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The Development of Chronic Physical Aggression: A Bio-Psycho-Social Model for the Next Generation of Preventive Interventions

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The Development of Chronic Physical Aggression: A Bio-Psycho-Social Model for the Next Generation of Preventive Interventions

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This review describes a bio-psycho-social approach to understanding and preventing the development of chronic physical aggression. The debate on the developmental origins of aggression has historically opposed genetic and environmental mechanisms. Recent studies have shown that the frequency of physical aggression peaks in early childhood and then decreases until old age. Molecular genetic studies and twin studies have confirmed important genetic influences. However, recent epigenetic studies have highlighted the important role of environments in gene expression and brain development. These studies suggest that interrelated bio-psycho-social channels involved in the development of chronic physical aggression are generally the product of an intergenerational transmission process occurring through assortative mating, genetic inheritance, and the inheritance of physical and social environmental conditions that handicap brain functioning and support the use of physical aggression to solve problems. Given these intergenerational mechanisms and physical aggression onset in infancy, it appears clear that preventive interventions should start early in pregnancy, at the latest. Expected final online publication date for the Annual Review of Psychology Volume 69 is January 4, 2018. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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Annual Review of Psychology
Developmental Origins of
Chronic Physical Aggression:
A Bio-Psycho-Social Model
for the Next Generation of
Preventive Interventions
Richard E. Tremblay,1Frank Vitaro,2
and Sylvana M. C ˆ
ot´
e3,4
1Department of Pediatrics and Department of Psychology, University of Montreal, Montreal
QC H3T 1J4, Canada; email: richard.ernest.tremblay@umontreal.ca
2School of Psychoeducation, University of Montreal, Montreal QC H3T 1J4, Canada;
email: frank.vitaro@umontreal.ca
3Department of Social and Preventive Medicine, University of Montreal, Montreal QC H3T
1J4, Canada; email: sylvana.cote.1@umontreal.ca
4INSERM U1219, University of Bordeaux, 33400 Talence, France
Annu. Rev. Psychol. 2018. 69:383–407
First published as a Review in Advance on October
16, 2017
The Annual Review of Psychology is online at
psych.annualreviews.org
https://doi.org/10.1146/annurev-psych- 010416-
044030
Copyright c
2018 by Annual Reviews.
All rights reserved
Keywords
physical aggression, development, prevention, genetics, epigenetics,
intergenerational
Abstract
This review describes a bio-psycho-social approach to understanding and
preventing the development of chronic physical aggression. The debate on
the developmental origins of aggression has historically opposed genetic and
environmental mechanisms. Recent studies have shown that the frequency
of physical aggression peaks in early childhood and then decreases until old
age. Molecular genetic studies and twin studies have confirmed important
genetic influences. However, recent epigenetic studies have highlighted the
important role of environments in gene expression and brain development.
These studies suggest that interrelated bio-psycho-social channels involved
in the development of chronic physical aggression are generally the prod-
uct of an intergenerational transmission process occurring through assorta-
tive mating, genetic inheritance, and the inheritance of physical and social
383
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ANNUAL
REVIEWS
Further
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environmental conditions that handicap brain functioning and support the use of physical aggres-
sion to solve problems. Given these intergenerational mechanisms and physical aggression onset
in infancy, it appears clear that preventive interventions should start early in pregnancy, at the
latest.
Contents
1. INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384
2.THE LONG-STANDINGNATURENURTUREDEBATE................... 384
3. DEVELOPMENTAL TRAJECTORIES OF PHYSICAL AGGRESSION FROM
EARLYCHILDHOOD TOOLDAGE........................................ 386
4. BIO-PSYCHO-SOCIAL MECHANISMS THAT SUPPORT
CHRONICPHYSICAL AGGRESSION ....................................... 387
4.1. Studies of Sex Differences. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388
4.2. Twin Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389
4.3. Molecular Genetic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 390
4.4.Environmental Effectson GeneExpression(Epigenetics)..................... 390
4.5.Environmental Effectson theBrainandAggressiveBehavior ................. 392
4.6. Intergenerational Transmission: Numerous Interrelated
Bio-Psycho-SocialChannels ................................................. 394
5. CAN CHRONIC PHYSICAL AGGRESSION BE PREVENTED? . . . . . . . . . . . . . . 396
5.1. Prevention Initiated During Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397
5.2. Prevention Initiated During Early Childhood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397
5.3. Prevention Initiated During the Elementary School Period . . . . . . . . . . . . . . . . . . . 398
5.4. Toward Integrated Bio-Psycho-Social Prevention Trials...................... 399
6.CONCLUSIONS .............................................................. 400
1. INTRODUCTION
The study of physical aggression among humans includes a very large spectrum of topics, from
the study of wars between countries to that of biting among toddlers in childcare centers. The
causes and consequences of physical aggression among humans and animals are studied by a wide
variety of specialists, such as anthropologists, biologists, criminologists, ethologists, historians,
psychologists, neurologists, philosophers, psychiatrists, and surgeons.
2. THE LONG-STANDING NATURE–NURTURE DEBATE
The focus of this review is recent research into the developmental origins of chronic physical
aggression by humans. However, to understand recent research questions and answers in a given
research area, it is always useful to keep in mind its long-term history.
As illustrated by the story of Cain and Abel in the Bible, the topic of aggression among humans
is probably as old as humanity, and questions concerning the developmental origins of aggression
were investigated by many philosophers from ancient Greece to modern times. Not surprisingly,
one central issue over the centuries has been the nature–nurture origin of aggression. For example,
Aristotle, in his book Politics, concluded that humans grow from irrational to rational behavior
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because “anger and will and desire are implanted in a child from their very birth, but reason and
understanding develop as they grow older” (Aristotle 1943, p. 405). Some 800 years later, Augustin
of Thagase and Hippo (Saint Augustine) played a major role in developing the idea of original
sin based, in part, on his observations of young children’s aggressive behavior [Augustine 1960
(397–401 AD)]. This line of reasoning was reiterated 1,200 years after Augustine by the British
philosopher Thomas Hobbes. He noted, “Unless you give infants everything they want, they
cry and get angry, they even beat their own parents,” and concluded that aggressive adults were
simply behaving like children [Hobbes 1998 (1647), p. 11]. However, a century later, Jean-Jacques
Rousseau [1979 (1762), p. 5], one of the most influential philosophers of the Enlightenment and
still a reference for many education specialists, strongly stated the nurture hypothesis in the first
phrase of his famous book on the education of children: “God makes all things good; man meddles
with them and they become evil.” He also summarized the research agenda for many developmental
psychologists, sociologists, and criminologists over the past century: “There is no original sin in
the human heart, the how and why of the entrance of every vice can be traced” [Rousseau 1979
(1762), p. 56].
One of the best illustrations of the modern nature–nurture clash concerning the develop-
ment of aggression is found in two books published approximately half a century ago. The first
was On Aggression by the ethologist Konrad Lorenz (1966), originally written in German; the
second was Aggression: A Social Learning Perspective by the psychologist Albert Bandura (1973).
Lorenz’s book was based on his observations of animal behavior and concluded that humans, like
all other animals, inherited an aggressive instinct, which could lead to the destruction of humanity.
Bandura’s book was based on studies of children in a laboratory situation, where they were shown
to spontaneously imitate an adult hitting a Bobo doll. Bandura, 200 years after Rousseau, reached
a similar conclusion: “People are not born with preformed repertories of aggressive behaviors;
they must learn them in one way or another” (Bandura 1973, p. 61). It is probably fair to say that
most psychologists trained during the last 30 years of the twentieth century were convinced that
humans learn to aggress from their environment, and most biologists trained during that period
were convinced that humans, like other animals, instinctively use aggression.
To understand this long-standing philosophical and scientific debate, it is important to note
that the term learn to aggress is used here to mean that, if a child never saw a human physically
aggress another, this child would not be able to aggress even if he needed to do so to defend
himself. The above quotations from Rousseau and Bandura appear to have that meaning. Those
who argue that there is a genetic-instinctual basis to physical aggression generally do not deny that
there are also learning components. It seems obvious that, for aggression, as for other physical
skills that have a strong genetic-instinctual basis (eating, running, jumping, smelling, tasting, etc.),
there is much that an individual must learn to use that skill effectively. This may be the reason
why play fighting is common during the early development of cats, dogs, monkeys, and humans
(Palagi et al. 2016, Parent & Meaney 2008).
At the end of the twentieth century, large-scale longitudinal studies were planned specifically
to investigate the developmental mechanisms by which children learn to aggress from their envi-
ronment. Many of these studies were driven partly by the hypothesis that children were becoming
more aggressive because of violence on television (Eron et al. 1963, Huesmann et al. 1984). A few
studies by psychologists during the 1930s had either observed young children’s physical aggres-
sion (Murphy 1937) or questioned parents on their children’s expression of anger (Goodenough
1931), but no studies had done long-term follow-ups from early childhood to adolescence to try
to address the nature–nurture issue. In fact, to our knowledge, even biologists and psychologists
who studied aggression in mammals, such as rats, mice, and primates, had not done develop-
mental studies to unravel the developmental origins of aggression, probably because it appeared
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obvious to them that aggression is an adaptive mechanism needed for a species to survive, as it
appeared obvious to social psychologists and sociologists that humans learn to aggress from their
environment.
3. DEVELOPMENTAL TRAJECTORIES OF PHYSICAL AGGRESSION
FROM EARLY CHILDHOOD TO OLD AGE
The first prospective longitudinal studies with yearly assessments of physical aggression from
childhood to adolescence reported surprising results from a social learning perspective, especially
regarding the negative influence of television violence on children’s aggression (Eron et al. 1963,
Huesmann et al. 1984). If observing physical aggression on television made children more physi-
cally violent, we would expect that children’s physical aggression would increase with age because
the exposure to violence on television increases with age. However, results from longitudinal
studies in North Carolina (Cairns et al. 1989) and Canada (Nagin & Tremblay 1999) showed,
surprisingly, a substantial decrease in the frequency of instances of physical aggression from school
entry to adolescence. To rule out the hypothesis that one particular group of children were in-
creasing their frequency of aggression with age whereas most others decreased their frequency
of aggression, developmental trajectory analyses of the data were made to identify differences in
developmental trajectories. Results showed that no significant group of children went from a low
frequency of physical aggression during childhood to a high frequency during adolescence. Those
who frequently aggressed in adolescence were those who frequently aggressed during childhood.
