Sociogenomic Personality Psychology

Brent W. Roberts and Joshua J. Jackson

University of Illinois, Urbana-Champaign

ABSTRACT In this article, we address a number of issues surround-

ing biological models of personality traits. Most traditional and many
contemporary biological models of personality traits assume that biolog-
ical systems underlying personality traits are causal and immutable. In
contrast, sociogenomic biology, which we introduce to readers in this ar-
ticle, directly contradicts the widely held assumption that something that
is biological, heritable, or temperamental, is unchangeable. We provide
examples of how seemingly unchanging biological systems, such as DNA,
are both dependent on environments for elicitation and can be modified
by environmental changes. Finally, we synthesize sociogenomic biology
with personality psychology in a model of personality traits that inte-
grates this more modern perspective on biology, physiology, and envi-
ronment that we term sociogenomic personality psychology. We end the
article with a discussion of the future directions of sociogenomic person-
ality psychology.

With the decoding of the human genome and technological break-

throughs, such as Functional Magnetic Resonance Imaging (fMRI),
personality psychology is poised to rediscover its biological roots. It
is now codified as ‘‘law’’ that personality traits are heritable (Turk-
heimer, 2000). Theoretical models have mapped out the pathways
between neurophysiological structures and temperament (Depue &
Lenzenweger, 2001). Brain imaging studies are beginning to reveal
the physiological correlates of traits, such as extraversion (Canli,
2004), agreeableness (Haas, Omura, Constable, & Canli, 2007), and

This research was supported by grant AG21178 from the National Institute of Aging.
We would like to thank Gene Robinson, Robert Hogan, Sam Gosling, Lars Penke,
Grant Edmonds, and Jennifer Fayard for comments on earlier drafts of this article.
Correspondence should be sent to Brent W. Roberts, Department of Psychology,
University of Illinois, 603 East Daniel Street, Champaign, IL 61820; E-mail: broberts
@cyrus.psych.uiuc.edu.

Journal of Personality 76:6, December 2008

r 2008, Copyright the Authors
Journal compilation r 2008, Wiley Periodicals, Inc.
DOI: 10.1111/j.1467-6494.2008.00530.x
1524 Roberts & Jackson

neuroticism (Hariri et al., 2002). Molecular genetics studies have

demonstrated the association between specific genetic markers and
personality traits (Sen et al., 2004). The resurgence of research on the
biological foundations of personality harkens back to the work of
Eysenck (1967) and a time when personality traits—relatively en-
during patterns of thoughts, feelings, and behaviors—were thought
to be rooted in biology.
These advances raise a number of interesting issues, especially in
light of the intervening decades in which the modal perspective on
personality psychology was situationist and openly skeptical of the
importance or existence of personality traits (Mischel, 1968). It ap-
pears that the situationist critique of personality traits has been put
to rest. There are few disputes about the stability of personality over
time, as this has been shown to exist even when using different judges
of personality at different ages (Block & Block, 2006). The perspec-
tive on the cross-situational consistency of personality has changed,
such that researchers have shown theoretically meaningful levels of
correlations across disparate situations (Borkenau et al., 2004).
Moreover, even the argument that personality traits are of little
use in predicting important behaviors has been soundly refuted.
Personality traits predict numerous, concrete, and important life
outcomes across multiple domains (Caspi, Roberts, & Shiner, 2005;
Ozer & Benet-Martinez, 2006). In fact, a recent review shows that
personality traits predict mortality, divorce, and occupational at-
tainment as well as, if not better than, socioeconomic status and in-
telligence (Roberts, Kuncel, Shiner, Caspi, & Goldberg, 2007).
With advances demonstrating the power of personality and the
pendulum swinging toward biological perspectives, it is time to re-
examine underling theories of biological personality psychology. The
current state of biological thinking in personality psychology is sur-
prisingly consistent with Eysenck’s perspectives espoused over 30
years ago. This is not to say that much work has not occurred in
biological personality but rather that the overarching biological
model underlying even modern biological investigations of person-
ality share key features with Eysenck’s original models. Alterna-
tively, personality psychology has the opportunity to take advantage
of the spectacular advances made in biology in the last few decades,
which as we describe below, provide an alternative biological model
for personality psychology to consider. In this article, we will review
Eysenckian biological models of personality and how they still
Sociogenomic Personality Psychology 1525

inform biological thinking in personality psychology to this day and

provide reasons for implementing an alternative perspective derived
from biology called sociogenomics (Robinson, Grozinger, & Whit-
field, 2005).

