Psych
Theory Into Practice, 52:241–248, 2013
Copyright © The College of Education and Human Ecology, The Ohio State University
ISSN: 0040-5841 print/1543-0421 online
DOI: 10.1080/00405841.2013.829726
Tracy Vaillancourt Shelley Hymel Patricia McDougall
The Biological Underpinnings of Peer Victimization: Understanding Why and How the Effects of Bullying Can Last a Lifetime
Recent research in the areas of neuroscience,
neuroendocrinology, and genetics is reviewed
providing convincing evidence for why and how
the effects of bullying can last a lifetime. Specif-
ically, the research reviewed herein indicates
that (a) the brain experiences peer victimization
Tracy Vaillancourt is full professor and Canada Re-
search Chair at the University of Ottawa; Shel-
ley Hymel is a full professor at the University of
British Columbia; Patricia McDougall is an asso-
ciate professor and vice-provost at the University of
Saskatchewan.
Correspondence should be addressed to Tracy Vail-
lancourt, Professor and Canada Research Chair, Chil-
dren’s Mental Health and Violence Prevention Faculty
of Education and School of Psychology, University
of Ottawa, 145 Jean-Jacques-Lussier, Ottawa, Ontario
KIN 6N5. E-mail: tracy.vaillancourt@uottawa.ca.
in a similar way to physical pain, (b) peer
victimization is robustly linked to dysregulation of
the neuroendocrine response to stress, (c) certain
genetic profiles place bullied children at greater
risk for poorer sequelae, and (d) the experiences
of peer victimization become biologically embed-
ded in the physiology of the developing person,
placing him or her at risk for life-long mental and
physical health problems. These studies highlight
the urgent need to prioritize the reduction of
bullying.
W ITH EACH NEW MEDIA REPORT of a
bullying-related youth suicide comes the
growing appreciation of the need to reduce,
if not eliminate, school bullying. It is clear
241
Emerging Issues in School Bullying Research and Prevention Science
from these media reports, and more importantly
from research, that bullying causes harm. Indeed,
bullying is consistently associated with poorer
physical and mental health as well as poorer
academic achievement, both concurrently (see
Card, Isaacs, & Hodges, 2007, for a review) and
longitudinally (see McDougall & Vaillancourt,
2013, for a review). Despite the growing body of
evidence over the past 3 decades pointing to the
harmful impact of bullying on victims, some still
view peer bullying as a normal part of growing
up and as something that can help kids to toughen
up and build character. In this article, we review
recent research in the areas of neuroscience,
neuroendocrinology, and genetics that provides
compelling evidence for why bullying hurts so
much and why, for many, the hurt persists well
beyond the actual abuse.
Neuroscience
The enduring pain associated with bullying
is well illustrated by a recent (Weldon, 2012)
news story that made headlines around the world.
Robin Tomlin, a married father of two who is
dying of a liver disease, sought to remedy a
longstanding issue that has caused him “pro-
longed grief.” Tomlin was severely bullied in
high school. The level of vitriol directed at him
was made public when school officials allowed
his 1970 high school yearbook picture to be pub-
lished with the authorized typewritten descriptor
“Fag.” In recounting his feelings about the inci-
dent, Tomlin told one reporter that “I feel like,
emotionally, they [his bullies] have been beating
me with a stick for 42 years” (Weldon, 2012).
Tomlin’s description is consistent with re-
search by Chen, Williams, Fitness, and Newton
(2008), who found that “individuals can relive
and re-experience social pain more easily and
more intensely than physical pain” (p. 789).
Social pain is the term used to describe the
feelings of pain that follow the experiences of
peer rejection, ostracism, or loss. Social pain can
also be used to describe the feelings associated
with being bullied (Vaillancourt, Hymel, & Mc-
Dougall, 2010), a humiliating experience that is
not easily, if ever, forgotten. In describing the
social and emotional pain that he continued to
experience long after the bullying had ceased,
Tomlin’s metaphor, “beating me with a stick,”
is consistent with how social pain is described
by people around the world (Eisenberger, 2012).
