Bullying behavior is a serious problem among school-age children and adolescents; it has short- and long-term effects on the individual who is bullied, the individual who bullies, the individual who is bullied and bullies others, and the bystander present during the bullying event. In this chapter, the committee presents the consequences of bullying behavior for children and youth. As referenced in Chapter 1, bullying can be either direct or indirect, and children and youth may experience different types of bullying. Specifically the committee examines physical (including neurobiological), mental, and behavioral health consequences. The committee also examines consequences for academic performance and achievement and explores evidence for some of the mechanisms proposed for the psychological effects of bullying. When applicable, we note the limited, correlational nature of much of the available research on the consequences of bullying.
Mounting evidence on bullying has highlighted the detrimental effects of being bullied on children’s health and behavior (Gini and Pozzoli, 2009; Lereya et al., 2015; Reijntjes et al., 2010; Ttofi et al., 2011). In this section, the committee reviews the research on physical, psychosocial, and academic achievement consequences for those children and youth who are bullied.
Physical Health Consequences
The physical health consequences of bullying can be immediate, such as physical injury, or they can involve long-term effects, such as headaches, sleep disturbances, or somatization.1 However, the long-term physical consequences of bullying can be difficult to identify and link with past bullying behavior versus being the result of other causes such as anxiety or other adverse childhood events that can also have physical effects into adulthood (Hager and Leadbeater, 2016). In one of the few longitudinal studies on the physical and mental effects of bullying, Bogart and colleagues (2014) studied 4,297 children and their parents from three urban locales: Birmingham, Alabama; 25 contiguous school districts in Los Angeles County, California; and one of the largest school districts in Houston, Texas. Bogart and her team were interested in the cumulative effects of bullying on an individual. They collected data when the cohort was in fifth grade (2004 to 2006), seventh grade (2006 to 2008), and tenth grade (2008 to 2010). Data consisted of responses to the Peer Experience Questionnaire, the Pediatric Quality of Life Inventory with its Psychosocial Subscale and Physical Health Subscale, and a Self-Perception Profile. The Physical Health Subscale measured perceptions of physical quality of life.
Bogart and colleagues (2014) found that children who were bullied experienced negative physical health compared to non-involved peers. Among seventh grade students with the worst-decile physical health, 6.4 percent were not bullied, 14.8 percent had been bullied in the past only, 23.9 per-
1 Somatization is “a syndrome of physical symptoms that are distressing and may not be fully explained by a known medical condition after appropriate investigation. In addition, the symptoms may be caused or exacerbated by anxiety, depression, and interpersonal conflicts, and it is common for somatization, depression, and anxiety to all occur together” (Greenberg, 2016).
cent had been bullied in the present only, and nearly a third (30.2%) had been bullied in both the past and present. These effects were not as strong when students were in tenth grade. Limitations to this study were that physical health was measured by participants’ perceptions of their health-related quality of life, rather than by objectively defined physical symptoms. It is critical to understand that this study, or other studies assessing correlations between behavior and events, cannot state that the events caused the behavior. Future research might build on this large multisite longitudinal study and obtain more in-depth evidence on individuals’ physical health as a consequence of bullying.
In their study of 2,232 twins reared together and separately as a part of the Environmental Risk (E-Risk) Longitudinal Twin Study, Baldwin and colleagues (2015) found that children who had experienced chronic bullying showed greater adiposity subsequently, but not at the time of victimization. The study revealed that at age 18, these children had a higher body mass index (b = 1.11, CI [0.33, 1.88]), waist-hip ratio (b = 0.017, CI [0.008, 0.026]), and were at a higher risk of being overweight (OR = 1.80, CI [1.28, 2.53]) than their nonbullied counterparts (Baldwin et al., 2015).
An important future direction for research is to gather more information on physical consequences such as elevated blood pressure, inflammatory markers, and obesity in light of work showing effects on these outcome of harsh language by parents and other types of early life adversity (Danese and Tan, 2014; Danese et al., 2007; Evans et al., 2007; Miller and Chen, 2010).
Most of the extant evidence on the physical consequences—somatic symptoms in particular—of bullying pertains to the individual who is bullied. The emotional effects of being bullied can be expressed through somatic disturbances, which, similar to somatization, are physical symptoms that originate from stress or an emotional condition. Common stress or anxiety-related symptoms include sleep disorders, gastrointestinal concerns, headaches, palpitations, and chronic pain. The relationship between peer victimization and sleep disturbances has been well documented (Hunter et al., 2014; van Geel et al., 2014).
For instance, Hunter and colleagues (2014) examined sleep difficulties (feeling too tired to do things, had trouble getting to sleep, and had trouble staying asleep) among a sample of 5,420 Scottish adolescents. The researchers found that youth who were bullied (OR = 1.72, 95% CI [1.07, 2.75]) and youth who bully (OR = 1.80, CI [1.16, 2.81]) were nearly twice as likely as youth who were not involved in bullying to experience sleep difficulties. One limitation of this study is that it was based on self-reports,
which have sometimes been criticized as being subject to specific biases. Patients with insomnia may overestimate how long it takes them to fall asleep (Harvey and Tang, 2012). Another limitation is that the study included young people at different stages of adolescence. Sleep patterns and sleep requirements vary across the different stages of adolescence.
A recent meta-analysis based on 21 studies involving an international sample of 363,539 children and adolescents examined the association between peer victimization and sleeping problems. A broader focus on peer victimization was used because of the definitional issues related to bullying. The authors defined peer victimization as “being the victim of relational, verbal or physical aggression by peers” (van Geel et al., 2015, p. 89). Children and youth who were victimized reported more sleeping problems than children who did not report victimization (OR = 2.21, 95% CI [2.01, 2.44]). Moreover, the relationship between peer victimization and sleeping problems was stronger for younger children than it was for older children (van Geel et al., 2015). This study was based on cross-sectional studies that varied widely in how peer victimization and sleeping problems were operationalized and thus cannot make any claims about causal relations between peer victimization and sleeping problems.