Current Biological Models in Psychology

Eysenck’s approach to the biological basis of personality still reso-
nates in today’s conceptualizations of biological personality psy-
chology. This is exemplified in Figure 1, in which we have
reproduced one of Eysenck’s (1972) models depicting the interface
between biology, personality, and society. In this model, Eysenck
proposed that at the foundation of personality traits were physio-
logical systems that are inherited and often associated with specific
brain functions and structures. These physiological systems cause
behaviors that then make up personality traits, which in turn cause
social phenomena such as crime. We do not intend to discuss the
intricacies of Eysenck’s model or the validity of its structure. We
invoke it here as a representative example of models that place the
causal primacy of physiological systems over psychological systems.
DNA is the root of physiological systems in Eysenck’s model
(Eysenck, 1997) and is often considered an immutable influence on
phenotypes throughout the lifespan. Many theories assume that
since genetic polymorphisms do not change, then the influence of
DNA on behavior must not change. This would result in a constant
genetic effect throughout the lifespan. This thinking is exemplified by

Figure 1
Eysneckian model of personality.
1526 Roberts & Jackson

theories of personality that dichotomize personality into tempera-

mental (biological) and characterological (learned) components.
Temperament is seen by many as individual differences that reflect
‘‘expressions of neurobiological mechanisms that have a strong ge-
netic basis’’ (De Fruyt et al., 2006, p. 539); see also Mervielde, De
Clercq, De Fruyt, & Van Leeuwen, 2005). Personality traits have
been defined similarly (e.g., McCrae et al., 2000), which would
equate personality traits with constructs rooted in physiology and
driven by genetic causes—a conceptualization quite similar to
Eysenck’s. Even those who distinguish between temperament and
trait still argue that they are linked such that temperaments are the
‘‘biologically based’’ developmental precursor to adult personality
traits and that the two sets of constructs are viewed as ‘‘biological’’
and linked through a common genetic basis (Deal, Halverson, Hav-
ill, & Martin, 2005). For example, ‘‘temperament has been equated
to the hard ice ball around which the softer snow of personality ac-
cumulates developmentally’’ (p. 1267, Graziano, Jensen-Campbell,
& Sullivan-Logan, 1998). These definitions of temperament and
personality traits are quite similar to Eysenck’s model in which the
biological substrate to personality is unaffected by environmental
influence and that which is biological is presumed to be causal and
not caused.
We think it is important to examine more closely what researchers
mean when they use the terms ‘‘biological,’’ ‘‘genetic’’ and ‘‘highly
heritable.’’ First, it is nonsensical to describe something as ‘‘biolog-
ical’’ because there is nothing psychological that is not biological.
That is to say, if a person is thinking, feeling, or behaving, multiple
biological systems have to be engaged. What we suspect people really
mean when they refer to personality traits or temperaments as ‘‘bi-
ological,’’ ‘‘genetic,’’ or ‘‘highly heritable’’ is that there is some com-
ponent to the trait or temperament that is unchanging. Moreover,
the implicit assumption is that this unchanging influence is either
DNA or some physiological structure that is largely the result of
genetic polymorphisms. As the metaphor alluded to above—tem-
perament is the ice ball—it does not change despite socialization. Or,
to invoke a different metaphor, temperament is the biological set
point at the core of any given personality trait. People can vary
around this set point, but when left to their own resources they
will naturally gravitate back toward their biologically driven modal
tendency.
Sociogenomic Personality Psychology 1527

At first glance, the biological personality model that Eysenck

espoused seems eminently reasonable. If personality traits and
temperaments are heritable (Turkheimer, 2000), and there are
known biological correlates of personality (Eysenck, 1967; Gray,
1970; Wacker, Chavanon, & Stemmler, 2006; Zuckerman, 1991),
then it would not be a radical leap to assume that there is some un-
changing biological system at the core of personality traits. How-
ever, the heritability of personality traits and the fact that personality
traits have biological correlates does not mean that the environment
does not play a role in determining personality traits and in shaping
the biological systems assumed to underlie traits. As will be seen
below, one of the key elements of sociogenomic biology is that it
brings a new perspective to the relation between the biology and
environment.