Comparing social pain to physical pain, however,
is more than a metaphor, as recent neuroscience
research has shown that social pain is, in fact,
experienced in a similar way to physical pain,
at least as far as the brain is concerned. Indeed,
recent studies have shown that social pain and
physical pain rely on similar neurobiological
and neural substrates (see Eisenberger, 2012;
Panksepp, 1998; Vaillancourt et al., 2010, for
reviews) and, as a result, are experienced physi-
ologically in a similar manner.
Neuroendocrinology
Researchers are just beginning to understand
the physiology that underlies peer victimization
and how such experiences get under the skin.
For example, they have long conceptualized peer
victimization as a stressful experience. However,
it is only recently that research has demon-
strated the biological mechanisms that verify
this assumption, although the picture is more
complicated than originally thought. Specifically,
a growing number of studies over the past
decade have converged to demonstrate that peer
victimization is linked to dysregulation of the
hypothalamic-pituitary-adrenal axis (HPA axis),
the body’s stress response system (e.g., Kliewer,
2006; Knack, Jensen-Campbell, & Baum, 2011;
Ouellet-Morin et al., 2011; Rudolph, Troop-
Gordon, & Granger, 2011; Vaillancourt et al.,
2011; Vaillancourt et al., 2008; see Knack &
Vaillancourt, 2012, for review). Simply put, when
exposed to stressful events, the body typically
reacts with the quick secretion of cortisol, the
end product of the HPA axis, which essentially
prepares the body for a flight-or-fight response
(see Lupien et al., 2005; Wolf, 2003, for review).
This rapid release of cortisol is followed by a
steady decline and this curve characterizes an
adaptive response to stress.
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Vaillancourt et al. Biological Underpinnings of Peer Victimization
With regard to peer victimization, several
studies have now shown that bullied children
tend to produce less cortisol than their nonbullied
peers (e.g., Kliewer, 2006; Knack et al., 2011;
Ouellet-Morin et al., 2011; Vaillancourt et al.,
2008). This pattern of hyposecretion has been
noted in relation to exposure to an acute so-
cial stressor (e.g., Knack et al., 2011; Ouellet-
Morin et al., 2011), as well as in relation to
daily average (diurnal) levels of cortisol (e.g.,
Hansen et al., 2006; Kliewer, 2006; Knack et al.,
2011; Vaillancourt et al., 2008). Although this
blunted pattern of cortisol production is opposite
to what is typically observed in response to acute
stress, it is consistent with studies examining
cortisol levels in relation to extreme or prolonged
stress. Indeed, this lowered production of cortisol
in response to on-going stress has been well
documented in research on child maltreatment
(e.g., Bremner & Vermetten, 2001; Shea, Walsh,
MacMillan, & Steiner, 2005). As well, among
adults, holocaust victims (Yehuda et al., 1995)
and repeated rape victims (Resnick, Yehuda,
Pitman, & Foy, 1995) have also been shown
to secrete lower levels of cortisol. What these
survivors have in common is that their exposure
to violence was severe, recurrent, and very likely
associated with terror. Not surprising then, is
the oft-replicated finding that individuals with
posttraumatic stress disorder (PTSD) also tend
to underproduce cortisol. For example, Morris,
Compas, and Garber’s (2012) meta-analytic re-
view of 47 studies showed that the daily output
of cortisol for individuals with PTSD was lower
(d D �.36), compared to nontraumatized con-
trols. PTSD can only be diagnosed if a person
has experienced a traumatic event or events that
“involve actual or threatened death or serious
injury, or a threat to the physical integrity of
oneself or others” (American Psychiatric Asso-
ciation, 2000, p. 463). Moreover, the individual’s
response to this threat must include “intense
fear, helplessness, or horror” (p. 463). Using
data from a nationally representative sample of
Norwegian children, Idsoe, Dyregrov, and Idsoe
(2012) reported that 28% of bullied boys and
40% of bullied girls in grades 8 and 9 scored
in the clinical range for PTSD.