Knack and colleagues (2011a) posited that bullying results in meaningful biological alterations that may result in changes in one’s sensitivity to pain responses. A recent meta-analysis by Gini and Pozzoli (2013) concluded that children and adolescents who are bullied were at least twice as likely to have psychosomatic disturbances (headache, stomachache, dizziness, bedwetting, etc.) than nonbullied children and adolescents (OR = 2.39, 95% CI [1.76, 3.24] for longitudinal studies; OR = 2.17, 95% CI [1.91, 2.46] for cross-sectional studies). Although the use of self-report measures are very common in bullying research and are usually considered to be valid and reliable (Ladd and Kochenderfer-Ladd, 2002), their use requires adequate self-awareness on the part of the respondent, and some children who are bullied may be in denial about their experience of having been bullied.
There is also evidence of gender differences in the physical effects of being bullied. For example, Kowalski and Limber (2013) examined the relation between experiences with cyberbullying or traditional bullying (i.e., bullying that does not involve digital electronic means of communication) and psychological and physical health, as well as academic performance, of 931 students in grades 6 through 12 living in rural Pennsylvania. Students were asked how often in the past 4 weeks they experienced 10 physical health symptoms, with scores across these 10 symptoms averaged to provide an overall health index (higher scores equal more health problems). Traditional bullying was defined as “aggressive acts that are meant to hurt another person, that happen repeatedly, and that involve an imbalance of
power” (Kowalski and Limber, 2013, p. S15). The authors found that girls who were traditionally bullied reported more anxiety and overall health problems than boys who were bullied (females: M = 1.65, SD = 0.41; males: M = 1.42, SD = 0.38). A limitation of this study is that it is correlational in nature and the authors cannot conclude that being a victim of traditional bullying caused the psychological or physical problems.
In summary, it is clear that children and youth who have been bullied also experience a range of somatic disturbances. There are also gender differences in the physical health consequences of being bullied.
Neuroendocrinology of Stress
Psychological and physical stressors, such as being the target of bullying, activate the stress system centered on the hypothalamic-pituitary-adrenal (HPA) axis (Dallman et al., 2003; McEwen and McEwen, 2015). The role of HPA and other hormones is to promote adaptation and survival, but chronically elevated hormones can also cause problems. Stress has ubiquitous effects on physiology and the brain, alters levels of many hormones and other biomarkers, and ultimately affects behavior. Therefore, both a general understanding of stress during early adolescence and, where known, specific links between stress and bullying can provide insight into the enduring effects of bullying.
The levels of the stress hormone cortisol have been shown to change in targets of repeated bullying, with being bullied associated with a blunted cortisol response (Booth et al., 2008; Kliewer, 2006; Knack et al., 2011b; Ouellet-Morin et al., 2011; Vaillancourt et al., 2008). To the committee’s knowledge, no study has examined bidirectional changes in cortisol, although there is evidence to suggest that cortisol is typically elevated immediately following many types of stress and trauma but blunted after prolonged stress (Judd et al., 2014; Miller et al., 2007). Kliewer (2006) did find that cortisol increased from pre-task to post-task (i.e., watching a video clip from the film Boyz ’n the Hood followed by a discussion) among youth who had been bullied, and in a more recent study, Kliewer and colleagues (2012) reported, among African American urban adolescents, that peer victimization was associated with greater sympathetic nervous system (fight or flight reaction) reactivity to a stress task (measured using salivary a-amylase, an enzyme that increases in saliva when the sympathetic nervous system is activated). However, in these studies, the immediate effect of being bullied on stress reactivity was not examined. In contrast, Ouellet-Morin and colleagues (2011) and Knack and colleagues (2011b) did not find an increase in cortisol in bullied youth following a psychosocial stress test but rather found a blunted pattern of response after the test had concluded (see Figures 4-1 and 4-2). In order to test whether, in the short-term, bullying
produces an increase in cortisol, whereas in the long-term it is associated with a blunted cortisol response (as seen with other types of psychosocial stressors; Judd et al., 2014; Miller et al., 2007), a longitudinal study is needed to examine bullying chronicity and regulation of the HPA axis. The importance of this future work notwithstanding, there is evidence to support a finding that when stress becomes prolonged, the stress hormone system becomes hypofunctional and a blunted stress response results (McEwen, 2014).
When stress becomes prolonged, the stress hormone system becomes hypofunctional and a blunted stress response results (Knack et al., 2012a; McEwen, 2014; Vaillancourt et al., 2013a). That is, the elevation in cortisol in response to stress fails to occur. Scientists are not exactly sure how this happens, but evidence suggests that the stress system has shut itself down through “negative feedback.” Although on the surface this may seem to be beneficial, it is not. Cortisol has many functions and serves to regulate myriad biological systems; a blunted stress response compromises the orchestration of cortisol’s biological functions. The critical importance of the massive over-activation of the stress system producing a blunted stress response is clinically relevant since it is associated with posttraumatic stress disorder and other psychiatric disorders (Heim et al., 1997). It is also relevant for understanding an individual’s inability to self-regulate and cope with stress.
Prolonged stress also disrupts the circadian or daily rhythm of cortisol, which is normally elevated in the morning and slowly decreases over the day to result in low levels at bedtime (Barra et al., 2015). An altered circadian rhythm results not only in difficulty awaking in the morning but also in difficulty falling asleep at night. It can cause profound disruption in sleep patterns that can initiate myriad additional problems; sleep deficits are associated with problems with emotional regulation, learning, mood disorders, and a heightened social threat detection and response system (McEwen and Karatsoreos, 2015). Recent research suggests that the consolidation of memories2 one learns each day continues during sleep (Barnes and Wilson, 2014; Shen et al., 1998). Sleep disturbances disrupt memory consolidation, and studies in animals suggest stress during learning engages unique neurochemical and molecular events that cause memory to be encoded by some unique mechanism (Baratta et al., 2015; Belujon and Grace, 2015; McGaugh, 2015; Rau and Fanselow, 2009). Although victims of bullying have sleep problems (Miller-Graff et al., 2015), causal relations between bullying, sleep disorders, learning/memory consolidation, and cortisol dysregulation have not been established. Indeed, these correla-
2 Consolidation of memory is a biological process where the information one learns is stabilized within neural circuits and placed into long-term memory through a complex orchestration of molecular-level change and gene activation within neurons.
tions between being a target of bullying and physiological problems may highlight important interactions between events and outcome, but it is also likely that unidentified variables might be the critical causal factors.
