.
doi:10.1017/s0954579410000611
Essex, M. J., Armstrong, J. M., Burk, L. R., Goldsmith, H. H., & Boyce, W. T. (2011).
Biological sensitivity to context moderates the effects of the early teacher-child
relationship on the development of mental health by adolescence. Development and
Psychopathology, 23(1), 149–161. doi:10.1017/s0954579410000702
Fortuna, K., van IJzendoorn, M. H., Mankuta, D., Kaitz, M., Avinun, R., Ebstein,
R. P., & Knafo, A. (2011). Differential genetic susceptibility to child risk at birth

An Evolutionary Perspective on Developmental Plasticity

11

in predicting observed maternal behavior. PLoS One, 6(5). doi:10.1371/journal.
pone.0019765
Frankenhuis, W. E., & Panchanathan, K. (2011). Individual differences in developmental plasticity may result from stochastic sampling. Perspectives on Psychological
Science, 6(4), 336–347. doi:10.1177/1745691611412602
Grazioplene, R. G., DeYoung, C. G., Rogosch, F. A., & Cicchetti, D. (2013). A novel
differential susceptibility gene: CHRNA4 and moderation of the effect of maltreatment on child personality. Journal of Child Psychology and Psychiatry, 54(8), 872–880.
Hankin, B. L., Nederhof, E., Oppenheimer, C. W., Jenness, J., Young, J. F., Abela, J. R.
Z., … Oldehinkel, A. J. (2011). Differential susceptibility in youth: Evidence that
5-HTTLPR x positive parenting is associated with positive affect ‘for better and
worse’. Translational Psychiatry, 1, e44. doi:10.1038/tp.2011.44
Kegel, C. A. T., Bus, A. G., & van IJzendoorn, M. H. (2011). Differential susceptibility in early literacy instruction through computer games: The role of the
dopamine D4 receptor gene (DRD4). Mind, Brain, and Education, 5(2), 71–78.
doi:10.1111/j.1751-228X.2011.01112.x
Kim, S., & Kochanska, G. (2012). Child temperament moderates effects of parent–
child mutuality on self-regulation: A relationship-based path for emotionally negative infants. Child Development, 83(4), 1275–1289. doi:10.1111/j.1467-8624.2012.
01778.x
Knafo, A., Israel, S., & Ebstein, R. P. (2011). Heritability of children’s prosocial
behavior and differential susceptibility to parenting by variation in the dopamine
receptor D4 gene. Development and Psychopathology, 23(1), 53–67. doi:10.1017/
s0954579410000647
Kochanska, G., Kim, S., Barry, R. A., & Philibert, R. A. (2011). Children’s genotypes interact with maternal responsive care in predicting children’s competence:
Diathesis-stress or differential susceptibility? Development and Psychopathology, 23,
605–616.
Kuepper, Y., Wielpuetz, C., Alexander, N., Mueller, E., Grant, P., & Hennig, J. (2012).
5-HTTLPR S-Allele: A genetic plasticity factor regarding the effects of life events
on personality? Genes, Brain, and Behavior. doi:10.1111/j.1601-183X.2012.00783.x
Luthar, S. S., Cicchetti, D., & Becker, B. (2000). The construct of resilience: a critical
evaluation and guidelines for future work. Child Development, 71(3), 543–562.
Obradović, J., Bush, N. R., & Boyce, W. T. (2011). The interactive effect of marital
conflict and stress reactivity on externalizing and internalizing symptoms: The
role of laboratory stressors. Development and Psychopathology, 23(01), 101–114.
Obradović, J., Bush, N. R., Stamperdahl, J., Adler, N. E., & Boyce, W. T. (2010). Biological sensitivity to context: The interactive effects of stress reactivity and family
adversity on socio-emotional behavior and school readiness. Child Development,
81(1), 270–289.
Park, A., Sher, K. J., Todorov, A. A., & Heath, A. C. (2011). Interaction between the
DRD4 VNTR polymorphism and proximal and distal environments in alcohol
dependence during emerging and young adulthood. Journal of Abnormal Psychology, 120(3), 585–595. doi:10.1037/a0022648