The findings on hypocortisolism in rela-
tion to extreme and prolonged stress are well-
documented and extend to an atypical circadian
cortisol pattern. For example, in a recent meta-
analytical review, Miller, Chen, and Zhou (2007)
showed that, whereas individuals typically show
a pattern of higher morning levels of cortisol
followed by lower afternoon levels of cortisol,
chronic and severe stressors tend to be associ-
ated with the opposite pattern—lower morning
levels of cortisol and higher afternoon levels of
cortisol, a similar pattern that has been observed
in response to physical threats to self. Thus, from
a physiological perspective, peer victimization
represents a relatively extreme and/or persistent
stressor, which ultimately leads to uncharacteris-
tic cortisol levels.
Moving one step closer to understanding the
biological mechanisms underlying responses to
peer victimization, it is important to consider
recent research conducted by Ouellet-Morin and
colleagues (2011). In this study, pairs of identical
twins were assessed at 5 and 10 years of age,
with one twin experiencing peer victimization
at age 10 and the other not. Ouellet-Morin
et al. found that peer victimization had a causal
effect on how the body responded to stress,
with victimized children displaying a blunted
cortisol response to a psychosocial stress test,
consistent with the research previously described.
By examining discordant monozygotic twins, the
effect could not be attributed to variations in
either genetic makeup, family environment, or
other concomitant factors, nor could they be
attributed to the twins’ perceptions of the degree
of stress experienced during the task. Rather, the
blunted cortisol reactivity was causally linked to
the stress of peer victimization.
Genetics
Related research also shows that exposure to
peer victimization influences DNA methylation.
DNA methylation is an epigenetic mechanism
that maintains gene activity or changes gene
expression by activating or silencing the gene,
resulting in the development of phenotypes that
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Emerging Issues in School Bullying Research and Prevention Science
are time-dependent and are not determined by
the DNA sequence at that locus. Epigenetic al-
terations seem to function as a “biological mech-
anism for translating environmental signals into
organismal molecular events” (Bick et al., 2012,
p. 1418). Scientists are particularly interested
in DNA methylation because it is implicated,
among other things, in the emergence of neu-
ropsychiatric disorders (see Tsankova, Renthal,
Kumar, & Nestler, 2007, for review). In a recent
study by Ouellett-Morin and colleagues (2012),
increased DNA methylation of the serotonin
transporter (SERT ) gene between ages 5 and 10
was found for those twins who had been bullied
but not for those who had not been bullied. Chil-
dren with higher SERT DNA methylation also
showed a blunted cortisol response to stress. An-
imal studies clearly support a pathway from early
life stress to changes in DNA methylation (e.g.,
Weaver et al., 2004; see Meaney, 2010, for re-
view), a finding that has also been demonstrated
in children who have experienced early adversity
(see Bick et al., 2012, for review), including child
maltreatment (Beach, Brody, Todorov, Gunter,
& Philibert, 2010; McGowan et al., 2009), and
can now be extended to children who have been
bullied by their peers.
Other evidence supporting the idea that vic-
timization can alter biology comes from re-
search by Shalev et al. (2012) examining another
biomarker of stress—telomere length. Telom-
ere refers to the repetitive nucleotide sequence
(TTAGGG) at the end of chromosomes that pro-
motes “chromosomal stability and also regulates
the cells’ cellular replicative lifespan” (Kiecolt-
Glaser et al., 2011, p. 16). Telomere erosion
has been linked to normal processes such as
aging, but it has also been associated with health
behaviors such as smoking and obesity, as well
as diseases such as cancer, diabetes, and cardio-
vascular problems (Kiecolt-Glaser et al., 2011).