These results from a Canadian longitudinal study were replicated with longitudinal studies in
Italy, New Zealand, and the United States (e.g., Broidy et al. 2003, Di Giunta et al. 2010).
The developmental trajectories of physical aggression during elementary school years and
adolescence suggest that, if children learn to aggress from their environment, then this must
happen before school entry. Thus, longitudinal studies of physical aggression were initiated with
birth cohorts. Results from these studies showed (see Figure 1) that physical aggression is often
initiated during the first year of life (e.g., Hay et al. 2014, Naerde et al. 2014, Tremblay et al.
1999), substantially increases in frequency with physical growth up to 3–4 years of age, and then
starts decreasing (Campbell et al. 2006, C ˆ
ot´
e et al. 2006, Dearing et al. 2015, Naerde et al.
2014).
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
17 29 42 54 60
Physical aggression score
Age (months)
Low: 32.5%
Moderate: 50.5%
High: 17%
Figure 1
Developmental trajectories of physical aggression from 17 to 60 months old. Figure adapted with permission
from C ˆ
ot´
e et al. (2007a).
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0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
4.0
4.5
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
4.0
4.5
13 14 15 16 17 13 14 15 16 17
Age (years) Age (years)
High
Moderate
Low
High
Moderate
Low
Mean reactive aggression
Mean proactive aggression
ab
Figure 2
Trajectories of (a) proactive aggression and (b) reactive aggression from 13 to 17 years old.
These longitudinal studies of physical aggression during adolescence and early adulthood
showed that the frequency of instances of physical aggression continues to decline with age for the
majority of children. However, among the most physically aggressive individuals, there is often a
slight increase during mid-adolescence, followed by a decline (Lacourse et al. 2002, van Lier et al.
2009; see Figure 2). Few studies have monitored the development of physical aggression from
adolescence through adulthood with longitudinal studies. The best data comes from court records
of a sample of male juvenile delinquents living in Boston in 1940 (Sampson & Laub 2003). The
results showed a clear decline in arrests for violent crimes from early adulthood to old age. Similar
results were obtained for physical aggression among couples from cross-sectional and short-term
longitudinal studies (Bookwala et al. 2005, O’Leary & Woodin 2005, Suitor et al. 1990, Vickerman
& Margolin 2008).
Thus, research on the development of physical aggression from infancy to old age indicates
that (a) humans start to physically aggress before the end of their first year after birth, and
(b) the frequency of physical aggression reaches a peak during the first 3–4 years after birth and then
decreases until old age. A small group of individuals, mainly males, tend to use physical aggression
more frequently than others throughout life, and they are more likely to increase the frequency of
their physical aggression during mid-adolescence. Thus, from a learning perspective, one of the
most important challenges for a young human is to learn not to physically aggress others.
4. BIO-PSYCHO-SOCIAL MECHANISMS THAT SUPPORT
CHRONIC PHYSICAL AGGRESSION
To identify the mechanisms that support the developmental trajectories of physical aggression
described above, we need studies that go beyond the mere description of these developmental tra-
jectories. The fact that humans start to use physical aggression before they reach their first birthday
suggests that they do not need to observe physical aggression by other humans to initiate physical
aggression themselves. It also suggests that there is, indeed, a strong genetic-instinctual basis to
human use of physical aggression. To understand the extent to which the different developmen-
tal trajectories of physical aggression are determined by genetic and environmental mechanisms,
we need genetically informative research designs. However, to understand the bio-psycho-social
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mechanisms that are triggered by genes and by environments at different periods during devel-
opment, we also need designs that assess the different developmental pathways from conception
to adulthood. These pathways may include neurophysiological as well as psychological and social
processes. As we discuss below, this will require hard work by future generations of scholars.
4.1. Studies of Sex Differences
It has long been common knowledge that human males use physical aggression more often than
human females. Sexual dimorphism is, indeed, one of the most robust findings from studies on
aggression (Daly & Wilson 1990, Quetelet 1833). Men are found to use aggression more than
females when studies focus on direct forms of aggression (e.g., physical or verbal aggression) and
when the target of the aggression is an individual not known to the perpetrator. Conversely,
females are found to use aggression more often than males when studies focus on indirect forms
of aggression (e.g., psychological or social aggression) and when the target of the aggression is an
individual known to the perpetrator (Archer 2000, Archer & C ˆ
ot´
e 2005).
However, the developmental origins of these sex differences in aggression have been studied
only recently with large population samples of children. For example, with a large sample of
Canadian children from 2 to 8 years of age (C ˆ
ot´
e et al. 2007b), significant differences were observed
in the proportions of boys and girls who followed the highest and the lowest developmental
trajectories of physical aggression, based on parent reports (see Figure 3). More boys than girls
(53.6% versus 46.4%) were on the high physical aggression trajectory, whereas more girls than boys
(57.2% versus 42.7%) were on the low physical aggression trajectory. The reverse was observed
for indirect aggression (e.g., when the individual is mad at someone, they get others to dislike that
person): More girls than boys (57.6% versus 42.3%) were on a high indirect aggression trajectory.
With another large population sample and a different statistical approach, Baillargeon et al. (2007)
reported that 5% of 17-month-old boys used physical aggression on a frequent basis compared
to 1% of girls the same age, and the magnitude of the difference was the same one year later.
Finally, in a comparison of six large longitudinal studies from Canada, New Zealand, and the
United States, Broidy et al. (2003) reported similar sex differences based on teacher reports from
school entry to adolescence.
468
4268
Mean physical aggression score
Low: 67.9%
High: 32.01%
0.0
0.5
1.0
1.5
2.0
2.5
3.0
Mean indirect aggression score
0.0
0.5
1.0
1.5
2.0
2.5
3.0
Low: 5%
Moderate-low: 36.3%
Moderate-high: 43.8%
High: 14.5%
Age (years)
ab
Age (years)
Figure 3
Developmental trajectories of (a) physical aggression between 2 and 8 years old and (b) indirect aggression
between 4 and 8 years old. Figure adapted with permission from C ˆ
ot´
e et al. 2007b.
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4.2. Twin Studies
One frequently used and genetically informative type of study involves comparing the frequency
of aggressive behavior within and between pairs of monozygotic (MZ) and dizygotic (DZ) twins
raised together. The basic logic behind these studies is that genetic mechanisms are likely to
play an important role if MZ twins are more similar than DZ twins in their propensity to use
physical aggression because MZ twins share the same genes, whereas DZ twins share only half
of their genes, like non-twin brothers and sisters. Twin studies with elementary school children,
adolescents, and adults have, indeed, shown that there is a relatively strong genetic component
to the use of physical aggression (Brendgen et al. 2005, 2008; Burt 2009; Hicks et al. 2004;
Rhee & Waldman 2002; Tuvblad et al. 2009). Not surprisingly, twin studies also indicate that
genetic effects are probably mediated by brain development. For example, with a sample of twins
in which continuity in proactive aggression (i.e., a type of predatory aggressive behavior) was
shown to be influenced by genetic factors (Tuvblad et al. 2009), associations were found between
the frequency of aggression, fear conditioning deficits (Gao et al. 2015), and a number of brain
morphology characteristics related to the fronto-limbic-striatal circuit, such as cortical thickness
in frontal regions (Yang et al. 2016).
To what extent are these genetic determinants of physical aggression active during early child-
hood? To address this question, a study of twins was initiated at birth and the frequency of physical
aggressions was reported by parents at 20, 36, and 50 months (Dionne et al. 2003). At 20 months,
the heritability of physical aggression was compared to the heritability of language development.
Interestingly, the strength of the genetic influences on individual differences was higher for phys-
ical aggression (58%) than for expressive vocabulary (39%), whereas the strength of the shared
environmental influence was high for expressive vocabulary (51%) but nil (0%) for physical ag-
gression. Further analyses of the data on the development of physical aggression using the same
twin sample indicated important genetic effects that changed over time (Lacourse et al. 2014). The
contribution of genetic factors to the variance in frequency of physical aggression at 20 months
was 60% and decreased to 50% at 50 months, whereas new genetic effects appeared at 36 and
50 months. Two separate sets of uncorrelated genetic factors accounted for the variation in initial
level and growth rate. Results did not indicate any environmental effects (shared or nonshared)
on the initial level of physical aggression (at 20 months) or on its stability and its growth rate
from 20 to 50 months. Thus, during early childhood, when physical aggression is on the rise,
genetic factors explain a substantial part of individual differences in the frequency of aggression
(as seen in Figure 1). The fact that the genes involved appear to change on a yearly basis is not
surprising considering that early childhood is a developmental period with accelerated growth
of key instruments for the use and control of aggression, such as limbs and muscles, as well as
neurological control over cognitive and emotional development.
Similar estimates of genetic effects were obtained from a larger longitudinal study with older
twins (at 3, 7, and 10 years of age) using an assessment of aggressive behavior that was not
limited to physical aggression (Hudziak et al. 2003). The developmental analyses from this study
identified a similar dynamic process where genetic effects at 3 years old interacted with new genetic
contributions at 7 years old. Interestingly, the important contribution of nonshared environmental
factors was specific to a given age.
Although these two twin studies assessed different aspects of aggressive behavior (physical and
nonphysical) by children from 20 months to 12 years old, they both support the hypothesis that
the stability of aggressive behavior is influenced by both genetic and environmental factors from
infancy to early adolescence. The larger study of children between 3 and 12 years of age had
sufficient power to show that genetic effects were larger for boys and shared environmental effects
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were larger for girls. It remains to be tested if this is true specifically for physical aggression, but
developmental analyses of physical aggression during early childhood have shown that girls learn
more quickly than boys to use alternatives to physical aggression and to replace physical aggression
with indirect aggression (Baillargeon et al. 2007, C ˆ
ot´
e et al. 2006, Hay et al. 2011).
4.3. Molecular Genetic Studies
Molecular genetic studies of animals and humans have identified numerous genes involved in
aggressive behavior. For example, a recent comparison of three genetic mouse models (Malki
et al. 2014) identified a network of 14 genes associated with aggression-related behavior. Another
mouse study (Yu et al. 2014) identified periods during development when the brain is particularly
sensitive to the effects of dopamine and serotonin on aggressive behavior. Research in humans has
similarly shown that various genes involved in serotonin and dopamine metabolism, for example,
the monoamine oxidase A (MAOA), dopamine receptor 2 (DRD2), and serotonin transporter (5-HTT
or SLC6A4) genes (Belsky & Pluess 2013, Caspi et al. 2002, Pavlov et al. 2012), are associated
with aggression in both humans and other animals. However, the genes that play a role in the
development of aggressive behavior are not the same at different developmental periods, as the
twin studies summarized above indicated. For example, Pingault et al. (2013a) modeled the age-
dependent contribution of the MAOA gene to the development of physical aggression between
6 and 12 years of age and found that its influence appears to emerge over time. Using the same
sample assessed during late adolescence and early adulthood, Ouellet-Morin et al. (2016) showed
that the genetic moderation of adverse family environment by the MAOA gene, with reference to
aggression and other forms of antisocial behavior, may be active only at certain levels of family
adversity and varies according to the different antisocial outcomes that are being assessed.