Sociogenomic Biology
Sociogenomic biology is based on one theoretical assumption and
two scientific discoveries that are by themselves innocuous but when
combined provide a different perspective on the meaning of biology
and potentially the meaning of biological personality psychology
(Robinson et al., 2005). The assumption, derived from evolutionary
theory and sociobiology (Wilson, 1975), is that all behavior is influ-
enced by genes and forces of evolution. The latter is necessarily true
for any heritable behavior that has some impact on survival or re-
production, even if it is small (Penke, Denissen, & Miller, 2007).
Thus, sociogenomic biology focuses on the behavior of animals that
live in groups in which members must cooperate and compete in
order to survive and thrive. Clearly, humans fall into this category.
The first scientific discovery that guides a sociogenomic perspec-
tive is that the genome has been highly conserved across species.
Therefore, understanding social behavior becomes a cross-species
effort as the same genes are involved in analogous behaviors in dis-
tinctly different animals. This is consistent with the argument that
personality psychologists can benefit by becoming intimately familiar
with personality processes and structures of other species (Gosling,
2001, 2008; King, Weiss, & Farmer, 2005; Mehta & Gosling, 2006).
Sociogenomics provides a profoundly compelling reason to do so—
other animals most likely share molecular pathways and genetic
1528 Roberts & Jackson

polymorphisms with humans that contribute to similar behavioral

syndromes.
The second scientific finding that is most relevant to our argument
that biological models of personality need to be updated is that genes
are intrinsically dynamic in the way they transact with the environ-
ment, which contrasts starkly with the perspectives on temperament
and personality traits provided above and directly contradicts an
Eysenckian model of personality. One of the most significant recent
findings in biology is that the genome, whether it is human or not, is
intrinsically dependent on the environment for activation and main-
tenance. DNA consists of tens of thousands of genes that are re-
sponsible for coding different proteins, which are the building blocks
of life (Penke et al., 2007). A gene, made of up a segment of DNA,
does not directly produce behaviors, emotions, or thoughts. More-
over, genes do not continuously produce proteins. A common mis-
conception is that DNA regulates when the production of protein
occurs, since DNA is thought as the prime mover for all things bi-
ological. In fact, gene expression can be switched on and off and
altered in response to both genetic and environmental factors. This is
a result of both biology and the environment being able to influence
the complex pathway that exists between DNA and protein produc-
tion. In a flashback to introductory biology, the production of pro-
tein is the result of RNA, not DNA. DNA directs the synthesis of
RNA, known as transcription. After transcription, RNA is trans-
lated into polypeptides, which ultimately form proteins. When,
where, and how much of each protein is produced is contingent on
the cellular environment. At each step in the process the cellular
environment can be influenced by the environment outside an indi-
vidual, ultimately affecting the production of proteins. Thus, the
regulation of gene expression links the influence of DNA with the
environment (Robinson, 2004).
Broadly speaking, differences in gene expression arise from at
least two different processes, which may work in concert together.
First, variation in gene activity may be inherited through variations
in the DNA sequence (genetic polymorphisms). This is what com-
monly is thought of as ‘‘nature.’’ Secondly, gene expression may be
influenced through variation in environments. This is commonly
considered to be ‘‘nurture.’’ These processes work in tandem, result-
ing in not nature versus nurture, and not even nature and nurture, as
commonly construed. Despite the common acknowledgment that
Sociogenomic Personality Psychology 1529

both nature and nurture are important, few conceptualize how the
two work together. What is apparent from recent discoveries in bi-
ology is that the dichotomy between nature and nurture is not only
false but a gross oversimplification (Balaban, 2006; Robinson, 2004).
It turns out that both act on the same substrate, the genome. Both
can influence gene expression and both impact the brain similarly,
with the effect being that nature and nurture should not be thought
of as two distinct processes but rather as two sides of the same coin.
To demonstrate the transactional relation between environment and
gene function, we will provide a few examples drawn from animal
biology and behavior genetics studies of humans where both genes
and the environment work together to influence behavior.
One of the most dramatic examples of how the environment
affects biology comes from the life-course ecological analysis of the
blue-headed wrasse (Stearns, 1992). The blue-headed wrasse is a reef
fish found in the tropics. The males of the species are typically larger
than the females and are, as the name implies, bright blue. Females
in contrast are smaller and dull brown. Typically, males gather a
harem of females that they guard and with whom they mate. Of
course, being bright blue and large makes the males conspicuous. In
the eternal reality of fish, this means the male is likely to be eaten by
a larger fish. Interesting things happen after the male is consumed by
a predator. The females in the harem do not initiate a search for a
new male consort. Rather, literally overnight, one of the females
transforms into a male. The effect is of course genetically mediated
but entirely caused by the loss of the male or a change in the envi-
ronment. That is to say, environmental change can change the sex of
a fish.
Recent methodological advances have allowed a genetic examin-
ation of instances, like the blue headed wrasse, where the environ-
ment and biology seemingly work together. What has been
uncovered is that differences in environment can result in differ-
ences in gene expression. For example, when born, worker honey-
bees start out as caretakers of the hive but eventually transition from
caretaker to food gatherer (Robinson, 2002). Genes guide this entire
process and timing of behavioral maturation. The transition from
caretaker to food gatherer is mediated entirely at the noncognitive,
cellular level. The behavioral maturation is associated with changes
in expression of at least 2,000 genes in the bee brain (Whitfield,
Cziko, & Robinson, 2003). Interestingly, the expression of a specific
1530 Roberts & Jackson