It is also noteworthy that the HPA axis showed heightened responsiveness during the peak ages of bullying (Blakemore, 2012; Dahl and Gunnar, 2009; Romeo, 2010; Spear, 2010). For example, cortisol response characteristics in children are such that, when cortisol is activated, the hormonal response is protracted and takes almost twice as much time to leave the blood and brain compared to adults (Romeo, 2010, 2015). The circadian rhythm of cortisol also seems altered during early adolescence, most notably associated with morning cortisol levels, with levels increasing with age and pubertal development (Barra et al., 2015). Animal models suggest that the extended cortisol response begins in pre-puberty and indicate that recovery from stressful events is more challenging during this age range (Romeo, 2015).
Emotional regulation, including a person’s ability to recover from a traumatic or stressful event, involves being able to regulate or normalize stress hormone levels. Before adolescence, children’s ability to regulate their stress response can be greatly assisted by parents or other significant caregivers—a process referred to as “social buffering” (Hostinar et al., 2014; Ouellet-Morin et al., 2011, 2013). Specifically, it is well documented in the human and animal research literature that a sensitive caregiver or a strong support system can greatly dampen the stress system’s response and actually reduce the amount of stress hormone released, as well as shorten the amount of time the stress hormones circulate within the body and brain. This results in dramatic decreases in stress-related behavior (Gee et al., 2014; Hostinar et al., 2014). The social cues actually reduce stress by reducing the activation of the stress system, or HPA axis, at the level of the hypothalamus (Hennessy et al., 2009, 2015; Moriceau and Sullivan, 2006). The social stimuli that buffer children as they transition into adolescence appear to begin to have greater reliance on peers rather than on the caregiver (Hostinar et al., 2015).
Other physiological effects of stress include the activation of the immune system by bullying-induced stress (Copeland et al., 2014; McCormick and Mathews, 2007), and a cardiovascular blunting among individuals with a history of being bullied (Newman, 2014). Other hormones and physiological mechanisms are also involved in the stress activation response. For example, cortisol is associated with an increase in testosterone, the male sex hormone associated with aggression in nonhuman animals and with dominance and social challenge in humans, particularly among boys and men (Archer, 2004). In fact, in rodents the combined assessment of testosterone and cortisol provides more predictive value of behavioral variability (McCormick and Mathews, 2007) compared to controls (Márquez et al., 2013). In humans, there is increasing evidence supporting an interaction
between testosterone and cortisol in the prediction of social aggression (see Montoya et al., 2012). In a study of 12-year-olds, Vaillancourt and colleagues (2009) found that testosterone levels were higher among bullied boys than nonbullied boys, but lower among bullied girls than nonbullied girls. The authors speculated that the androgen dynamics were possibly adrenocortical in origin, highlighting the need to examine testosterone and cortisol in consort. To date, researchers have only investigated cortisol response to being bullied (Kliewer, 2006; Knack et al., 2011b; Ouellet-Morin et al., 2011; Vaillancourt et al., 2008), and only one study has examined testosterone and peer victimization (Vaillancourt et al., 2009). There are no studies examining these two important hormones together in relation to bullying perpetration or to being bullied.
Together, the research on both humans and animals suggests that stress is beneficial when it is experienced at low-to-moderate levels, whereas prolonged or repeated stress becomes toxic by engaging a unique neural and molecular cascade within the brain that is thought to initiate a different developmental pathway. Indeed, from animal models, brain architecture is altered by chronic stress, with amygdala activity being enhanced, hippocampal function impaired, and medial prefrontal cortex function being reduced, leading to increased anxiety and aggression and decreased capacity for self-regulation, as well as a more labile mood (Chattarji et al., 2015; McEwen and Morrison, 2013; McEwen et al., 2015). This stress effect on the brain is particularly strong when experienced during adolescence, but it is even more pronounced if combined with early life adversity (Gee et al., 2014; Hanson et al., 2015; Richter-Levin et al., 2015; Romeo, 2015; Sandi and Haller 2015). This could produce behavioral responses that become maladaptive by compromising emotional and cognitive functioning or perhaps it could produce adaptive behavior for a dangerous environment that results in socially inappropriate behavior.
Consequences of Bullying on Brain Function
Being a child or youth who is bullied changes behavior, and neuroscience research suggests this experience may also change the brain (Bradshaw et al., 2012; Vaillancourt et al., 2013a). The major technique used to monitor brain function in humans is functional magnetic resonance imaging (fMRI), which works by monitoring blood flow to indirectly assess the functioning of thousands of brain cells over an area of the brain. This technique has rarely been used on either the perpetrator or target of a bullying incident during this very particular social interaction, and for that reason little is known about whether or not the brain of a child who bullies or of a child who has been bullied is different before these experiences or is changed by them. These very specific studies are required before one can
make definitive statements about the brain for this topic or for how this information might help develop novel interventions or prevention.
Additionally, it is important to consider two limitations for understanding fMRI. First, one cannot scan the brain of a child during the action of bullying or being a target of bullying. Instead, one must rely on the child staying perfectly still as the investigator tries to approximate one or two aspects of the complex experience that occur in this complicated behavioral interaction. For example, the fMRI task used during a brain imaging session might mimic social exclusion as one facet of bullying, without the full social and emotional context of the real bullying process. Although this is an important methodology, these results need to be assessed with caution at this time and not directly applied as an accepted scientific interpretation of bullying. Therefore, the examples used below to assess brain function rely not on monitoring actual instances of bullying behavior but on monitoring components of behaviors that are thought to occur during a bullying incident.