That is, smoking, obesity, and disease, as well
as aging, have all been associated with shorter
telomere length. Importantly, shorter telomere
length has also been linked to psychological
stress (e.g., Epel et al., 2004) and mortality (e.g.,
Kimura et al., 2008; van der Harst et al., 2010;
Willeit et al., 2010). In a recent longitudinal study
of children who were tested at age 5 and 10,
Shalev et al. found that exposure to violence,
including peer victimization, was associated with
significant telomere erosion. That is, children
who were exposed to violence showed greater
reduction of telomere length at age 10 than did
those who were not exposed to violence. This
finding replicates other studies linking exposure
to childhood adversity, including child abuse, to
shortened telomere length (Kiecolt-Glaser et al.,
2011; Tyrka et al., 2010).
Taken together, the emerging studies reviewed
herein show quite clearly that peer victimization
experiences are hurtful and can alter normal bi-
ological functioning. Although the physiological
data show that victimization does get under the
skin, it does not explain why the visible impact
of victimization differs across bullied youth. Why
is it that some victimized children show negative
long-term effects, but others do not?
Gene � Environment Interactions
To date, research addressing heterogeneity
in outcomes associated with peer victimization
have focused on characteristics of the individual
victim or his or her immediate social environ-
ment that serve as moderators and mediators of
risk. For example, Rueger, Malecki, and Dem-
aray’s (2011) research indicates that girls are
more affected by peer victimization in the long-
run than boys. Sugimura and Rudolph (2012)
found that child variables, such as temperament
or gender, moderated the relationship between
peer victimization and aggression and depressive
symptoms. As one example, peer victimization
predicted depression among girls who were high
on negative emotionality. Bonanno and Hymel
(2010) found that suicidal ideation was higher
among victimized youths who perceived their
situation as socially hopeless and those who
perceived themselves to have less social support.
Even though these studies are important in try-
ing to identify factors that can be targeted and
manipulated in helping victimized children to
minimize the negative effects of peer harassment,
they implicitly focus responsibility on the victim
who becomes the agent of change. We contend
that biological processes, many of which are less
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Vaillancourt et al. Biological Underpinnings of Peer Victimization
directly under the control of the individual or
his/her immediate social environment, may also
be implicated and worthy of consideration.
Again, recent research on biological processes
provides some initial insights into the mecha-
nisms that may be operating. Particularly note-
worthy here is research on the polymorphism in
the promoter region of the serotonin transporter
gene (5-HTTLPR). The 5-HTTLPR polymor-
phism affects the rate of gene transcription with
the short allele being less effective than the long
allele (Karg, Burmeister, Shedden, & Sen, 2011).
An allele is an alternative form of the same gene.
Caspi et al. (2003) reported that among severely
maltreated children, those who had a short-short
allele for 5-HTTLPR, were far more likely to be
depressed in adulthood than those with a short-
long or long-long allele. Moreover, those who
had a long-long allele were at no greater risk for
depression than those who were not maltreated in
childhood. A recent meta-analysis (Karg et al.,
2011) documents the accumulated evidence of
the moderating role of the serotonin transporter
gene in the relationship between stress and de-
pression.
Extending this research to peer bullying, Ben-
jet, Thompson, and Gotlib (2010) found that,
among girls who endured relational victimization
by peers, those with a short-short allele were
far more likely to be depressed, as compared
to those with a long-long allele. Similarly, in
a longitudinal study of children from age 5 to
age 12, Sugden et al. (2010) found that children
with the short-short genotype for 5-HTTLPR
were at far greater risk for developing emotional
problems if frequently bullied, an effect that per-
sisted even when controlling for previctimization
emotional problems. These studies demonstrate
that genes matter and interact with environmental
triggers in determining the long-term impact of
peer victimization. As in the case of 5-HTTLPR,
biology can be a protective (long-long allele) or
risk (short-short allele) factor.