Thus, molecular genetic studies with animals and humans have shown that numerous brain-
related genes play an important role in the developmental trajectories of aggression. However,
the genes involved vary with age and interact with the environment in which the individuals live.
4.4. Environmental Effects on Gene Expression (Epigenetics)
The study of environmental impacts on gene expression (epigenetics) and human aggressive be-
havior began only a decade ago. The basic point to remember concerning genetic influences and
epigenetics is that genes can be turned on and off by environmental events through chemical sig-
nals, and genes can have effects only if they are turned on (Szyf 2009). Thousands of studies have
shown that environments can play important roles in the development of behaviors and diseases
by programming gene expression at different points during development. The study that led us
to use epigenetic research to understand the development of chronic physical aggression was a
mouse study where frequency of maternal licking at birth was shown to have a long-term impact
on the offspring’s ability to cope with stress through DNA methylation of the glucocorticoid receptor
gene (Weaver et al. 2004).
It will take a few years before we have data on human behavior development and epigenetics
as good as those provided by the mouse studies (Meaney & Szyf 2005), but numerous studies
have shown that the epigenetic mechanisms observed in the mouse model probably apply to hu-
mans from the prenatal period onwards. For example, a recent study showed associations between
placental methylation and the newborn reactive–poorly regulated profile, a well-known neurobe-
havioral profile (Paquette et al. 2015).
One of the key advantages of epigenetic research is that it provides a tool to study intergenera-
tional transmission of behavior and health problems. The basic hypothesis is that parents’ behavior
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from conception onwards can impact offspring brain development, behavior, and health through
its impact on the offspring’s gene expression programming. This type of gene–environment inter-
play is well illustrated in the study of maternal mouse licking at birth, mentioned above. Parental
behaviors in humans probably have epigenetic impacts on their offspring throughout development,
and these epigenetic effects on brain development are likely to start early on during pregnancy
(Glover 2011). One example of this mechanism is the putative impact of maternal mental health
on offspring development. Numerous studies have shown associations between maternal mental
health and children’s behavior problems (e.g., C ˆ
ot´
e et al. 2007a, Herba et al. 2013). One of the
underlying mechanisms of this link, besides genetic transmission, may be epigenetic impacts of
maternal neuroendocrine functioning and behavior on offspring’s brain development during preg-
nancy. For instance, Braithwaite et al. (2015) showed that maternal depression during pregnancy
is associated with increased DNA methylation of 2-month-old male offspring’s glucocorticoid re-
ceptor gene promotor region, which plays a critical role in the ability to respond to stress. Maternal
depression during pregnancy was also associated with 2-month-old female and male brain-derived
neurotrophic factor gene promotor, which plays an essential role in neurodevelopment.
The long-term epigenetic effects of maternal smoking during pregnancy are another good
example of intergenerational effects of parental behavior on offspring’s development. With a
variety of research designs, researchers have associated smoking during pregnancy with many
behavior problems in offspring, including chronic physical aggression during early childhood
(Dolan et al. 2016, Gaysina et al. 2013, Huijbregts et al. 2008). In a UK longitudinal study of 800
newborn children (Richmond et al. 2015), epigenetic analyses of umbilical cord blood showed an
association between maternal smoking during pregnancy and DNA methylation in seven gene
regions. The duration and intensity of smoking during pregnancy also led to a dose-dependent
response. The children were followed throughout development and blood samples were taken
again at 7 and 17 years of age. The longitudinal analysis revealed that some methylation sites were
persistently perturbed, whereas others showed reversibility. The investigators then focused on
the methylation sites that were perturbed from birth to 17 years of age. Controlling for postnatal
smoke exposure from mothers and fathers, they found that a critical window of exposure during
pregnancy made the major contribution to the long-term perturbed DNA methylation sites.
The first epigenetic study on human chronic physical aggression (Provenc¸al et al. 2013) com-
pared DNA methylation in cytokines and their regulators in T cells and monocytes between
Canadian boys who were on a chronic and a normal physical aggression trajectory from kinder-
garten to adolescence (Nagin & Tremblay 1999). Results provided evidence for an association
between male physical aggression and differential DNA methylation in cytokines and their reg-
ulators in T cells and monocytes. A second study (Provenc¸al et al. 2014), comparing the same
two groups of boys (chronic aggression trajectory versus normal trajectory), used an epigenome-
wide approach and identified 448 distinct gene promoters that were differentially methylated
in the two groups. An identical study with females (Guillemin et al. 2014) showed that, for
both males and females, the methylation of 31 gene promoters was associated with physical
aggression.
Two further studies with the same sample of males focused on the association among chronic
physical aggression, brain functioning, and DNA methylation. The first study (Booij et al. 2010)
used positron emission tomography to compare brain serotonin synthesis in males on a high
physical aggression trajectory with that of males on a low physical aggression trajectory. Results
showed that males on the high-aggression trajectory had lower brain serotonin synthesis in the
orbitofrontal cortex. The second study (Wang et al. 2012) hypothesized that this lower brain
serotonin synthesis was associated with DNA methylation of critical genes in the serotonin pathway
and detectable in peripheral white blood cells. Higher levels of methylation were, indeed, observed
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in T cells and monocytes for the high-aggression group, who also showed lower brain serotonin
synthesis.
Finally, Checknita et al. (2015) examined the association between the serotonergic system’s
MAOA promoter gene methylation and antisocial behavior during adulthood. The males from
Wang et al.’s (2012) study who were on the normal trajectory from childhood to adolescence
were compared to prisoners with an antisocial personality diagnosis. Results showed that MAOA
promoter gene hypermethylation was associated with the antisocial personality disorder diagnosis,
supporting the hypothesis that this hypermethylation is the mechanism that explains why impulsive
aggression and antisocial behavior are associated with serotonergic system dysregulation.
4.5. Environmental Effects on the Brain and Aggressive Behavior
The epigenetic studies described above have shown that the environment can impact the devel-
opment of aggressive behavior through its impact on gene expression, which, in turn, impacts
brain development and eventually behavior. But the impact of the environment on behavior can
be directly mediated by the brain. The clearest studies come from observations of animal behavior
because they enable a more extensive control of the environment and more precise measurements
of brain functioning and behavior. A useful recent example is a rat study that tested the hypoth-
esis that chronic passive exposure to aggressive behavior can lead to aggressive behavior in the
individual exposed. Suzuki & Lucas (2015) randomly exposed 72 rats to aggressive behavior for
either 1 day or 23 days. Results showed that those who were exposed for 23 days had reduced
dopamine density in the bilateral nucleus accumbens shell and increased amygdaloid receptor
densities (serotonin). These effects on brain functioning interacted to lead to high levels of ag-
gression. Thus, being forced to observe physical aggressions for long periods of time has an impact
on brain functioning (dopamine–serotonin interactions) that can lead to high levels of aggression.
However, this does not mean that a newborn rat needs to observe aggression to learn to aggress.
Aggression, like mating, is a goal-directed innate social behavior associated with brain-regulated
emotions and motivations and that can be measured in mice and flies as well as humans (Anderson
2016).
Numerous studies of school-age children have shown that aggression is associated with char-
acteristics of the social environment (e.g., Anderson et al. 2010, Huesmann et al. 2017). In a large
population sample study of the earliest social environment, the family, results showed that the
best predictors of a high physical aggression trajectory between 17 and 42 months old were the
following: young siblings, mothers with high levels of antisocial behavior before the end of high
school, mothers who started having children at an early age, mothers who smoked during preg-
nancy, mothers with coercive parenting behavior, families with low income, and dysfunctional
families (Tremblay et al. 2004).
However, few social environmental studies of aggression control for genetic effects on phys-
ical aggression or on social environmental variables that are correlated with physical aggression.
Studies of genetically identical (MZ) twins are one of the best research designs to control for
genetic effects while testing for environmental effects in human children. With a longitudinal
study of 223 MZ twin pairs in Canada, Vitaro et al. (2011) examined whether having an aggressive
friend increases one’s aggression. This was done by testing if the difference in aggression between
members of an MZ twin pair increased from kindergarten to first grade when one member of a
pair had the more highly aggressive friend in kindergarten than the other. Results for both boys
and girls showed that within-pair differences in friends’ aggression among pairs of MZ twins in
kindergarten significantly predicted increased within-pair differences in aggression the following
year (first grade). These results clearly show that children’s use of aggression can be influenced
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through their close friendships even when we control for genetic effects. However, in a follow-
up study that used the same sample of MZ twins and a similar control for genetic influences,
Vitaro et al. (2016) found no effect of friends’ aggression from middle childhood to early ado-
lescence, possibly because older children, as compared to younger children, increasingly select
their social environment in tune with their genetic dispositions (through a process known as a
gene–environment correlation).
The same investigators also found that, although social experiences (such as friends’ aggression)
do not always predict changes in children’s behavior, they may nevertheless operate to trigger the
genetic liability for aggression. First, in two separate studies, they found that the genetic com-
ponent associated with physical aggression was stronger when children had aggressive friends
than when they had nonaggressive friends (Brendgen et al. 2008, van Lier et al. 2007). They also
found that genetic influences were moderated by social experiences at the group level, such as
classroom norms toward aggression. As expected, results confirmed that genetic factors did influ-
ence children’s aggressive behavior, but that the genetic effects on aggression were attenuated or
exacerbated depending on whether classroom norms were unfavorable or favorable to aggression,
respectively, thus confirming that peer group norms impact genetic effects (Brendgen et al. 2013,
Vitaro et al. 2015).