Second, fMRI monitors a large brain area, which is composed of many smaller brain areas, each of which is involved in many, many behaviors, many of which are not yet fully understood. Thus, it is difficult to determine why the brain area one is examining changed, since that brain area is involved in hundreds of diverse behaviors. For this reason, the results reviewed below need to be viewed as preliminary and should not be misinterpreted as explaining any aspect of the experience of bullying. Rather, these preliminary results highlight the importance of brain assessment before and after bullying experiences, including developing monitorable tasks that more closely approximate the bullying experience within the physical constraints of an immobile subject during an fMRI brain scan. The value of neuroscience is that it enables exploration of brain mechanisms controlling behavior that are not obvious from behavioral assessment.
Whereas there are no studies directly examining bullying using neural imaging techniques, there are several studies examining how the brain processes social pain. Social pain describes the “feelings of pain that follow the experiences of peer rejection, ostracism, or loss” (Vaillancourt et al., 2013a, p. 242). Social pain is consistent with how people describe their feeling about being bullied. For example, one victim of bullying described the emotional toll of his experience by saying, “I feel like, emotionally, they [his bullies] have been beating me with a stick for 42 years” (Vaillancourt et al., 2013a, p. 242).
Researchers have demonstrated that when people experience social pain, they activate regions in their brain similar to those activated
when they experience physical pain (Eisenberger, 2012; Eisenberger and Lieberman, 2004; Eisenberger et al., 2003; Kross et al., 2011; Vaillancourt et al., 2010a). Specifically, the dorsal anterior cingulate cortex, which is part of the prefrontal cortex, seems to be implicated in the processing of both physical and social pain. The fact that physical and social pain have overlapping neural systems might explain why people tend to use physical pain metaphors (e.g., “It broke my heart when she called me ugly.”) when describing their experiences with being humiliated, oppressed, or rejected (Eisenberger, 2012). Eisenberger and Leiberman (2004) noted that these fMRI results are correlations between pain and the anterior cingulate cortex and could reflect other functions of that brain region, such as detecting conflict or errors, different ideas or goals about the task, or individual differences in the task difficulty. In a recent fMRI study by Rudolph and colleagues (2016), adolescent girls were socially excluded during a laboratory task (i.e., cyberball; Williams et al., 2000). Results indicated that activation of the social pain network—the dorsal anterior cingulate cortex, subgenual anterior cingulate cortex, and anterior insula—was associated with internalizing symptoms. Of note, this effect was particularly pronounced among adolescent girls with a history of peer victimization.3
In addition to studies on social pain, there are some studies examining how the brains of children who had been bullied reacted subsequently to different stimuli. Experiences of being bullied can alter an individual’s view of the world. While no brain imaging study has directly addressed this issue, a longitudinal study investigating the risk factors of depression found that being a child who was bullied at ages 11 and 12 was associated with a decreased response to reward in the medial prefrontal cortex at age 16, although it was unclear if these brain differences were present before the bullying experiences or developed after them (Casement et al., 2014). The medial prefrontal cortex, which is a brain area involved in memory and learning, was found to be disrupted in children who have been bullied (Vaillancourt et al., 2011). Because it also has countless other functions including decision making, risk taking, and conflict monitoring, disruption of this region compromises one’s ability to interpret results with respect to bullying (Euston et al., 2012; Vaillancourt et al., 2011).
In another fMRI study involving children, 10-12 years old, who were presented with a task that examined their response to negative feedback stimuli of emotional faces, greater and more extensive brain activation was found in the amygdala, orbitofrontal cortex, and ventrolateral prefrontal cortex of children who had been rejected by their peers, compared with
3 Peer victimization was measured with a 21-item revised version of the Social Experiences Questionnaire. The measure assesses overt and relational victimization and frequency of different acts of victimization (Rudolph et al., 2016).
children in a control group who had not been rejected by peers (Lee et al., 2014), a condition that is highly correlated with being bullied by peers (r = .57; Knack et al., 2012a). The prefrontal cortex is a very large brain area with many subareas, all of which serve diverse functions in many different behaviors, not just executive function. Indeed, the prefrontal cortex processes pain, self-regulation, stress integration, and safety signals and has been implicated in psychiatric disorders, higher order learning, extinction (active process to suppress a memory), personality, social behavior, planning, decision making, and many other behaviors and percepts including social exclusion, social/physical pain, and empathy (Casey and Jones, 2010; Spear, 2013). These few studies are consistent with other imaging studies demonstrating functional brain differences among individuals who were maltreated in childhood (Lim et al., 2014, 2015). Taken together, this work supports a finding that being exposed to such adversity during maturation has enduring effects on brain function, although additional research is needed to establish the parameters controlling these effects (and qualifying the generalization).