Implications
Recognizing the biological implications and
consequences of peer victimization serves to
underscore the urgent need to eliminate bullying
among children and youth. The emerging liter-
ature reviewed herein clearly indicates that the
experience of peer victimization has immediate
and lasting effects on biological functioning, even
to the extent of creating ghosts in the genome
(i.e., changes in methylation) that have impor-
tant implications for future mental and physical
health, as well life longevity (e.g., Kimura et al.,
2008; van der Harst et al., 2010; Willeit et al.,
2010). We offer two final examples in making our
point; the first involving a well-documented link
between peer victimization and poorer academic
achievement (e.g., Nakamoto, & Schwartz, 2010
meta-analysis), and the second connecting peer
victimization to poorer physical health (e.g., Gini
& Pozzoli, 2009 meta-analysis).
Extending research on stress and human mem-
ory, which has demonstrated the deleterious ef-
fects of cortisol on brain structure and function-
ing, Vaillancourt et al. (2011) have shown a simi-
lar relationship with respect to peer victimization.
Specifically, Vaillancourt and colleagues found
direct predictive links from peer victimization
and HPA dyregulation to poorer memory over
the course of 4 months. However, they also
found that peer victimization predicted depres-
sion (6 months later), which in turn predicted
HPA dysregulation (6 months later), and this dys-
regulation of the HPA axis was associated with
future memory impairment (4 months later) in
the areas of the brain that have been shown to be
especially sensitive to the effects of high circulat-
ing glucocorticoids (i.e., cortisol). In particular,
deficits were noted in prefrontal executive func-
tions and medial temporal lobe memory func-
tions. Vaillancourt et al. suggested that perhaps
the academic issues seen among bullied children
are mediated by poorer memory functioning.
As the final example, Knack et al. (2011)
found that peer victimization was associated with
poorer health and a flattened cortisol awakening
response (CAR). This altered atypical CAR was
linked to health issues, suggesting that the re-
lationship between peer victimization and poor
physical health was mediated by differences in
neuroendocrine functioning. This finding is in-
teresting in that the early adversity literature
suggests that the “epigenetic structure of genes
245
Emerging Issues in School Bullying Research and Prevention Science
underlying critical stress response and the im-
mune systems are especially vulnerable to envi-
ronmental signalling” (Bick et al., 2012, p. 1423;
italics added).
In summation, it is clear from the extant lit-
erature that peer victimization is associated with
significant concurrent and longitudinal problems
in the area of physical and mental health, as well
as in the academic domain. What has often been
neglected in this area of research is a more com-
prehensive understanding of why these sequelae
exist. Consistent with Bick et al.’s (2012) thesis
and extended to peer victimization, we suggest
that the experience of being bullied by peers
becomes biologically embedded in the physiol-
ogy of the developing person, which in turn
modifies his or her health and, perhaps, learn-
ing trajectory. The evidence presented herein
dispels any myth that the experience of peer
victimization builds anything remotely positive
or strong within individuals. On the contrary,
the accumulating evidence clearly demonstrates
that peer victimization erodes functioning at all
levels, perhaps most important at the level of
altering individual physiology.
It is not clear (as yet) if the biological
scars brought on by peer victimization can be
reversed—putting people back on to a healthier
trajectory, although there is evidence suggest-
ing hope. For example, two recent longitudinal
studies have demonstrated positive neuroplastic
changes to the amygdala (a brain structure that
plays an important role in detecting stressful
stimuli and initiating a response to cope) among
individuals who participated in a mindfulness-
based stress-reduction intervention (Hölzel et al.,
2010; Hölzel et al., 2011). Within the area
of DNA methylation changes induced by early
adversity, there is also the suggestion that the
effects may be reversed through behavioral or
pharmacological interventions (Szyf & Bick,
2013; Vialou, Feng, Robison, & Nestler, 2013);
granted, at this point in time, the mechanism
remains nascent. The promise of this future work
notwithstanding, we believe that a much simpler
answer would be to fight the root cause directly,
by having researchers and practitioners prioritize
the reduction of bullying.
Acknowledgements
Tracy Vaillancourt is supported by the Canada
Research Chair program and grants from the
Canadian Institutes for Heath Research. Shelley
Hymel is supported by the Edith Lando Profes-
sorship in Social and Emotional Learning and by
a SSRHC Prevention Science Cluster grant.
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