These peer group effects on the development of children’s aggressive or antisocial behavior
have been hotly debated as childcare has become a norm in Western societies (e.g., Belsky &
Steinberg 1978). Data from a US longitudinal study specifically designed to investigate the effects
of childcare did show that children who attended childcare for long periods of time were more
likely to be disruptive during their elementary school years (Belsky et al. 2007). However, other
longitudinal studies that also followed large random samples of children until the end of elementary
school did not find these negative impacts (e.g., Zachrisson et al. 2013). Indeed, one population-
based longitudinal study in Canada found that early initiation of childcare for children of mothers
with low education helped these children learn not to physically aggress between 17 and 60 months
(C ˆ
ot´
e et al. 2007a). Another study with the same sample compared the development of physical
aggression, opposition, shyness, and social withdrawal between 6 and 12 years of age for children
who went to childcare and those who did not (home care). Figure 4 shows that, during their
kindergarten year (age 6 years), the children who had not been in childcare were rated by teachers
as less physically aggressive and less oppositional than those who had been in childcare. However,
the difference between the two groups for both physical aggression and opposition disappeared
by the second year in school (age 7 years). It is important to note that the reverse phenomenon
was observed for teacher ratings of shyness and withdrawal. These results highlight the fact that,
throughout development, humans adapt their social behavior to social group norms, but that this
process takes time.
As with the twin studies discussed above, this does not mean that the social behavior of the
children is totally explained by the group norms. The genetic and environmental effects can be
observed when the research design is appropriate. An interesting example of this is a molecular
genetic study (Belsky & Pluess 2013) using the same data as the US childcare study by Belsky
et al. (2007). Results showed that the dopamine receptor D4 (DRD4) gene moderated the effect of
childcare quality on teacher-reported social skills (e.g., “makes friends easily,” “controls temper
when arguing with other children,” “asks permission before using someone else’s property”), but
only in kindergarten and first grade. Interestingly, this time period is exactly the same school entry
period in which significant differences in social behavior were observed between children with and
without childcare experience in the Canadian study described in Figure 3 (Pingault et al. 2015).
These results highlight the fact that longitudinal studies need to differentiate transition periods
from stable social environment periods.
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10 126810 1268
10 126810 12
68
Teachers’ ratings
Teachers’ ratings
Teachers’ ratings
Teachers’ ratings
0
1
2
3
0
1
2
3
0
1
2
3
0
0.5
Childcare use
Parental care
1.0
1.5
2.0
Age (years)
Age (years)
a Shyness
b Social withdrawal
c Opposition
d Aggression
Age (years)
Age (years)
Figure 4
Developmental trajectories of behavior problems from 6 to 12 years old according to early childcare use.
(a) Shyness. (b) Social withdrawal. (c) Opposition. (d) Aggression. Figure adapted with permission from
Pingault et al. (2015).
Finally, it is important to briefly mention a completely different and very recent line of research
on the interplay between the environment and the brain that has been labeled the gut-brain
hypotheses. The human gut microbiome is a bacterial environment shown to have important
impacts on the brain and on behavior. It has been linked to physical health problems but also
to anxiety, depression, alcoholism, and aggression. Recent studies with animals have shown that
the gut microbiome is important from the prenatal period to adulthood and that changing the
bacterial environment of the gut can have significant and sex-specific impacts on social behavior,
including aggression (e.g., Bailey & Coe 1999, Robertson et al. 2017, Sylvia et al. 2017).
4.6. Intergenerational Transmission: Numerous Interrelated
Bio-Psycho-Social Channels
Intergenerational research on antisocial behavior, especially on the bio-psycho-social mechanisms
involved, has been relatively limited. Longitudinal studies have shown that children of parents who
were convicted of criminal behavior are more at risk of being themselves convicted of criminal
behavior during adolescence and adulthood (see Farrington et al. 2017, Theobald et al. 2016).
Adoption studies have also shown that children of parents with a criminal history are less at risk
of criminal behavior when adopted by parents without a criminal record (Mednick et al. 1984). A
Canadian longitudinal study on the early development of chronic physical aggression highlighted
the fact that this association between the antisocial behavior of parents and that of children starts
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very early in life (Tremblay et al. 2004). The study showed that maternal reports of antisocial
behavior during their own adolescence predicted the chronic physical aggression of their child
between 17 and 42 months old. This study further showed that the mothers of children who
became chronically aggressive were, at the child’s birth, more likely to be among the youngest and
poorest, to be separated from the father, to have not completed high school, to have smoked during
pregnancy, and to have had postpartum depression. This network of associations illustrates well
the fact that the intergenerational transmission of behavior problems occurs through numerous
interrelated bio-psycho-social channels. The child inherits a mix of their parent’s genes, and
their mother’s smoking, stress, poverty, and depression during pregnancy impact the fetus’ brain
development through epigenetic mechanisms. From the postnatal period onwards, the physical
and social environments created by a poor, young, depressed woman with low education, behavior
problems, and coercive parenting in a dysfunctional family clearly fail to provide the care and
education needed by the brain of a young child to learn to control their emotions and behavior.
On the contrary, they may exacerbate further the expression of the child’s genetic liability and
contribute further epigenetic effects of their own.
However, the problems do not start with conception. We often forget that assortative mating
(mating with someone who has similar characteristics) is one of the initial mechanisms that lead
to the numerous interrelated bio-psycho-social channels that impact human development from
pregnancy onwards. In a recent large (N =707,263) population study in Sweden, Nordsletten
et al. (2016) showed that there was more assortative mating for mental illnesses than for physical
illnesses. The odds that a male with a psychiatric diagnosis had a mate with a psychiatric diagnosis
was OR 2.24 (CI,2.21–2.27; P <0.001), and the odds that a female with a psychiatric diagnosis
had a mate with a diagnosis was OR 2.11(CI,2.08–2.14; P <0.001). The correlation among
mates in terms of diagnosis was 0.45 for attention deficit/hyperactivity disorder, which is strongly
associated with chronic physical aggression from early childhood onwards (Carbonneau et al.
2016, Pingault et al. 2013b). It is important to emphasize that assortative mating brings together,
for the reproduction of the next generation, mates that have similar histories, not only for physical
and mental health problems but also for education, ability to self-control, and values on numerous
crucial issues for children’s development, such as nutrition, discipline, lifestyle, and respect for
others (Domingue et al. 2014, Frisell et al. 2012, Grant et al. 2007, Kandler et al. 2012, Keller
et al. 2013, Tognetti et al. 2014, Zietsch et al. 2011).
Figure 5 illustrates the complex network of interrelated genetic, epigenetic, neuropsycholog-
ical, and social factors that are involved in the transmission of chronic physical aggression from
one generation to another. This perspective is in line with the suggestion by the Nobel Prize
winner and ethologist Nikolaas Tinbergen (1963) that behavior needs to be explained from four
perspectives: the historical and survival value of the behavior in past generations as well as the
development of the behavior within an individual’s life and the proximal causal factors.
From the left to the right of Figure 5, we follow the intergenerational process with two lines
of ancestors transmitting their genetic, economic, educational, cultural, health, and lifestyle char-
acteristics to a male and a female who become parents of a child. The developmental changes
in this child’s DNA expression, brain, and behavior are shown to be determined by their inter-
generational inheritance but also by the environments in which they will grow and interact. The
uniqueness of this individual is largely determined by the genetic, economic, educational, cultural,
health, and lifestyle characteristics they received from their ancestors through their parents but
also by the unique environment in which they grow up.
To understand this complex process, it is useful to consider the developmental differences
between MZ twins, DZ twins, and singleton siblings living with their parents or adopted by
unrelated adults (e.g., Kendler et al. 2015, McAdams et al. 2015). Members of twin pairs, whether
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Female
Utero
3 Y 6 Y
BRA BRAIN BRAIN
BEH BEHAVI BEHAVIOR
ENVIRONMENT
ENVIRONMENT
ENVIRONMENT
ENVIRONMENT
1 Y
BRAI
BEHA
Siblings
Male
Prenatal Prenatal
Conception
AncestorsAncestors
Genes
Genes
DNA
expression
DNA
expression
DNA
expression
DNA
expression
Childcare peers
and friends
Classroom peers
and friends
Figure 5
Network of interrelated intergenerational, genetic, epigenetic, neuropsychological, and social factors involved in the development of
chronic physical aggression.
MZ or DZ, have the same ancestors and parents. When we consider DZ twins, we see that, with
time, they become as different as ordinary siblings, but, because they share half of their genes,
they become much more similar than adopted children living with the same parents. When we
consider MZ twins, we see that, with time, they become much more similar than DZ twins and
normal singleton siblings because they share the same genes. These comparisons highlight the
power of genes. However, there is a limit to the power of genes, as can be seen from the fact that
differences between MZ twins will increase with time because of the power of the environment,
which impacts not only how they perceive the world and behave but also when their genes are
expressed and, thus, how their brain functions and how they behave.
5. CAN CHRONIC PHYSICAL AGGRESSION BE PREVENTED?
Although understanding the development of physical aggression is, by itself, interesting, the aim
of these studies is usually to provide information that will help prevent the development of chronic
physical aggression problems and possibly reduce physical aggressions among humans. The nu-
merous mechanisms involved in the development of chronic physical aggression described above
suggest that we need to target many risk and protective factors. These include parents’ behavior
problems, family functioning, peer interactions, childcare, and school environments, as well as
biological mechanisms related to brain functioning. However, one of the main findings of these
studies is that humans start to use physical aggression during early childhood, and the children
who are on a high physical aggression trajectory at that time are more likely to maintain higher
frequencies of physical aggression into adulthood. This, of course, suggests that early childhood
interventions are more likely to prevent chronic aggression problems than later interventions.
This is clearly not a new idea. Erasmus [1529 (1985), p. 321] summarized it well in his essay on
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education: “We should be especially careful with our children during their first years. For at this
stage their behavior is guided by instinct more than by reason, so that they are inclined equally to
good and evil—more to the latter perhaps—and it is always easier to forget good habits than to
unlearn bad ones.” However, the idea that physical aggression and other antisocial behaviors are
learned from the environment mainly during adolescence led both the Surgeon General of the
United States (Surg. Gen. US 2001) and the World Health Organization (WHO 2002, p. 31) to
conclude that violent behavior starts during adolescence and that these violent adolescents neither
were highly aggressive during childhood nor had behavior problems during early childhood. The
result of these beliefs is that most experiments to prevent aggressive or antisocial behaviors target
preadolescents and adolescents. In this section, we focus on the few studies that have targeted
young children, starting with interventions during pregnancy.
5.1. Prevention Initiated During Pregnancy
The best known experimental intervention targeting pregnant women at high risk of having chil-
dren with chronic antisocial behavior is the Elmira project in the United States (Eckenrode et al.