There is also evidence that stressful events, such as might occur with bullying experiences, impact emotional brain circuits, an inference that is supported by changes in amygdala architecture and function described earlier in animal models in adulthood but more robust changes in brain structure are produced by stress during early life and around adolescence (Chattarji et al., 2015; McEwen and Morrison, 2013; McEwen et al., 2015). This point is critical because the stress system of adolescents seems to have a heightened sensitivity, and experiencing bullying can increase stress hormones (Romeo, 2010, 2015; Spear, 2013; Vaillancourt et al., 2011). Human brain scanning experiments suggest the prefrontal cortex is affected by stress through attenuating the connectivity to the hippocampus and amygdala, which are brain areas critical for emotional regulation and emotional memories (Ganzel et al., 2008; Liston et al., 2009). Animal research shows that this connectivity loss is caused by stress-induced atrophy of the prefrontal cortex (Radley et al., 2006), although this brain region does show the ability to recover once the stress has terminated (Liston et al., 2009). One aspect of being a target of bullying is that the memory of the experience seems to be enduring; the unique function of the prefrontal cortex and emotional circuits during preadolescence and adolescence may provide insight into the enduring memories of being bullied. Specifically, one function of the prefrontal cortex is to help suppress memories that are no longer important or true. Typically, memories are not simply forgotten or unlearned. Rather, as we update information in our brain, the old memory is suppressed by overlaying a new memory to attenuate the old memory, an active brain process called extinction (Milaid and Quirk, 2012). With respect to memories of trauma, of being bullied, or of experiencing a threat, the prefrontal cortex is important for attenuating
(extinguishing) memories in emotional brain areas, such as the amygdala. Importantly, dramatic changes occur in the extinction system during adolescence, where fear extinction learning is attenuated relative to children and adults (Pattwell et al., 2012, 2013). This learning mode has been modeled in animals to understand how the process occurs in the adolescent brain (Kim and Richardson, 2010; Nair and Gonzalez-Lima, 1999; Pattwell et al., 2012). The research suggests that around the time of adolescence, it is more difficult to decrease emotionally aversive memories, such as experiences of being bullied, than at other times in the life cycle. Furthermore, anxious teens (anxiety is sometimes comorbid with experience of being bullied) show even greater difficulties with processing extinction of fear memory (Jovanovic et al., 2013).
In conclusion, the available evidence indicates that the brain functioning of individuals who are bullied is altered (see reviews by Bradshaw et al., 2012; Vaillancourt et al., 2013a). However, it is difficult to ascertain fully what it means when fMRI scans detect an alteration in brain activity. In terms of understanding the prolonged and repeated stress associated with bullying, this research suggests that greater experience with being bullied and repeated exposure as a target of bullying produces a neural signature in the brain that could underlie some of the behavioral outcomes associated with being bullied.
In this section, the committee examines what is known about the psychosocial consequences of being bullied. A common method of examining mental health issues separates internalizing and externalizing problems (Sigurdson et al., 2015). Internalizing symptoms include problems directed within the individual, such as depression, anxiety, fear, and withdrawal from social contacts. Externalizing symptoms reflect behavior that is typically directed outwards toward others, such as anger, aggression, and conduct problems, including a tendency to engage in risky and impulsive behavior, as well as criminal behavior. Externalizing problems also include the use and abuse of substances.
Psychological problems are common after being bullied (see review by Hawker and Boulton, 2000) and include internalizing problems, such as depression, anxiety, and, especially for girls, self-harming behavior (Kidger et al., 2015; Klomek et al., 2009, 2015). There can also be subsequent externalizing problems, especially for boys (see review by McDougall and Vaillancourt, 2015). Rueger and colleagues (2011) found consistent concurrent association with timing of peer victimization and maladjustment. Both psychological and academic outcomes were particularly strong for students who experienced sustained victimization over the school year.
A robust literature documents that youth who are bullied often have low self-esteem and feel depressed, anxious, and lonely (Juvonen and Graham, 2014). Data from developmental psychopathology research indicate that stressful life events can lead to the onset and maintenance of depression, anxiety, and other psychiatric symptoms and that for many youth, being bullied is a major life stressor (Swearer and Hymel, 2015). Based on sociometric nominations, targets of bullying also are disliked by the general peer group (Knack et al., 2012b).
Several meta-analyses have specifically explored the relation between depression and being bullied at school (Ttofi et al., 2011) and victimized by peers4 (Hawker and Boulton, 2000; Reijntjes et al., 2010). Individuals who had been cyberbullied reported higher levels of depression and suicidal ideation, as well as increased emotional distress, externalized hostility, and delinquency, compared with peers who were not bullied (Patchin, 2006; Ybarra et al., 2006). Furthermore, severity of depression in youth who have been cyberbullied has been shown to correlate with the degree and severity of cyberbullying (Didden et al., 2009).
Two meta-analyses found that across several different longitudinal studies using different study populations, internalizing emotional problems increases both the risk and the harmful consequences of being bullied (Cook et al., 2010; Reijntjes et al., 2010). Internalizing problems can thus function
4Reijntjes and colleagues (2010, p. 244) defined peer victimization as taking “various forms, including direct bullying behaviors (e.g., teasing, physical aggression) as well as more indirect manifestations such as group exclusion or malicious gossip.” Hawker and Boulton (2000, p. 441) defined peer victimization as “the experience among children of being a target of the aggressive behavior of other children, who are not siblings and not necessarily age-mates.”
as both antecedents and consequences of bullying (Reijntjes et al., 2010; Vaillancourt et al., 2013b). Although most longitudinal studies suggest that psychological problems result from being bullied (see review by McDougall and Vaillancourt, 2015) and meta-analyses (Reijntjes et al., 2010; Ttofi et al., 2011) support this directionality, there is some evidence that for some youth, the temporal pattern begins with mental health problems (Kochel et al., 2012; Vaillancourt et al., 2013b).
In a large cohort of Canadian children followed every year from grade 5 to grade 8, Vaillancourt and colleagues (2013b) found that internalizing problems in grades 5 and 7 predicted increased self-reported bullying behavior the following year. They noted that these findings provide evidence for the “symptom-driven pathway” across time with increased internalizing problems predicting greater self-reported peer victimization. This “symptom-drive pathway” was noted from grade 5 to grade 6 and again from grade 7 to grade 8 and was consistent with other published work. For instance, Kochel et al. (2012) reported a symptom-driven pathway in which depressive symptoms predicted peer victimization5 1 year later (grade 4 to grade 5 and grade 5 to grade 6) and argued that this pathway may result from depressed youth displaying “social deficits,” selecting “maladaptive relationships,” and/or displaying a behavioral style that is perceived poorly by the peer group (Kochel et al., 2012, p. 638). Vaillancourt and colleagues (2013b) have also argued that depressed youth could be more “treat sensitive.” That is, these youth may select information from their environment that is consistent with their negative self-opinion. The idea that certain individuals may be more sensitive to environmental cues or make more hostile interpretation of ambiguous social data has been well documented in the literature (Crick and Dodge, 1994; Dodge, 1986). This work is consistent with studies showing that social information processing differs in children based on their experience with being bullied and that hypersensitivity can impact their interpretation of social behavior and their self-reports of subsequent incidents of being bullied (Camodeca et al., 2003; Smalley and Banerjee, 2013).