gene, the for gene, has been linked to rather subtle shifts in the en-
vironment. In one such shift, expression of the for gene is activated in
some of the caretaker bees when there is a shortage of food gatherers
in the hive, creating a cascade of biological changes that transition
the caretaker bee into a food gatherer (Ben-Sharar, Robichon, Sko-
lowiski, & Robinson, 2002). Here an environmental change triggers
the expression of a gene, which results in higher mRNA levels in the
brain that ultimately lead to increased protein products that cause
changes in behavior. In other words, the specific gene is similar
across all bees, but the influence of the gene is contingent on an en-
vironmental stimulus.
Changes in gene expression that do not depend on variations in
the DNA sequence (genetic polymorphisms) are referred to as epi-
genetic effects (for reviews, see Feinberg, 2008; Jirtle & Skinner,
2007; Whitelaw & Whitelaw, 2006). Epigenetic effects can occur
through multiple mechanisms, one of the best studied being meth-
ylation. Methylation represses transcription of the gene, stopping the
production of specific proteins. In a fascinating line of studies, meth-
ylation clarified the mechanism behind the putatively inherited be-
havior of stress reaction in rats (Francis, Caldji, Champagne,
Plotsky, & Meaney, 1999). Specifically, rats that handled stress bet-
ter had been treated differently by their mothers when young. These
rats had been licked more by their mothers, and variation in licking
behavior was heritable. Therefore, the individual differences in re-
sponse to stress could be due to genetic factors that were passed
down from the mother, or it could be environmentally mediated
through the licking behavior. Through a cross-fostering design, re-
searchers found that the causal pathway was through licking behav-
ior and its effect on gene expression (Weaver et al., 2004). Maternal
licking influenced DNA methylation, which resulted in differences in
expression of the glucocorticoid receptor gene. These differences in
genetic expression resulted in different activity levels in glucocorti-
coid receptors. Rats with more active glucocorticoid receptors are
better able to tolerate stress than rats with less active receptors.
Thus, the difference in stress response was not due to variations in
gene sequence but through an epigenetic modification of DNA ex-
pression through methylation (Weaver et al., 2004). Again, the effect
of the gene was conditional upon the environment.
There is now provisional evidence for epigenetic effects on the
human genome. Recently, the methylation patterns of Catechol-
Sociogenomic Personality Psychology 1531

O-Methyltransferase (COMT) gene of 12 monozygotic twins were

examined (Mill et al., 2005). While the methylation patterns were
highly correlated, they were not perfectly correlated, despite the fact
that these were identical twins. This finding indicates that some event
occurred during the life course of the twins that changed the way
identical genes were expressed. Moreover, epigenetic effects were
replicated in a second, larger study of twins that also showed that the
level of discordance was correlated with age and amount of time the
twins had spent together in their lives (Fraga et al., 2005). Specifi-
cally, older twins and twins who spent less time together showed
greater evidence of epigenetic effects. This means that even within
identical twins, some environmental or biological factors can differ-
entially change the way in which identical alleles are expressed (Mill
et al., 2005). This highlights the fact that gene expression in humans,
like that of other animals, is not solely based on sequences of DNA.
Rather, the environment can shape gene expression in humans as
well.
Genetic expression has been difficult to examine in humans be-
cause current technologies do not permit a direct examination of
expression levels in the brain (with the exception of post-mortem
autopsies, e.g., Thalmeier et al., 2007). However, a number of nat-
uralistic studies of heritability and gene-by-environment interactions
suggest that the effects of DNA are contingent on the environment.
As we noted above, one of the general laws of behavior genetics is
that almost any psychological construct is heritable (Turkheimer,
2000), with most estimates of the heritability of personality traits
hovering around 50% (Krueger & Johnson, in press). Some have
argued that the 50% estimate is conservative and that the true her-
itability is not only higher but high enough to rule out environmental
effects on personality traits (McCrae et al., 2000). Many of the initial
estimates of heritability were based on a model that did not objec-
tively include environmental effects and was therefore misspecified.
In contrast, when measures of environmental influence are explicitly
modeled, estimates of heritability are moderated by the environmen-
tal effects (Krueger, South, Johnson, & Iacono, in press). For ex-
ample, the heritability of negative emotionality decreases and the
effect of shared environment increases at high levels of parental
conflict (Krueger et al., in press).
Recent research has also shown that specific genetic poly-
morphisms interact with life experiences to predict such complex
1532 Roberts & Jackson