12

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Pitzer, M., Jennen-Steinmetz, C., Esser, G., Schmidt, M. H., & Laucht, M. (2011). Differential susceptibility to environmental influences: The role of early temperament
and parenting in the development of externalizing problems. Comprehensive Psychiatry, 52(6), 650–658. doi:10.1016/j.comppsych.2010.10.017
Pluess, M., Belsky, J., Way, B. M., & Taylor, S. E. (2010). 5-HTTLPR moderates effects
of life events on neuroticism: Differential susceptibility to environmental influences. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 34, 1070–1074.
Poehlmann, J., Hane, A., Burnson, C., Maleck, S., Hamburger, E., & Shah, P. E. (2012).
Preterm infants who are prone to distress: Differential effects of parenting on
36-month behavioral and cognitive outcomes. Journal of Child Psychology and Psychiatry, and Allied Disciplines. doi:10.1111/j.1469-7610.2012.02564.x
Raver, C. C., Blair, C., & Willoughby, M. (2012). Poverty as a predictor of 4-year-olds’
executive function: New perspectives on models of differential susceptibility.
Developmental Psychology. doi:10.1037/a0028343
Roiser, J. P., Rogers, R. D., Cook, L. J., & Sahakian, B. J. (2006). The effect of polymorphism at the serotonin transporter gene on decision-making, memory and executive function in ecstasy users and controls. Psychopharmacology, 188(2), 213–227.
doi:10.1007/s00213-006-0495-z
Roisman, G. I., Newman, D. A., Fraley, R. C., Haltigan, J. D., Groh, A. M., & Haydon,
K. C. (2012). Distinguishing differential susceptibility from diathesis-stress: Recommendations for evaluating interaction effects. Development and Psychopathology,
24(2), 389–409. doi:10.1017/S0954579412000065
Scott, S., & O’Connor, T. G. (2012). An experimental test of differential susceptibility to parenting among emotionally-dysregulated children in a randomized controlled trial for oppositional behavior. Journal of Child Psychology and Psychiatry,
and Allied Disciplines. doi:10.1111/j.1469-7610.2012.02586.x
Sih, A. (2011). Effects of early stress on behavioral syndromes: An integrated
adaptive perspective. Neuroscience and Biobehavioral Reviews, 35(7), 1452–1465.
doi:10.1016/j.neubiorev.2011.03.015
van IJzendoorn, M. H., Belsky, J., & Bakermans-Kranenburg, M. J. (2012). Serotonin transporter genotype 5HTTLPR as a marker of differential susceptibility? A
meta-analysis of child and adolescent gene-by-environment studies. Translational
Psychiatry.
Verschoor, E., & Markus, C. R. (2011). Affective and neuroendocrine stress reactivity
to an academic examination: Influence of the 5-HTTLPR genotype and trait neuroticism. Biological Psychology, 87(3), 439–449. doi:10.1016/j.biopsycho.2011.06.001

SARAH HARTMAN SHORT BIOGRAPHY
Sarah Hartman received her BS degree in psychology with an emphasis
in biology from University of California, Davis, in 2009. During 2012, she
received her MA degree in psychology from CSU Stanislaus with distinction.
She is currently a PhD student at University of California, Davis working
under the supervision of Professor Jay Belsky.

An Evolutionary Perspective on Developmental Plasticity

13

JAY BELSKY SHORT BIOGRAPHY
Jay Belsky is the Robert M. and Natalie Reid Dorn Professor of Human
Development at the University of California, Davis. He is an internationally
recognized expert in the field of child development and family studies.
His areas of special expertise include the effects of day care, parent–child
relations during the infancy and early childhood years, the transition to
parenthood, the etiology of child maltreatment, and the evolutionary basis of
parent and child functioning. He obtained his PhD in 1978 in Human Development and Family Studies from Cornell University. From 1999 to 2010, he
served as founding Director of the Institute for the Study of Children, Families and Social Issues and Professor of Psychology at Birkbeck University of
London. Before that, he served on the faculty at Penn State University for 21
years, rising to the rank of Distinguished Professor of Human Development.
In 1983, he won the Boyd McCandless Award for Distinguished Early
Contribution from the Developmental Psychology Division of the American
Psychological Association. In 2002, the Institute of Scientific Information,
Philadelphia, PA granted him the Highly-Cited-Researcher designation. In
2007, he was awarded the American Psychological Association Urie Bronfenbrenner Award for Lifetime Contribution to Developmental Psychology
in the Service of Science and Society. In 2010, he was made a member of the
Academy of Europe.
Webpage: http://hcd.ucdavis.edu/faculty/webpages/jbelsky/

RELATED ESSAYS
Economics of Early Education (Economics), W. Steven Barnett
Kin-Directed Behavior in Primates (Anthropology), Carol M. Berman
Neighborhoods and Cognitive Development (Psychology), Jondou Chen and
Jeanne Brooks-Gunn
Genetics and the Life Course (Sociology), Evan Charney
Cognitive Processes Involved in Stereotyping (Psychology), Susan T. Fiske
and Cydney H. Dupree
Social Class and Parental Investment in Children (Sociology), Anne H.
Gauthier
Changing Family Patterns (Sociology), Kathleen Gerson and Stacy Torres
Language and Thought (Psychology), Susan Goldin-Meadow
Family Relationships and Development (Psychology), Joan E. Grusec
Genetics and Social Behavior (Anthropology), Henry Harpending and Gregory Cochran
Grandmothers and the Evolution of Human Sociality (Anthropology), Kristen
Hawkes and James Coxworth

14

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Childhood (Anthropology), Karen L. Kramer
Two-Systems View of Children’s Theory-of-Mind Understanding (Psychology), Jason Low
Evolutionary Perspectives on Animal and Human Personality (Anthropology), Joseph H. Manson and Lynn A. Fairbanks
Neural and Cognitive Plasticity (Psychology), Eduardo Mercado III
A Bio-Social-Cultural Approach to Early Cognitive Development: Entering
the Community of Minds (Psychology), Katherine Nelson
The Intrinsic Dynamics of Development (Psychology), Paul van Geert and
Marijn van Dijk
How Form Constrains Function in the Human Brain (Psychology), Timothy
D. Verstynen
Theory of Mind (Psychology), Henry Wellman
Behavioral Heterochrony (Anthropology), Victoria Wobber and Brian Hare