2010, Olds et al. 1986). The pregnant women were young, unmarried, and poor. Nurses visited
the women once a month between the twenty-fourth week of pregnancy and the child’s second
birthday, giving support to the mothers in three areas of their life: (a) personal development,
including education, workforce integration, and family planning; (b) health-related behavior, in-
cluding smoking prevention and adequate nutrition for the mother and child; and (c) competent
care of the child and maternal sensitivity. The nurses also helped link mother and child with
community services. Results showed that the intervention reduced child abuse and neglect and
maternal delinquency (Olds et al. 1986, 2007) and showed, at the 19-year follow-up, a significant
reduction of arrests for the female offspring (Eckenrode et al. 2010). The latter finding is an espe-
cially important and encouraging result because female offspring will become the mothers of the
next generation.
A more recent pregnancy experiment was carried out in a poor neighborhood of Dublin,
Ireland (Doyle & PFL Eval. Team 2016). The study randomly allocated 230 pregnant women to
a high- and a low-support program. The high-support program included home visits up to school
entry at 4 or 5 years of age and a parenting support program. Results after 5 years showed signif-
icant differences between the two groups of children in numerous developmental outcomes, such
as overall cognitive development, language development, attention, hyperactivity, motor skills,
social competence, autonomy, and amount of hospital services used from birth to school entry.
Surprisingly, however, there were no significant impacts on children’s aggression, oppositional
defiance, anxiety, and prosocial and respectful behavior, as assessed by teachers. One would expect
that, if the wide-ranging positive impacts are maintained in the long run, they will reduce the
likelihood of aggressive antisocial behavior by favoring social acceptance from normative peers
and improved academic performance.
5.2. Prevention Initiated During Early Childhood
Children’s cognitive abilities and parents’ disciplinary skills have been the focus of most prevention
programs during the preschool period. Head Start programs for socially disadvantaged children
aged 3–5 years in the United States were shown to improve academic success in the short term and
to prevent arrests and court referrals in the long term (Garces et al. 2002). The best known of these
programs is the High-Scope Perry Preschool project, which targeted African American children
age 3–4 years with parents with a low IQ. The 2-year program included a daily preschool program
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aimed at increasing cognitive abilities and weekly home visits. Several long-term assessments up
to age 40 showed that children who participated in the program were more likely to be employed,
more likely to earn higher annual incomes, more likely to have graduated from high school, and
less likely to have been arrested compared to the children who were part of the control group
(Schweinhart et al. 1993). A study of the mechanisms that could explain these important long-
term results concluded that the preschool program had impacts on the social skills of the children
rather than on the targeted cognitive skills (Heckman et al. 2013).
Several parent training programs have been tested for preschool-aged children (e.g., Patterson
1982, Sanders et al. 2000). One of these programs for parents of preschoolers with behavior
problems included components that also targeted the child and the teacher. A randomized control
trial of its impact was made with a sample of 159 4- to 7-year-old children with oppositional
defiant disorder (Webster-Stratton et al. 2001). The children were assigned to one of the following
conditions: the parent program only; the child program only; the parent and teacher programs; the
child and teacher programs; and the child, parent, and teacher programs. The five conditions were
compared to a waiting-list control condition. At the end of a 6-month intervention period, children
in the three conditions with the child program showed more prosocial skills with peers than the
children in the control condition. No difference between treatment and control was observed for
children in the two conditions without the child program. Similarly, parents in the three parent
program conditions manifested less negative and more positive parenting and reported fewer
child behavior problems than parents in the control condition and parents in the two conditions
without parent training. Finally, children’s behavior problems at school were reduced for those
whose teacher participated in the teacher program relative to the control children. Overall, the
conditions that included all three programs produced the best results after 6 months. At a 2-year
follow-up, teachers reported an equal proportion of children with behavior problems across all
five treatment conditions (i.e., around 50%). However, parents in the condition that included both
the parent and teacher programs reported fewer cases of behaviorally disordered children relative
to only one other condition, the parent-program-only condition, suggesting that more than one
component may be necessary to achieve optimal results (see also Gardner et al. 2006). In an 8- to
12-year follow-up study of the children in the parent training condition, Webster-Stratton and her
colleagues (2011) found that the majority maintained their postintervention progress, although
one out of four reported major delinquent acts or had contact with the justice system.
5.3. Prevention Initiated During the Elementary School Period
Multitarget, multicomponent programs for preventing conduct problems in at-risk children have
also been assessed during the elementary school years. For example, the Fast Track program
(Conduct Probl. Prev. Res. Group 1992, 2004) had six components: (a) group parent training;
(b) home visits; (c) group-based social skills training with the children; (d) peer-pairing, in which
a target child and a no-risk peer participated in guided play sessions; (e) academic tutoring; and
(f) teacher support. The program was implemented in four sites in the United States and targeted
a large sample of children age 7 who scored above the ninetieth percentile on the aggressive–
disruptive scale of the Child Behavior Checklist. The program was initially set to last until the
end of elementary school but was eventually extended to tenth grade. After the first three years,
the evaluation results were, at best, moderate, with effect sizes varying between 0.2 and 0.5 on
teacher ratings of disruptive behavior. After five years (by age 11 or fifth grade), 37% of the
randomly assigned Fast Track children had no conduct problem dysfunction, compared to 27%
of control children (Conduct Probl. Prev. Res. Group 2002). Evaluations in late adolescence
showed that the children in the prevention group were significantly better off with respect to
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important outcomes, such as Diagnostic and Statistical Manual of Mental Disorders diagnoses for
conduct disorder, criminal offenses, and interpersonal violence, compared to their counterparts in
the control group, although the effect sizes remained moderate (Conduct Probl. Prev. Res. Group
2010). Finally, by age 25, 69% of the participants in the control group manifested at least one
externalized, internalized, or substance-related problem, compared to 59% in the experimental
group. Interestingly and importantly, mediation analyses showed that about one third of Fast
Track’s impact on later crime outcomes was accounted for by improvements in social and self-
regulation skills during childhood (ages 6–11), such as prosocial behavior, emotion regulation,
and problem solving (Sorensen et al. 2016).
A less intensive and shorter program was tested experimentally in Canada at approximately
the same time and targeted kindergarten boys from schools in low socioeconomic areas who
were among the most aggressive and hyperactive. The 2-year program (between 7 and 9 years
of age) included a home-based parent training component and a school-based social-cognitive
skills training component. Notably, the social-cognitive component was delivered at school in a
small-group format that included one or two target boys and three or four prosocial peers. In
comparison to the control group, boys who participated in the intervention were found to have
less self-reported delinquency and substance use throughout adolescence (Castellanos-Ryan et al.
2013, Lacourse et al. 2002, Tremblay et al. 1995, Vitaro et al. 2001) and to have fewer criminal
records by 24 years of age (Boisjoli et al. 2007). In addition, the intervention reduced property
crime by age 28 but did not seem to impact violent crimes (Vitaro et al. 2013).
The experimental preventive interventions reviewed above show important short-, medium-,
and long-term effects. But we must admit that we are far from having the impact we would like to
have on the lives of these unfortunate children and parents that suffer from their behavior problems
and create much suffering around them. How can we push forward to better understand the onset
of these behavior problems and the means to change the life-course of these unfortunate people?
Long-term interventions that aim for long-term impacts will, of course, always appear to lag
behind the advancement of knowledge when they are eventually published. For example, the
preventive interventions described above did not include genetic, epigenetic, or brain imaging
assessments because they were all initiated before the advancement of knowledge in these areas.
We clearly need a new generation of preventive experiments that will make use of the recent
knowledge on chronic aggression development to plan the interventions and to assess the long-
term impacts. For example, to have significant long-term impacts, we will most likely need to tailor
interventions with babies to their genetic, epigenetic, and neuroendocrine profiles, in the same
way we tried to tailor the past interventions to the differences in behavior profiles and profiles of
the family needs. We may also need to adopt a developmentally sensitive approach that includes
the notion of stepwise continuous prevention for the extreme cases of individuals who do not
revert to normative behavior during a given developmental period (Vitaro & Tremblay 2016).
The next section gives examples of prevention experiments that would help achieve these aims.
5.4. Toward Integrated Bio-Psycho-Social Prevention Trials
We suggest that the intergenerational nature of physical and mental health problems highlighted
above (Figure 5) is key in planning future prevention experiments and that this should lead to pre-
vention experiments that start during early pregnancy at the latest. Parents who have had behavior
problems carry with them pervasive high-risk environmental conditions (e.g., low education, low
income, poor neighborhoods, and risky lifestyle choices such as use of tobacco, alcohol and drugs
and unhealthy nutrition), which impact childhood and adulthood psychopathology through many
interrelated channels, including impacts on the children’s DNA methylation. Interventions that
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do not start close to conception could not impact the many causal pathways that are already present
during fetal life. Bovet (1951) already suggested using this intergenerational perspective in the first
World Health Organization report, which happened to be on juvenile delinquency. Epigenetic
research has now provided access to one of the important mechanisms by which the intergenera-
tional problems are transmitted. If brain development is compromised through epigenetic effects
during pregnancy, and if the child’s parents also lack self-control, then it is easy to understand
that the child will lack the cognitive and environmental support needed to develop the self-control
that is essential to learning effective alternatives to physical aggression.
From this perspective, mothers are likely to have the greatest impact on early gene expression
because their lifestyle during pregnancy has direct biological impacts on the child’s development.
Epigenetic effects during pregnancy suggest that we need to fundamentally revisit our thinking
concerning early prevention of chronic physical aggression because, although male children are
much more severely affected, pregnant women need to be our prime target to prevent a new gener-
ation of males and females with chronic physical aggression and similar intergenerational physical
and mental health problems. This epigenetic perspective suggests that successful prevention of
many physical and mental health problems may be easier to achieve by ameliorating the pre- and
early postnatal environment, rather than by chasing bad genes (Bernet et al. 2007, Gluckman et al.
2008) or trying to change individuals’ environments once they clearly have physical or mental
health problems. Finally, we emphasize the fact that mothers, fathers, and children should not be
blamed for the genes and the environment they inherit at conception and onwards. These families
need to receive intensive and long-lasting support to break the intergenerational cycle of chronic
behavior problems.
Intergenerational prevention trials should be initiated by enrolling in longitudinal and experi-
mental studies large samples of young primiparous pregnant women with low levels of education.