psychological phenomena as depression (Caspi et al., 2003; Jacobs

et al., 2006; Kendler, Kuhn, Vittum, Prescott, & Riley, 2005), de-
linquency (Caspi et al., 2002; Foley et al., 2004; Kim-Cohen et al.,
2006) and aggression (Verona, Joiner, Johnson, & Bender, 2006).
These gene-by-environment interactions (G  E) reflect that certain
forms of a gene are more susceptible to the environment than others.
For example, in the Caspi et al. (2003) study, a functional polymor-
phism in the promoter region of the serotonin transporter gene
moderated the influence of stressful life events on depression. In each
of these cases there was no genetic main effect; the association only
came about when taking the environment into consideration. These
studies illustrate that the effect of genes may often not be direct.
Genetic polymorphisms do not determine behavior; rather, different
alleles modulate responses to the environment.
These findings from both animal biology and human psychology
provide clear evidence that DNA sequences are not the simple, un-
changing causal mechanisms depicted in typical biological person-
ality models. Moreover, consistent with a sociogenomic perspective,
the co-action between environment and allelic variation is necessary
for natural selection to occur (Ridley, 2003). As we have seen above,
alleles do not directly code for behavior; rather, alleles affect re-
sponses to the environment. The DNA sequences that get passed on
have evolved to work with specific environments. Thus, survival of
an allele in biological evolution depends on the interplay between
itself and the environment. Furthermore, since personality develop-
ment is an environmentally dependent process, genes are involved in
this process the entire time development occurs, which many have
argued is lifelong (Gottlieb, 2003; Johnston & Edwards, 2002; Rob-
erts & Woods, 2006). The critical point to take from these examples
is that genetic effects, once thought to be a constant influence, are
often dependent on environments to be triggered. Interestingly these
environmental contingencies do not solely occur in childhood and
young adulthood when the brain is still developing. The interplay
between the environment and one’s genome is lifelong. In terms of
Eysenck’s model, it is clear that environments can and do affect
physiological systems, even one as basic as DNA.
If environments are capable of shaping genetic expression, and
triggering dramatic physiological changes, then it would seem rea-
sonable to expect that functional neuroanatomical structures should
also change in response to environmental input. Consistent with this
Sociogenomic Personality Psychology 1533

perspective, there is ample evidence that human hormone levels, ne-

urotransmitter functioning, and brain structures change in response
to environmental intervention. For example, men who get married
or engage in a committed relationship have a significant drop in
testosterone (Mazur & Michalek, 1998; McIntyre et al., 2006). Re-
cent research shows that cognitive behavioral therapy changes blood
flow and functioning in the brain (Felmingham et al., 2007). Finally,
long-term studies of the experience of stress has shown that struc-
tural changes in the brain result from the accumulation of what is
called allostatic load, which is where the usually adaptive stress re-
sponse functions improperly and works against the body (McEwen,
Liston, & Morrison, 2006). Specifically, the prefrontal cortex is re-
modeled under long-term stress, with atrophy in the medial prefron-
tal cortex and the hippocampus and expansion in the orbitofrontal
cortex and basolateral amygdala. Thus, just as is the case for non-
human animals, human physiology can be affected quite significantly
by environmental interventions.
Given the evidence that environments influence genetic expression
across species and that both personality and physiology in humans
change through environmental influence, it is impossible to endorse or
support the original Eysenckian model or similar modern variants of
deterministic biological personality models (e.g., McCrae & Costa,
1999). As a point of reference, we provide a new model that is
associated with a sociogenomic personality position that folds in en-
vironment, biology, traits, and states into one comprehensive model
(see Figure 2). In contrast to Eysenck’s original model, traits are latent
constructs, as is the environment. We have left biological effects
as manifest variables because it is quite possible that some aspects of
biological effects, such as neuoranatomical structure, may not fit a
latent conceptualization. This model was created so as to account for
the multiple pathways through which environmental effects could
shape genetic expression, physiology, and personality traits.
Several aspects of the new model are unique. Unlike Eysenck’s
original model, the proposed model involves reciprocity between
many of the connected variables. For example, the environment
can affect biological factors directly. Accidents can impart serious
biological insults that affect personality, such as in the case of
Phineas Gage, who after having a tamping rod removed from his
brain became more aggressive and hostile than before his injury.
Environments can also affect biological systems indirectly through
1534 Roberts & Jackson