Most longitudinal studies to date are of relatively short duration (i.e., less than 2 years) and focus on a narrow developmental period such as childhood or adolescence (McDougall and Vaillancourt, 2015). Nevertheless, there are several recently published studies examining the long-term adult outcomes of childhood bullying. These studies indicate that being bullied does affect future mental health functioning, as reviewed in the following paragraphs.
5 Peer victimization was measured using peer, self-, and teacher reports, including peer nominations, a four-item self-report victimization scale, and a six-item teacher report victimization scale (Kochel et al., 2012).
Most long-term studies of childhood bullying have focused on links to internalizing problems in adulthood, demonstrating robust long-standing effects (Gibb et al., 2011; Olweus, 1993b; Sourander et al., 2007; Stapinski et al., 2014). For example, Bowes and colleagues (2015) examined depression in a large sample of participants who reported being the target of bullying at age 13 and found higher rates of depression at age 18 compared to peers who had not been bullied. Specifically, they reported that 14.8 percent of participants who reported being frequently bullied in childhood at age 13 were clinically depressed at age 18 (OR = 2.96, 95% CI [2.21, 3.97]) and that the population attributable fraction was 29.2 percent, suggesting that close to a third of the variance in depression could be explained by being bullied in childhood (Bowes et al., 2015).
In another longitudinal study using two large population-based cohorts from the United Kingdom (the ALSPAC Cohort) and the United States (the GSMS Cohort), Lereya and colleagues (2015) reported that the effects of childhood bullying on adult mental health were stronger in magnitude than the effects of being maltreated by a caregiver in childhood. Being bullied only (and not maltreated) placed individuals at higher risk for mental health difficulties than being maltreated only (and not bullied) (OR = 1.6, 95% CI [1.1, 2.2] for ALSPAC cohort; OR = 3.8, 95% CI [1.8, 7.9] for GSMS cohort). Children who were bullied were more likely than maltreated children to be anxious (OR = 4.9, 95% CI [2.0, 12.0] for GSMS cohort), depressed (OR = 1.7, 95% CI [1.1, 2.7] for ALSPAC cohort), and to engage in self-harming behavior (OR = 1.7, 95% CI [1.1-2.6] for ALSPAC cohort) in adulthood (Lereya et al., 2015).
Similarly, Stapinski and colleagues (2014) found that adolescents who experienced frequent peer victimization6 were two to three times more likely to develop an anxiety disorder 5 years later at age 18 than nonvictimized adolescents (OR = 2.49, 95% CI [1.62, 3.85]). The association remained after adjusting for potentially confounding individual and family factors and was not attributable to diagnostic overlap with depression. Frequently victimized adolescents were also more likely to develop multiple internalizing problems in adulthood (Stapinski et al., 2014). After controlling for childhood psychiatric problems or family hardship, Copeland and colleagues (2013) found that individuals who were bullied continued to have higher prevalence of generalized anxiety (OR = 2.7, 95% CI [1.1, 6.3]).
These findings suggest that being bullied and internalizing problems such as depression are mutually reinforcing, with the experience of one increasing the risk of the other in a harmful cycle that contributes to the
6Stapinski et al. (2014) used a modified version of the Bullying and Friendship Interview Schedule to assess self-reported peer victimization. This measure includes items on overt victimization, such as threats, physical violence, and relational victimization.
high stability of being both bullied and experiencing other internalizing problems. These studies also suggest that the long-term consequences of being bullied, which extend into adulthood, can be more severe than being maltreated as a child by a caregiver.
Alcohol and drug abuse and dependence have been associated with being bullied as a child (Radliff et al., 2012). A longitudinal study of adolescents found that those who reported being bullied were more likely to report use of alcohol, cigarettes, and inhalants 12 months later (Tharp-Taylor et al., 2009), compared to those who did not report being bullied. More longitudinal research that tracks children through adulthood is needed to fully understand the link between being bullied and substance abuse (see review by McDougall and Vaillancourt, 2015).
Several studies show links between being bullied and violence or crime, especially for men (Gibb et al., 2011; McGee et al., 2011; Sourander et al., 2007, 2011). A meta-analysis by Reijntjes and colleagues (2011) that included studies with data on 5,825 participants showed that after controlling for externalizing symptoms at baseline, peer victimization—under which they included being the target of teasing, deliberate exclusion, and being the target of physical threats and malicious gossip—was associated over time with exhibiting externalizing problems such as aggression, truancy, and delinquency (r = .14, 95% CI [.09, .19]). This research team also found that externalizing problems predicted changes in peer victimization over time (r = .13, 95% CI [.04, .21]) and concluded that there is a bidirectional relationship between peer victimization and externalizing problems.
Evidence from the broader research on childhood trauma and stress indicates that earlier adverse life experiences, such as child abuse, are associated with the development of psychotic symptoms later in life (Institute of Medicine and National Research Council, 2014b). Until recently, the association between bullying and psychotic symptoms has been understudied (van Dam et al., 2012). Two recent meta-analyses support the association between bullying and the development of psychotic symptoms later in life (Cunningham et al., 2015; van Dam et al., 2012). van Dam and colleagues (2012) conducted a meta-analysis of 14 studies to assess whether being bullied in childhood is related to the development of psychotic (either
clinical or nonclinical) symptoms. (Nonclinical psychotic symptoms7 place individuals at risk for the development of psychotic disorders (Cougnard et al., 2007).) Results from the analyses of studies that examined the association between bullying and nonclinical symptoms (six studies) were more definitive (adjusted OR = 2.3; 95% CI [1.5, 3.4]), with stronger associations when there was an increased frequency, severity, and persistence of bullying (Cougnard et al., 2007). Although some research has found this association, a recent longitudinal study from New Zealand found that the link between bullying and the development of psychosis later in life is likely not causal but instead reflects the fact that individuals who display disordered behaviors across childhood and adolescences are more likely to become bullying targets (Boden et al., 2016) An analysis of studies that examined the association between bullying and psychosis in clinical samples was inconclusive (van Dam et al., 2012).