Intensive preventive interventions should be randomly allocated, especially to pregnant women
with a history of antisocial behavior problems and their spouses, specifically targeting their lifestyle
during pregnancy (i.e., smoking, drinking, drugs, spousal abuse) and their parental care and family
life from birth onwards. Judging by the results of past experiments with these families (Boisjoli
et al. 2007, Conduct Probl. Prev. Res. Group, 2005, Doyle & PFL Eval. Team 2016, Eckenrode
et al. 2010), it is likely that supportive interventions maintained until the children are young adults
will have the strongest impacts. Data collection would include genetic and repeated epigenetic in-
formation on parents and children and parenting behavior, as well as brain imaging and cognitive,
health, and behavior development of the children. Longitudinal and experimental studies such as
these will assess the short- and long-term impacts of the preventive interventions, but they will
also advance knowledge on the causal mechanisms involved in the development of problem behav-
iors. The identification of these mechanisms will, in turn, help researchers design the following
generation of interventions.
We believe that we will substantially advance our understanding of the mechanisms that lead to
chronic physical aggression if, in these longitudinal and experimental studies, we regularly monitor
the changes in epigenetic profiles, brain structure, brain functioning, cognition, and language, as
well as changes in social-emotional behavior from birth onwards. This monitoring should, of
course, include the changes in the children’s environmental factors, such as parenting practices,
family functioning, peer relationships, and social environments.
6. CONCLUSIONS
The aim of this review was to describe a bio-psycho-social approach to understanding and pre-
venting the development of chronic physical aggression. We first highlighted the fact that, from a
400 Tremblay ·Vitaro ·Cˆ
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long-term historical perspective, the debate on the developmental origins of aggression opposed
those who supported a genetic mechanism (nature) to those who supported an environmental
mechanism (nurture). We then presented recent longitudinal studies that show that human phys-
ical aggression starts at the end of the first year of life, reaches a peak in frequency before entry
into kindergarten, and then decreases in frequency until old age. The appearance of physical ag-
gression during the first year of life suggests that a human’s very first acts of physical aggression
are spontaneous reactions to anger (nature), rather than imitations of physical aggression in their
environment (nurture). The very high frequency of physical aggression during early childhood
and its decline throughout life also indicate that there are important brain maturation processes
that are involved in the development of the ability to control physical aggression and that the
environment plays an important role in learning alternatives to the use of physical aggression
to solve problems. Molecular genetic studies with animals and humans, as well as twin studies,
have confirmed important genetic influences on the use of physical aggression. However, more
recently, epigenetic studies have highlighted the important role environments play, from concep-
tion onwards, in the expression of genes that impact brain development and behavior. From the
present state of knowledge, we can conclude that the development of chronic physical aggres-
sion is generally influenced by genetic and environmental factors through numerous interrelated
bio-psycho-social channels from conception onwards. The general mechanism that can be hy-
pothesized from the recent bio-psycho-social studies is that the interrelated bio-psycho-social
factors involved in the development of chronic physical aggression are generally the product of
an intergenerational transmission process through assortative mating, genetic inheritance, and
inheritance of physical and social environmental conditions that handicap brain development and
support the tendency to use physical aggression as a means of solving problems.
Given these intergenerational mechanisms and the onset of physical aggression in infancy, it
appears clear that preventive interventions should start early in pregnancy at the latest and continue
throughout childhood and adolescence. In many cases, it may take more than one generation to
break the intergenerational transmission. To our knowledge, no experimental preventive interven-
tion with pregnant women has, to this day, specifically targeted risk for chronic physical aggression.
We suggest that the life-long beneficial impacts of preventive interventions with families of
children at high risk of chronic physical aggression will be obtained only if intensive interventions
are initiated early in pregnancy and maintained throughout the children’s development. Based
on results from previous studies (Eckenrode et al. 2010) and the key role of maternal health and
lifestyle in brain development during fetal life and early childhood, we hypothesize that the effects
of these very early preventive interventions will be greater for girls and that these effects will have
a still greater impact on the next generation of boys and girls.
DISCLOSURE STATEMENT
The authors are not aware of any affiliations, memberships, funding, or financial holdings that
might be perceived as affecting the objectivity of this review.
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Volume 69, 2018
Contents
The Properties and Antecedents of Hedonic Decline
Jeff Galak and Joseph P. Redden pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp1
How We Hear: The Perception and Neural Coding of Sound
Andrew J. Oxenham pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp27
The Psychology of Music: Rhythm and Movement
Daniel J. Levitin, Jessica A. Grahn, and Justin London pppppppppppppppppppppppppppppppppppp51
Multistable Perception and the Role of Frontoparietal Cortex
in Perceptual Inference
Jan Brascamp, Philipp Sterzer, Randolph Blake, and Tomas Knapen pppppppppppppppppppppp77
Ensemble Perception
David Whitney and Allison Yamanashi Leib pppppppppppppppppppppppppppppppppppppppppppppp105
Neuro-, Cardio-, and Immunoplasticity: Effects of Early Adversity
Eric Pakulak, Courtney Stevens, and Helen Neville pppppppppppppppppppppppppppppppppppppp131
Prefrontal Cortex and Neurological Impairments of Active Thought
Tim Shallice and Lisa Cipolotti ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp157
Infant Statistical Learning
Jenny R. Saffran and Natasha Z. Kirkham ppppppppppppppppppppppppppppppppppppppppppppppp181
How Children Solve the Two Challenges of Cooperation
Felix Warneken ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp205
Linking Language and Cognition in Infancy
Danielle R. Perszyk and Sandra R. Waxman ppppppppppppppppppppppppppppppppppppppppppppp231
Cognitive Foundations of Learning from Testimony
Paul L. Harris, Melissa A. Koenig, Kathleen H. Corriveau, and Vikram K. Jaswal ppp251
Gender Stereotypes
Naomi Ellemers pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp275
Attitudes and Attitude Change
Dolores Albarracin and Sharon Shavitt pppppppppppppppppppppppppppppppppppppppppppppppppppp299
vi
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Persuasion, Influence, and Value: Perspectives from Communication
and Social Neuroscience
Emily Falk and Christin Scholz pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp329
Social Mobilization
Todd Rogers, Noah J. Goldstein, and Craig R. Fox ppppppppppppppppppppppppppppppppppppppp357
Developmental Origins of Chronic Physical Aggression:
A Bio-Psycho-Social Model for the Next Generation of Preventive
Interventions
Richard E. Tremblay, Frank Vitaro, and Sylvana M. Cˆot´epppppppppppppppppppppppppppppp383
Improving Student Outcomes in Higher Education: The Science
of Targeted Intervention
Judith M. Harackiewicz and Stacy J. Priniski pppppppppppppppppppppppppppppppppppppppppppp409
Why Social Relationships Are Important for Physical Health: A Systems
Approach to Understanding and Modifying Risk and Protection
Julianne Holt-Lunstad pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp437
Principles and Challenges of Applying Epigenetic Epidemiology
to Psychology
Meaghan J. Jones, Sarah R. Moore, and Michael S. Kobor pppppppppppppppppppppppppppppp459
Psychology, Science, and Knowledge Construction: Broadening
Perspectives from the Replication Crisis
Patrick E. Shrout and Joseph L. Rodgers ppppppppppppppppppppppppppppppppppppppppppppppppppp487
Psychology’s Renaissance
Leif D. Nelson, Joseph Simmons, and Uri Simonsohn pppppppppppppppppppppppppppppppppppp511
Indexes
Cumulative Index of Contributing Authors, Volumes 59–69 ppppppppppppppppppppppppppp535
Cumulative Index of Article Titles, Volumes 59–69 ppppppppppppppppppppppppppppppppppppp540
Errata
An online log of corrections to Annual Review of Psychology articles may be found at
http://www.annualreviews.org/errata/psych
Contents vii
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... A recent review of aggressive behavior stated: "Men are found to use aggression more than females when studies focus on direct forms of aggression (e.g., physical or verbal aggression) and when the target of the aggression is an individual not known to the perpetrator. Conversely, females are found to use aggression more often than males when studies focus on indirect forms of aggression (e.g., psychological or social aggression) and when the target of the aggression is an individual known to the perpetrator" (20). Robust evidence from prospective, longitudinal investigations of birth and population cohorts conducted in different countries confirm that aggressive behavior is observed during the first year of life, that it increases to about the age of 4 years, then declines. ...
... Robust evidence from prospective, longitudinal investigations of birth and population cohorts conducted in different countries confirm that aggressive behavior is observed during the first year of life, that it increases to about the age of 4 years, then declines. All studies identify one group of individuals who display high levels of aggressive behavior through childhood, adolescence, and adulthood (20). In a representative sample of 1,183 Canadian children 12.5% of boys and 11.0% of girls were reported to present the highest levels of aggressive behavior and of indirect aggression from ages 2 to 8 years. ...
... Other studies report that from toddlerhood through adolescence (∼5% of boys display high levels of physically aggressive behavior as do 1% of girls (23); for a review see (24). As for all types of aggressive behavior, across adolescence, stable high trajectories of both proactive and reactive aggression have been observed (20). ...
Article
Full-text available
The percentage of forensic psychiatric patients who are female varies from 5 to 13% in Europe, rises to 18% in England and Wales, and sits at 15% in Canada. Similarly, many fewer women than men are incarcerated in correctional facilities. While these statistics supposedly reflect less antisocial and aggressive behavior (AAB) among females than males, not all findings support this supposition. Data from prospective longitudinal studies show that aggressive and antisocial behavior onsets in childhood, and in a small group of females it remains stable across the life-span. Unlike similar males, few of these females are convicted of crimes. This article begins with a review of descriptive studies of females sentenced by criminal courts to treatment in forensic psychiatric hospitals and moves on to present evidence showing that most female AAB does not lead to criminal prosecution. Next, studies of female AAB are reviewed, noting that it onsets in early childhood and, that in a small group remains stable across the life-span. Subsequent sections of the article focus on the two most common mental disorders presented by female forensic patients, schizophrenia and borderline personality disorder, highlighting what is known about the sub-groups of women with these disorders who present AAB. The article concludes with recommendations for earlier identification by psychiatric services of women presenting mental disorders and AAB, treatments to reduce both the symptoms of their mental disorders and their life-long AAB, and the research that is needed in order to improve the effectiveness of these treatments. The real possibilities of prevention of the development of AAB, and even perhaps aspects of the mental disorders that plague female forensic patients, are described.