M M M

Biological Environment
factors

M M M

States

Traits

Figure 2
Sociogenomic model of personality.

the way environments make people think, feel, or behave in any

given situation (e.g., states). For example, it is clear that environ-
mental factors can affect state levels of thoughts, feelings, and be-
haviors, and in turn, how someone thinks, feels, and behaves can
affect their biology. On the other hand, some pathways are direct
and unidirectional. Biological factors will not affect the environment
directly but indirectly through the personality trait or state. Viewed
this way, personality serves as the conduit between biology and sig-
nificant life outcomes. Furthermore, the trait can be directly affected
by biological functions—children are born with a wide variety of
temperamental starting values that are then shaped by environmen-
tal experiences. In turn, traits will not affect biological structures
directly but indirectly through the effect of continuous state effects.
For example, as noted in the McEwen et al. (2006) research, con-
tinuous states of anxiety and stress can lead to neuronatomical
changes in brain structures. Stressful states likely interact with genes
responsive to stress, which, in turn, will affect the neuroanatomy
that shapes the habitual ability of the person to respond to future
environmental insults—thus a trait-like phenomenon.
We also incorporate the fact that environments interact with
genes to affect states and traits. For example, individuals with two
copies of the short form of the serotonin transporter gene (5-HTT)
are prone to higher levels of aggression when provoked in an
experimental setting (Verona et al., 2006). We believe that similar
Sociogenomic Personality Psychology 1535

processes played out over long periods of time can account for the
gene-by-environment effects on delinquency and depression that oc-
cur decades apart (Caspi et al., 2002, 2003). That is, the stable de-
pression that emerges from the interaction between significant life
events in adolescence and the 5-HT transporter gene occurs because
of the continuous state experiences (e.g., rumination) that result in
longstanding changes in neurotransmitter levels or neuroanatomical
structures that then cause consistent, global depression.
One of the keys to the sociogenomic-inspired personality model
that differs not only from Eysenck but from many other personality
models is the placement and prominence of the role of states. The
necessity of states being the prime mediator in the model became
apparent when we attempted to answer the question of how envi-
ronments literally get under the skin. As already noted, environ-
ments can cause change through gross physiological insults. On the
other hand, environmental effects typically act on momentary
thoughts, feelings, and behaviors—that is, environments cause
changes in states that then affect changes in traits in a bottom-up
fashion (Roberts, 2006). This bottom-up nature of the socialization
effect of environmental experiences is an important distinction. En-
vironments will not affect personality traits directly unless they in-
volve some dramatic change in physiology. On the other hand, the
slow incremental effects of environmental experience, which appears
to be the most common pattern of development (Roberts, Wood, &
Caspi, in press) can be explained by the mediation of states. Only
through prolonged effects on momentary thoughts, feelings, and
behaviors will neuroanatomical structures or gene expression be
changed enough to change the model level of the system and thus
change the personality trait (e.g., McEwen et al., 2006).
The structure of this new model is highly relevant to the pre-
sumption that if a personality trait is ‘‘biological,’’ ‘‘heritable,’’ or
‘‘genetic,’’ it is immutable and therefore causal. As we saw above,
many psychologists assume, explicitly or implicitly, that if something
is biologically based, it is causal because it cannot be changed. The
assumption that biology reflects the ultimate level of causality is built
on the assumption that biological systems are distal causal factors
that are not affected by any other link, as in Eysenck’s original per-
sonality model. The evidence from animal biology, behavior genet-
ics, and personality development research directly contradicts this
notion. Just because something is rooted in DNA does not mean that
1536 Roberts & Jackson

it is impervious to environmental influences, even after the DNA

sequence is set. Thinking of personality psychology through this
sociogenomic lens leads to a number of questions and insights that
we turn to now.