A recent meta-analysis conducted by Cunningham and colleagues (2015) examined ten European prospective studies, four from the Avon Longitudinal Study of Parents and Children. This analysis found that individuals who were bullied were more than twice as likely to develop later psychotic symptoms, compared to those who were not bullied (OR = 2.1, 95% CI [1.1, 4.0]). These results were consistent in all but one of the studies included in the meta-analysis. More longitudinal research is needed to more fully understand the mechanisms through which trauma such as bullying may lead to the development of psychotic symptoms (Cunningham et al., 2015; van Dam et al., 2012). Importantly, this research will need to be prospective and examine the development of bullying and psychotic symptoms in order to truly identify the temporal priority. The inclusion criteria for the Cunningham and colleagues (2015) meta-analysis included that the study had to be prospective and had to include a measure of psychosis and that bullying needed to be reported before the age of 18. Although the authors stated that “bullying appears to cause later development of psychosis,” such a conclusion requires that mental health functioning be assessed early and over time, as it is possible that premorbid characteristics may make individuals targets for poor peer treatment (see Kochel et al., 2012; Vaillancourt et al., 2013b, regarding depression leading to peer victimization).
Academic Performance Consequences
A growing literature has documented that targets of bullying suffer diminished academic achievement whether measured by grades or standard-
7 Nonclinical psychotic symptoms are symptoms that do not meet the clinical definition for those psychotic disorders associated with such symptoms.
ized test scores (Espelage et al., 2013; Nakamoto and Schwartz, 2010). Cross-sectional research indicates that children who are bullied are at increased risk for poor academic achievement (Beran, 2009; Beran and Lupart, 2009; Beran et al., 2008; Glew et al., 2005; Neary and Joseph, 1994; see also meta-analysis by Nakamoto and Schwartz, 2010) and increased absenteeism (Juvonen et al., 2000; Kochenderfer and Ladd, 1996; Vaillancourt et al., 2013b).
The negative relation between being bullied and academic achievement is evident as early as kindergarten (Kochenderfer and Ladd, 1996) and continues into high school (Espinoza et al., 2013; Glew et al., 2008). In a 2-week daily diary study with ninth and tenth grade Latino students, Espinoza and colleagues (2013) reported that on days when adolescents’ reports of being bullied were greater than what was typical for them, they also reported more academic challenges such as doing poorly on a quiz, test, or homework and felt like less of a good student. Thus, even episodic encounters of being bullied can interfere with a student’s ability to concentrate on any given day. In a cross-sectional study of more than 5,000 students in grades 7, 9, and 11, Glew and colleagues (2008) found that for every 1-point increase in grade point average (GPA), the odds of being a child who was bullied (versus a bystander) decreased by 10 percent. However, due to the cross-sectional nature of this study, this association does not establish whether lower academic achievement among children who were bullied was a consequence of having been bullied.
Several short-term (one academic year) longitudinal studies indicate that being bullied predicts academic problems rather than academic problems predicting being a target of bullying (Kochenderfer and Ladd, 1996; Schwartz et al., 2005). Given the impairments in brain architecture associated with self-regulation and memory in animal models and the currently limited imaging data in human subjects, this is a reasonable inference, although reverse causation is possible. For instance, early life abuse and neglect impair these same abilities, lower self-esteem, and may make an individual more likely to be a target of bullying. In one of the few longitudinal studies to extend beyond one year, Juvonen and colleagues (2011) examined the relation between victimization8 and academic achievement across the three years of middle school. Academic adjustment was measured by both year-end grades and teacher reports of engagement. These authors found that more self-reported victimization was related to lower school achievement from sixth to eighth grade. For every 1-unit increase in victimization (on a 1-4 scale), GPA declined by 0.3 points.
8 Peer victimization was measured using a modified six-item version of the Peer Victimization Scale, which asks students to select a statement that is most like them. Higher scores indicated higher levels of peer victimization (Juvonen et al., 2011).
Other short-term longitudinal studies found similar results. For example, Nansel and colleagues (2003) found that being bullied in a given year (grade 6 or 7) predicted poor academic outcomes the following year, after controlling for prior school adjustment and if they were previously targets of bullying or not. Similarly, Schwartz and colleagues (2005) reported a negative association for third and fourth grade children between victimization9 and achievement 1 year later. In addition, Baly and colleagues (2014) found that the cumulative impact of being bullied over 3 years from sixth grade to eighth grade had a negative impact on GPA and standardized test scores.
However, other studies have not found such associations. For instance, Kochenderfer and Ladd (1996) found no relation between being bullied and subsequent academic achievement in their study of students assessed in the fall and spring of kindergarten, nor did Rueger and Jenkins (2014) in their study of seventh and eighth graders assessed in the fall and spring of one academic year. Feldman and colleagues (2014) also reported no association between being a target of bullying and academic achievement in their 5-year longitudinal study of youth ages 11-14. Poor academic performance can also be a predictor of peer victimization (Vaillancourt et al., 2013b). The authors found that poor writing performance in third grade predicted increased bullying behavior in fifth grade that was stable until the end of eighth grade.