... Early childhood and family visitation programs have already been found rather effective for preventing delinquency later in life (e.g., see meta-analyses by Piquero et al., 2009Piquero et al., , 2016 and reviews by Webster-Stratton & Taylor, 2001;Welsh & Farrington, 2007). In fact, Tremblay et al. (2018), when discussing prevention programs intended to reduce aggression, specifically urge to target not only the age of infancy and early childhood but also the prenatal development, given the intergenerational transmission of aggression and its early onset in infancy. Adding microbiome-friendly enhancements to the range of early interventions could be a small effect with a big payoff. ...
... In fact,O'Mahony et al. (2017) suggest that ACEs may lead to brain-related socioemotional and behavioral issues due to the detrimental impact of early adversity on the gut microbiome. Several studies show associations between adverse early experiences and stress, functional brain connectivity, and the gut microbiome composition in adulthood(Callaghan et al., 2020;Coley et al., 2021).Evidence from population-wide longitudinal studies also finds the confluence of poor health, crime, poverty, and other social adversities concentrated within the same populations(Richmond-Rakerd et al., 2020;Semenza et al., 2020), which underscores the importance of early interventions to disrupt the possible intergenerational health effects(Foster & Hagan, 2015;Tremblay et al., 2018). The concentration of various adversities, including ACEs and health problems, within deprived neighborhoods(Powell-Wiley et al., 2020;Ribeiro et al., 2019;Rocha et al., 2017) points to a reciprocal process starting in early childhood and likely involving brain structure abnormalities(Carlisi et al., 2020;Rocque et al., 2015;Semenza et al., 2020). ...
Article
Research in biosocial criminology and other related disciplines has established links between nutrition and aggressive behavior. In addition to observational studies, randomized trials of nutritional supplements like vitamins, omega‐3 fatty acids, and folic acid provide evidence of the dietary impact on aggression. However, the exact mechanism of the diet‐aggression link is not well understood. The current article proposes that the gut microbiome plays an important role in the process, with the microbiota–gut–brain axis serving as such a mediating mechanism between diet and behavior. Based on animal and human studies, this review synthesizes a wide array of research across several academic fields: from the effects of dietary interventions on aggression, to the results of microbiota transplantation on socioemotional and behavioral outcomes, to the connections between early adversity, stress, microbiome, and aggression. Possibilities for integrating the microbiotic perspective with the more traditional, sociologically oriented theories in criminology are discussed, using social disorganization and self‐control theories as examples. To extend the existing lines of research further, the article considers harnessing the experimental potential of noninvasive and low‐cost dietary interventions to help establish the causal impact of the gut microbiome on aggressive behavior, while adhering to the high ethical standards and modern research requirements. Implications of this research for criminal justice policy and practice are essential: not only can it help determine whether the improved gut microbiome functioning moderates aggressive and violent behavior but also provide ways to prevent and reduce such behavior, alone or in combination with other crime prevention programs.
... Maladaptive aggression is common across childhoodonset psychiatric disorders (Connor et al. 2019) and constitutes one of the main reasons for referral to mental health services (Costello et al. 2014). The causal pathways to childhood aggression involve multiple interacting biological, environmental, and psychosocial risk factors (Tremblay et al. 2018). One inf luential theory, the social information-processing model, identifies deficits in the detection and interpretation of social cues, as well as in the generation and enactment of socially appropriate responses, as key factors that can lead to maladaptive aggression (Crick and Dodge 1994). ...
... This distortion in processing social informationreferred to as hostile attribution bias-often leads to increased anger arousal and aggressive behavior (Verhoef et al. 2019). The construct of "aggression" refers to a broad category of behaviors, which often results in harm to self or others (Tremblay et al. 2018). In children with psychiatric disorders, affective, impulsive aggressionalso referred to as reactive aggression-represents one of the most clinically challenging behaviors (Vitiello and Stoff 1997). ...
Article
Aggressive behavior is common across childhood-onset psychiatric disorders and is associated with impairments in social cognition and communication. The present study examined whether amygdala connectivity and reactivity during face emotion processing in children with maladaptive aggression are moderated by social impairment. This cross-sectional study included a well-characterized transdiagnostic sample of 101 children of age 8-16 years old with clinically significant levels of aggressive behavior and 32 typically developing children without aggressive behavior. Children completed a face emotion perception task of fearful and calm faces during functional magnetic resonance imaging. Aggressive behavior and social functioning were measured by standardized parent ratings. Relative to controls, children with aggressive behavior showed reduced connectivity between the amygdala and the dorsolateral prefrontal cortex (PFC) during implicit emotion processing. In children with aggressive behavior, the association between reduced amygdala-ventrolateral PFC connectivity and greater severity of aggression was moderated by greater social impairment. Amygdala reactivity to fearful faces was also associated with severity of aggressive behavior for children without social deficits but not for children with social deficits. Social impairments entail difficulties in interpreting social cues and enacting socially appropriate responses to frustration or provocation, which increase the propensity for an aggressive response via diminished connectivity between the amygdala and the ventral PFC.
... There is strong evidence that these health and educational problems in kindergarten were often preceded by developmental problems during pregnancy and infancy (Galéra et al., 2011;Tremblay et al., 2018). Pregnant women with low levels of education are more at risk of physical and mental health problems (Akhtar-Danesh & Landeen, 2007). ...
... Les études du développement des enfants montrent que les problèmes observés à la maternelle découlent souvent des problèmes du développement au prénatal et/ou à la petite enfance (Galéra et al., 2011;Tremblay et al., 2018). Les femmes enceintes qui ont un faible niveau d'éducation sont plus à risque de problèmes de santé physique et mentale (Akhtar-Danesh & Landeen, 2007). ...
Article
A large research-based consensus was achieved over the past 30 years concerning the importance of prenatal and early childhood development: Preventive interventions are needed early in life because physical and psychological problems during pregnancy and early childhood often lead to serious physical, psychological, educational, and social problems throughout the life course. These problems are also transmitted to the next generation. The COVID-19 pandemic is likely to have increased the number of families who need these early-life preventive interventions. Without intensive support, children from high-risk families are likely to fail in school, to have serious physical and mental health problems, and to reproduce another generation of children with similar physical, cognitive, and mental health problems. We underline the need to: (1) assess the extent of the COVID-19 damage on pregnant women and on their spouses, as well as on the families with preschool children; (2) help service providers identify the state-of-the art services they should implement; (3) assess the implementation of these services; and (4) help service providers maintain highly effective interventions. For the next 20 to 30 years at least, governments will be under intense pressure to invest massively in the health and care of the baby boomers. We are thus facing abysmal health care and retirement costs for the next 3 decades. Governments should be pressured to substantially invest in the support of pregnant women and preschool children, rather than in the sustained quality of life of the aging baby boomers.
... These are the children who become criminal offenders in adolescence and adulthood. In these studies of large birth and population cohorts there is no evidence of aggressive behavior emerging later than toddlerhood (Tremblay, Vitaro, & Côté, 2018). ...
Chapter
Effective treatments for traumatic brain injuries (TBIs) are limited. Prevention is key to reduce the societal burden of TBIs. This chapter reviews research on TBIs and aggressive behavior and criminality to illustrate the importance of disentangling pre- and post-injury characteristics, family environments, and experiences. The assumption that TBIs lead to aggressive behavior and violent criminality, or even cause such behaviors, has been challenged by findings from investigations that collected data, prospectively, over many years on population cohorts. Most individuals who engage in aggressive behavior and crime have a history of conduct problems that emerged in childhood, parents who engaged in harsh parenting and physical maltreatment, and an elevated risk of accidents. A prospective, longitudinal investigation has shown that childhood conduct problems and inattention at age 10 were associated with TBIs sustained up to age 34. Effective treatments that reduce childhood CP and inattention could potentially be modified to prevent TBIs.
... Prior research has demonstrated aggression to be a common type of behavioral problem in peer relationships that increases in frequency and intensity during the early childhood period (Basten et al., 2016;Crick et al., 1997;Furniss et al., 2006;Tremblay et al., 2018). However, a significant amount of research attention has been devoted to physical aggression. ...
Article
Full-text available
Purpose: To conduct a systematic review study of school based interventions to decrease aggressive behaviour among adolescents. The main goal of this review is to know about various interventions and to evaluate the effect of interventions on aggressive behaviour. The study's second goal is to find research gaps that could lead to more research in this area. The findings could be used as a foundation for developing interventional programs aimed at reducing adolescents' aggression. Design/Methodology/Approach: The purpose of this study is to develop a module as coping techniques to reduce the aggressive behaviour and analyse the ABCD model of the same. For this purpose we conducted a search 122 articles for relevant articles in the specified area. We looked for articles published between 2000 and 2022 using the primary databases; Google Scholar, Research Gate, Academia, SSRN, Shodhganga, PubMed, Rayyan and Elsevier. The words like aggressive behaviour, interventions and aggression were used for searching articles. All abstracts and entire articles were scrutinized to see various interventions as a coping strategy to decrease aggressions among students. Findings/Result: These findings reveal a clear link between self-control abilities and aggressive behaviour: those with greater self-control have less aggression, while people with lower self-control have more aggression. This relationship shows to hold true across a range of ages i.e. from childhood onwards. Based on these review study it also discussed and put forward future research into various interventions and strategies for regulating aggressiveness. Originality/Value: This review summarizes selected studies identifying the effect of various interventions on aggressive behaviour and find out the coping strategies. The future direction of existing research on emotional stability, first focusing on stressors and barriers associated with aggressive behavior, and considering the increased risk of stress, anxiety, and depression reported in this population. Next, it then describes recent trends and issues and seeks to fill gaps in existing literature that require additional research effort. We also conclude that there exists a need for future research on psychological intervention and coping strategies, cognitive behavioral therapy, parent management training, anger rumination and relaxation therapy for enhancing emotional well being and self-control of adolescents. Implementing parental interventions in parallel with the child's interventions may raise mental health.
Chapter
There is a discernible shift from paradigm 1 towards paradigm 2 for understanding bullying, but some of the most helpful lessons learned from past decades of research on individual and family factors need to be retained. There is a greater focus on everyday social processes underlying bullying, under paradigm 2, with a further movement towards an integrated view (paradigm 3?) discernible in the work of several authors. In this chapter, an Integrated Bullying Framework is put forward, in the form of both a statement and a supplementary diagram. It unites a top-down paradigm 2 perspective with the bottom-up evolutionary and psychological perspectives explored in this book to present a process-based systemic framework for understanding bullying in functional terms, which hinges on social identity and the basic human need to belong. The chapter ends with an illustrative case study.