Unfinished Business in the Move Toward a Sociogenomic

Personality Psychology
If current trends are any indication, personality researchers will ex-
plore the biological foundations of personality in the coming years.
Our hope is that personality psychologists not only move in the di-
rection of biology but actually move all the way over to become
more like some of our colleagues in biological sciences. It is clear
from our limited forays into animal biology that many biologists do
not suffer from naı̈ve assumptions of nature versus nurture (Bala-
ban, 2006; Robinson, 2004). Though many people endorse the per-
spective that it should be nature and nurture, few if any psychologists
can articulate what that means (cf. Johnson, 2007). In contrast, soc-
iogenomic biologists have provided personality psychologists keen
insights through their work detailing how evolution, genes, physio-
logical systems, and the environment work in conjunction with
one another. We believe that a biological model of personality
psychology that adopts a similar approach will avoid meaningless
arguments over nature and nurture. It is not only both but most
interestingly both.
What would a sociogenomic personality psychology look like?
First, a sociogenomic personality psychology would be comparative
from the start. Possibly one of the most important foundations of
sociogenomic biology is the fact that the genome is conserved across
species (Robinson et al., 2005). This means that many of the molec-
ular pathways and genetic polymorphisms associated with human
personality exist in other species and are often involved in analogous
behavioral syndromes (e.g., Winstanley, Dalley, Theobald, & Rob-
bins, 2003). This fact is even more significant given the fact that
many animals exhibit similar personality traits as humans (Gosling,
2001; Gosling & Graybeal, 2007; Sih, Bell, Johnson, & Ziemba,
2004). It also has the potential to skewer ‘‘homocentric’’ perspectives
on personality that arise from solely focusing on humans. For ex-
ample, it is often assumed that ‘‘characterological’’ traits in humans,
such as self-control, are primarily the result of socialization and act
Sociogenomic Personality Psychology 1537

as a control mechanism over more biologically driven emotional

temperaments that are presumed to be in place from birth, such as
neuroticism (Bell, Backstrom, Huntingford, Pottinger, & Winberg,
2007; Carver & Miller, 2006). On the other hand, individual differ-
ences in control mechanisms are identifiable in species that predate
human evolution, such as stickleback fish, and these control systems
are dependent on the environment for their development (Bell et al.,
2007). Moreover, the same physiological system that involves the
serotonin neurotransmitter appears to be involved in control of fish
and human behavior (Carver & Miller, 2006). Therefore, it is a dis-
tinct possibility that humans have a control system that is analogous
to control systems in many other species with whom we share similar
genes that help to structure these systems. Integrating findings
across species, such as these, may provide keen insights into
human personality and human personality development (Gosling,
2001). In this case, it may dispel the myth that character traits
are particular to human development and solely dependent on the
environment.
Our point in invoking the animal examples is to illustrate the
point made by sociogenomic biology that key insights into social
behavior can be gleaned from an examination of multiple species (see
also Mehta & Gosling, 2006). That is to say that humanity, per se,
should not be the sole focus of personality psychology. Rather, the
genome is the target we should be training our attention on. Since
the genome has proven to be a remarkably conserved across species,
when looked upon with a sober eye, it has to be given significant
credit for both the existence of human psychological functioning and
of the behaviors and actions of all of the successful life forms on the
planet. Although it is important to know how the genome affects
humanity, it is also important to keep in mind the immense capac-
ities of the genome as exemplified in other species. Based on this,
studying other species can shed light onto how the human genome
operates. For example, technological limitations prohibit direct ex-
amination of gene expression in the human brain. However, brain
expression can be examined in mice, which share similar genes and
neural systems. By focusing on the genome across species we will
come to a better understanding of the way in which genes in-
teract with environments to cause personality and in turn shape
the development of humans and other animals across their life
course (Howell et al., 2007).
1538 Roberts & Jackson