Chapter
To place bullying a very broad context, this chapter outlines evidence that modern humans have evolved as an essentially social species, in which biological and cultural evolution are intertwined. Sociality, especially close emotional relationships within a broader social environment, enables our very survival. It plays a central role in the dynamic systemic processes that constitute our developmental path and determine our wellbeing. Being bullied is a threat to the basic human need for belonging.
Chapter
This chapter summarises the objections raised to the paradigm 1 approach to school bullying and presents Schott’s hypotheses under paradigm 2. These are based on theories about social relations on a large scale, involving the ongoing formation and maintenance of groups, in a dynamic, continuous process in which power is central. Certain groups are granted more power and are motivated to defend their status, at the expense of some others. If one’s belonging to a group is threatened (‘social exclusion anxiety’), defence often takes the form of marginalising someone else. We can see these processes in areas not usually considered as ‘bullying’, including indirect aggression, sexual and racial harassment and peer group popularity contests. Conversely, we can see traditionally defined bullying as serving the purpose of marginalisation. The ‘marginalisation’ perspective therefore offers a unifying theory for understanding all forms of peer victimisation in schools
Article
In the prevention of physical aggression, possible etiological links with language development are rarely taken into account. Indeed, little is known about when language and aggressive behavior become linked during development and which mechanisms are responsible for this association. This study investigated the association between physical aggression and language in late infancy with a genetic design that involved 562 19-month-old twins. A modest but significant correlation (r = -.20) was found between physical aggression and expressive vocabulary. Substantial heritability was found for physical aggression. Quantitative genetic modeling suggests that the correlation between expressive vocabulary and physical aggression cannot be explained by shared etiologies. However, phenotype-to-phenotype models indicate that the covariation can be entirely accounted for by a significant phenotypic path from expressive vocabulary to physical aggression. The implications of these results for early prevention of chronic physical aggression are discussed.
Article
We examine the hypothesis that children's exposure to ethnic-political conflict and violence over the course of a year stimulates their increased aggression toward their own in-group peers in subsequent years. In addition, we examine what social cognitive and emotional processes mediate these effects and how these effects are moderated by gender, age, and ethnic group. To accomplish these aims, we collected three waves of data from 901 Israeli and 600 Palestinian youths (three age cohorts: 8, 11, and 14 years old) and their parents at 1-year intervals. Exposure to ethnic-political violence was correlated with aggression at in-group peers among all age cohorts. Using a cross-lagged structural equation model from Year 1 to Year 3, we found that the relation between exposure and aggression is more plausibly due to exposure to ethnic-political violence stimulating later aggression at peers than vice versa, and this effect was not moderated significantly by gender, age cohort, or ethnic group. Using three-wave structural equation models, we then showed that this effect was significantly mediated by changes in normative beliefs about aggression, aggressive script rehearsal, and emotional distress produced by the exposure. Again the best fitting model did not allow for moderation by gender, age cohort, or ethnic group. The findings are consistent with recent theorizing that exposure to violence leads to changes both in emotional processes promoting aggression and in the acquisition through observational learning of social cognitions promoting aggression.
Article
The gut microbiome is a diverse, host-specific, and symbiotic bacterial environment that is critical for mammalian survival and exerts a surprising yet powerful influence on brain and behavior. Gut dysbiosis has been linked to a wide range of physical and psychological disorders, including autism spectrum disorders and anxiety, as well as autoimmune and inflammatory disorders. A wealth of information on the effects of dysbiosis on anxiety and depression has been reported in laboratory model systems (e.g., germ-free mice); however, the effects of microbiome disruption on social behaviors (e.g., aggression) of non-model species that may be particularly important in understanding many aspects of physiology and behavior have yet to be fully explored. Here we assessed the sex-specific effects of a broad-spectrum antibiotic on the gut microbiome and its effects on social behaviors in male and female Siberian hamsters (Phodopus sungorus). In Experiment 1, we administered a broad-spectrum antibiotic on a short-term basis and found that antibiotic treatment altered the microbial communities in the gut in male and female hamsters. In Experiment 2, we tested the effects of single versus repeated antibiotic treatment (including a recovery phase) on behavior, and found that two, but not one, treatments caused marked decreases in aggressive behavior, but not other social behaviors, in males; aggression returned to normal levels following recovery. Antibiotic-treated females, in contrast, showed decreased aggression after a single treatment, with all other social behaviors unaffected. Unlike males, female aggression did not return to normal during either recovery period. The present findings demonstrate that modest antibiotic treatment results in marked disruption of the gut microbiome in hamsters, akin to research done in other rodent species and humans. Further, we show that treatment with a broad-spectrum antibiotic, which has dysbiotic effects, also has robust, sex-specific effects on aggression, a critical behavior in the survival and reproductive success of many rodent species.
Article
Verbal and physical aggression begin early in life and steadily decline thereafter in normal development. As a result, elevated aggressive behavior in adolescence may signal atypical development and greater vulnerability for negative mental and health outcomes. Converging evidence suggests that brain disturbances in regions involved in impulse control, emotional regulation, and sensation seeking may contribute to heightened aggression. However, little is known regarding the neural mechanisms underlying subtypes of aggression (i.e., proactive and reactive aggression) and whether they differ between males and females. Using a sample of 106 14-year-old adolescent twins, this study found that striatal enlargement was associated with both proactive and reactive aggression. We also found that volumetric alterations in several frontal regions including smaller middle frontal and larger orbitofrontal cortex were correlated with higher levels of aggression in adolescent twins. In addition, cortical thickness analysis showed that thickness alterations in many overlapping regions including middle frontal, superior frontal, and anterior cingulate cortex and temporal regions were associated with aggression in adolescent twins. Results support the involvement of fronto-limbic-striatal circuit in the etiology of aggression during adolescence. Aggr. Behav. 9999:1–11, 2016.
Article
Goal-directed social behaviours such as mating and fighting are associated with scalable and persistent internal states of emotion, motivation, arousal or drive. How those internal states are encoded and coupled to behavioural decision making and action selection is not clear. Recent studies in Drosophila melanogaster and mice have identified circuit nodes that have causal roles in the control of innate social behaviours. Remarkably, in both species, these relatively small groups of neurons can influence both aggression and mating, and also play a part in the encoding of internal states that promote these social behaviours. These similarities may be superficial and coincidental, or may reflect conserved or analogous neural circuit modules for the control of social behaviours in flies and mice.
Article
Background: Dating violence is an important problem. Evidence suggests that women are more likely to perpetrate dating violence. Aims: The present study investigates the prevalence of dating violence compared with cohabiting violence in a community sample of men and women and assesses to what extent child and adolescent explanatory factors predict this behaviour. A secondary aim is to construct a risk score for dating violence based on the strongest risk factors. Methods: The Cambridge Study in Delinquent Development is a prospective longitudinal survey of 411 men (generation 2) born in the 1950s in an inner London area. Most recently, their sons and daughters [generation 3 (G3)] have been interviewed regarding their perpetration of dating and cohabiting violence, utilising the Conflict Tactics Scale. Risk factors were measured in four domains (family, parental, socio-economic and individual). Results: A larger proportion of women than men perpetrated at least one act of violence towards their dating partner (36.4 vs 21.7%). There was a similar pattern for cohabiting violence (39.6 vs 21.4%). A number of risk factors were significantly associated with the perpetration of dating violence. For G3 women, these included a convicted father, parental conflict, large family size and poor housing. For G3 men, these included having a young father or mother, separation from the father before age 16, early school leaving, frequent truancy and having a criminal conviction. A risk score for both men and women, based on 10 risk factors, significantly predicted dating violence. Conclusion: Risk factors from four domains were important in predicting dating violence, but they were different for G3 men and women. It may be important to consider different risk factors and different risk assessments for male compared with female perpetration of dating violence. Early identification and interventions are recommended. Copyright © 2016 John Wiley & Sons, Ltd.
Article
The Cambridge Study in Delinquent Development is a prospective longitudinal survey of 411 London males from age 8 to age 56. This article compares the convictions of 343 adult sons (searched up to the median age of 29) with the convictions of their fathers up to the same age. There was significant intergenerational transmission of convictions, since 43% of the sons of convicted fathers were themselves convicted, compared with 18% of the sons of unconvicted fathers. There was significant intergenerational transmission of burglary, serious and minor theft, violence, threatening behavior, carrying an offensive weapon, and serious motoring offenses. The most important mediators between parental and child convictions were the family renting rather than owning their own home, poor parental supervision, an antiestablishment attitude of the father, parental physical punishment of the child, and separation of the son from his father. Implications for the prevention of intergenerational transmission are drawn.
Article
Background: Neurodevelopment is strongly influenced by maternal and early-postnatal diet. Omega-3 polyunsaturated fatty acids (n-3 PUFA) are vital structural and functional components of the developing brain. The gut microbiota is also influenced by n-3 PUFA status, however, little is known about the role of maternal and early-life n-3 PUFA intake on offspring gut microbiota development and subsequent interactions with central nervous system functioning and behavioural outcomes. Methods: Pregnant female C57BL/6 mice and their male offspring were fed a control (CON), omega-3 deficient (O3-) or omega-3 supplemented (O3+) diet. Cognitive, depressive and social behaviours were assessed through a battery of behaviour tests in the male offspring at both adolescence (week 4-5) and adulthood (week 11-13). Hypothalamic-pituitary-adrenal axis (HPA) activation was assessed by analysis of stress-induced corticosterone production. Fecal microbiota composition was analysed by 16s sequencing at both adolescent and adulthood. In addition, stimulated spleen cytokine levels were assessed. Results: n-3 PUFA interventions induced subtle changes in offspring early-life and adolescent behaviours, which were further evident in adulthood, such that O3- animals displayed impaired communication, social and depression-related behaviours and O3+ animals displayed enhanced cognition. O3- mice displayed an elevated Firmicutes:Bacteroidetes ratio and blunted systemic LPS responsiveness. Contrastingly, O3+ mice displayed greater fecal Bifidobacterium and Lactobacillus abundance and dampened HPA-axis activity. Conclusions: Neurobehavioural development related to cognitive, anxiety and social behaviours, is highly dependent upon in utero and lifelong n-3 PUFA availability. In addition, neurobehavioural changes induced by altering n-3 PUFA status are closely associated with comprehensive alterations in gut microbiota composition, HPA-axis activity and inflammation.