Of course, a sociogenomic personality psychology would embrace

the current explosion of research on the genetic architecture of per-
sonality. Nonetheless, it would also argue for a different approach
than the robotic pursuit of genetic associations with self-reports,
which have resulted in single genes being associated with a multitude
of diverse phenotypes but with few, if any, strong and replicable
associations (Caspi & Moffitt, 2006; Ebstein, 2006). Rather than
a direct genotype to phenotype account of functioning, a socio-
genomic approach would integrate the environment into personality
genetics and embed research questions in evolutionarily relevant
contexts.
This poses interesting questions. What are the evolutionarily rel-
evant contexts for personality trait development? Moreover, what
are the effects of these environments on genetic expression and
neurophysiology? If environments influence certain epigenetic mech-
anisms, then is it possible to reverse genetic effects or gene-by-
environment interaction effects? What are the important times in
development that certain environments are most potent? At this
stage in our understanding of personality development, we know
almost nothing about the relevant environmental stimuli responsible
for the development of specific personality traits. This is at once ap-
palling and invigorating. It seems an egregious oversight in our un-
derstanding of human nature that we cannot articulate the most
relevant and important environments for personality development
and their timing across the life course. At the same time, this is an
opportunity, both theoretically and empirically, for a new generation
of personality researchers to tackle a key research need.
A sociogenomic perspective would additionally lay out the com-
plex pathway from genes to behavior. What are the genes that are
expressed when someone goes through a traumatic incident, and
how do allelic differences result in interindividual differences in re-
sponses to such an incident? Do these immediately expressed genes
trigger other genes to be expressed causing a biological cocktail of
factors that influence multiple brain areas? What if someone inter-
venes and helps to change that person’s reaction to the traumatic
event? Do the changed cognitions and emotions that result from the
environmental intervention engage other molecular pathways to
counteract these biological processes and possibly change associated
traits? What physiological pathways are influenced by these thoughts
and feelings? These are just some of the questions that must be laid
Sociogenomic Personality Psychology 1539

out in understanding how biological systems relate to manifest be-

havior and personality.
As the lines between biology and psychology blur, it is necessary
to put these complex biological pathways into perspective. As
neuroscience continues to unravel the complexities of our brains,
there still exists the need to concentrate on the phenotypic structure
of personality. A sociogenomic personality psychology would em-
brace a detailed understanding and differentiation of the constructs
we measure. On this front, personality psychology has excelled. No
other field cares more about nor obsesses more over measurement
issues than personality psychology. Nonetheless, confronting bio-
logical systems may necessitate additional work on the measurement
and assessment of personality. Take an example from recent research
on the links between serotonin functioning and both impulse
control and depression (Carver & Miller, 2006). Carver and
colleagues argue that to understand the role of serotonin, one
must differentiate between two modes of self-regulation. Specifi-
cally, they propose that, in the first mode, people have a quick,
associative, emotionally based system organized around approach
and avoidance emotions. The second mode is represented by an
effortful control system that is used either to engage in voluntary
behavior—working out to improve fitness—or inhibit inappropriate
behavior—not hitting the person who makes you angry.
Presumably, this effortful control system is synonymous with
conscientiousness.
Using this system, one can gain a keen understanding of specific
psychological syndromes and constructs. Depression reflects a rela-
tively inactive approach system and inactive effortful control sys-
tem—neither the negative emotions are controlled or the behaviors
and thoughts necessary to shake the negative spirals symptomatic of
depression. Analogously, impulse control conflates high approach
and low effortful control. According to Carver, Johnson, and Joor-
man (2007), the serotonin system facilitates greater effortful control
and thus has pervasive effects on seemingly unrelated psychological
constructs, such as depression, angry hostility, and impulsivity.
From a measurement perspective, we must ask ourselves whether
our current crop of personality measures capture the systems like
those proposed by Carver and others. It is likely that we will make
further strides in personality science if we hone our measures to bet-
ter capture physiological systems currently being identified.
1540 Roberts & Jackson

Fully implementing a sociogenomic personality psychology will

require training of new methods, the learning of new terminology,
and the consilience of vastly different disciplines (Wilson, 1999). This
prospect is both exciting and overwhelming. The field of personality
psychology will undoubtedly become more cross-disciplinary in the
future to aid in these advances. Of course, this does not mean that all
personality psychologists must capitulate and get advanced training
in biology. There are many questions that do not necessitate bridging
levels of analysis. For example, investigating the predictive validity
of personality traits, personality development, or the mechanisms
that explain the effect personality has on behavior remain significant
and important scientific endeavors despite not being intrinsically
connected to biological systems.
In sum, we have discussed issues relevant to the reinvigoration of
biological studies in personality psychology and in doing so have
borrowed and elaborated on a theoretical model from biology. In
our move toward a sociogenomic personality psychology, we see that
DNA is not always at the helm of the causal ship. Environments
interact with genes to produce the biology behind behavior. Given
these findings, we believe that an integration of psychological and
biological concepts that move beyond traditional biological models
like those found in Eysenck’s work will be instrumental to the future
viability of a biological personality psychology.

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