The longitudinal associations between peer victimization and school attendance are also equivocal, with some showing positive associations (Baly et al., 2014; Buhs et al., 2006; Gastic, 2008; Kochenderfer and Ladd, 1996; Smith et al., 2004) and others not finding a statistically significant association (Forero et al., 1999; Glew et al., 2008; Rueger et al., 2011; Vaillancourt et al., 2013b).10
In summary, there have been a number of cross-sectional and longitudinal studies that have provided support for a relation between being bullied and increased risk for poor academic achievement. However, given the inconsistent results found with longitudinal studies, more research is warranted in this area to more fully ascertain the relation between being bullied and academic achievement over time.
10 Peer victimization is used here to include the broader category of bullying, peer victimization, and bullying behavior.
There is evidence that supports a finding that individuals who bully others have contradictory attributes (Institute of Medicine and National Research Council, 2014a; Vaillancourt et al., 2010b). Research suggests that there are children and adolescents who bully others because they have some form of maladjustment (Olweus, 1993a) or, as mentioned in Chapter 3, are motivated by establishing their status in a social network (Faris and Ennett, 2012; Rodkin et al., 2015; Sijtsema et al., 2009; Vaillancourt et al., 2003). Consequently, the relation between bullying, being bullied, acceptance, and rejection is complex (Veenstra et al., 2010). This complexity is also linked to a stereotype held by the general public about individuals who bully. This stereotype casts children and youth who bully others as being high on psychopathology, low on social skills, and possessing few assets and competencies that the peer group values (Vaillancourt et al., 2010b). Although some occurrence of this “stereotypical bully” or “classic bully” is supported by research (Kumpulainen et al., 2001; Olweus, 1993a; Sourander et al., 2007), when researchers consider social status in relation to perpetration of bullying behavior, a different profile emerges. These studies suggest that most children and youth who bully others wield considerable power within their peer network and that high-status perpetrators tend to be perceived by peers as being popular, socially skilled, and leaders (de Bruyn et al., 2010; Dijkstra et al., 2008; Peeters et al., 2010; Thunfors and Cornell, 2008; Vaillancourt et al., 2003). High-status bullies have also been found to rank high on assets and competencies that the peer group values such as being attractive or being good athletes (Farmer et al., 2003; Vaillancourt et al., 2003); they have also been found to rank low on psychopathology and to use aggression instrumentally to achieve and maintain hegemony (for reviews, see Rodkin et al., 2015, and Vaillancourt et al., 2010b). Considering these findings of contrasting characteristics of perpetrators of bullying behavior, it makes sense that the research on outcomes of perpetrating is mixed. Unfortunately, most research on the short- and long-term outcomes of perpetrating bullying behavior has not taken into account this heterogeneity when considering the impact to children and youth who have bullied their peers.
Findings from cross-sectional studies that reported data on individuals who bullied others have shown that these individuals are at risk of developing psychosomatic problems (Gini, 2008; Srabstein et al., 2006). Gini and Pozzoli (2009) conducted a meta-analysis to test whether children involved in bullying behavior in any role are at risk for psychosomatic
problems. They included studies (n = 11) that examined the association between bullying involvement and psychosomatic complaints in children and adolescents between the ages of 7 and 16. The studies included in the meta-analysis used self-report questionnaires; reports from peers, parents, or teachers; and clinical interviews that resulted in a clinical rating of the subject’s behaviors and health problems. The included studies also had enough information to calculate effect sizes. An analysis of six studies that met the selection criteria revealed that children who bully had a higher risk (OR = 1.65, 95% CI [1.34, 2.04]) of exhibiting psychosomatic problems than their uninvolved peers.
This meta-analysis was limited because of its inclusion of cross-sectional and observational studies. Such studies do not allow firm conclusions on cause and effect; hence, the association between bullying perpetration and psychosomatic problems may be difficult to interpret. The methodologies used in the studies make them susceptible to bias and misclassification due to the reluctance of individuals who bully to identify themselves as perpetrators of bullying behavior. Also, the different forms of victimization included in the underlying studies were not reported in this meta-analysis. Additional research is needed to examine the involvement in perpetrating bullying behavior and its short- and long-term psychosomatic consequences.
Using a population-based cohort study, Wolke and colleagues (2014) examined whether bullying perpetration and being a target of bullying in elementary school predicted psychotic experiences11 in adolescence. The authors assessed 4,720 individuals between the ages of 8 and 11 who were involved in bullying either as perpetrators or targets. At age 18, suspected or definite psychotic experiences were assessed using semistructured interviews. After controlling for the child’s gender, intelligence quotient at age 8, and childhood behavioral and emotional problems, the researchers found that both individuals who are bullied (child report at age 10: OR = 2.4, 95% CI [1.6, 3.4]; mother report: OR = 1.6, 95% CI [1.1, 2.3]) and individuals who bullied others (child report at age 10: OR = 4.9, 95% CI [1.3, 17.7]; mother report: OR = 1.2, 95% CI [0.46, 3.1]) had a higher prevalence of psychotic experiences at age 18. The authors concluded that “involvement in any role in bullying may increase the risk of developing psychotic experiences in adolescence” (Wolke et al., 2014, p. 2208).
In summary, several studies have focused on the consequences of bully-
11 Psychotic experiences included hallucinations (visual and auditory), delusions (spied on, persecution, thoughts read, reference, control, grandiosity), and experiences of thought interference (broadcasting, insertion, and withdrawal), and any unspecified delusions.
ing for individuals who are bullied and have also reported more broadly on consequences for perpetrators of aggressive behavior (see Gini and Pozzoli, 2009; Lereya et al., 2015; Reijntjes et al., 2010; Ttofi et al., 2011), but the consequences of bullying involvement for individuals who perpetrate bullying behavior have been rarely studied to date. That is, although there is a rich literature on aggressors and the outcomes of being aggressive, there are few studies examining bullying perpetration specifically, taking into account the power imbalance, repetition, and intentionality that differentiates aggression from bullying from other forms of peer aggression. As discussed in Chapter 2, the available research on the prevalence of bullying behavior focuses almost entirely on the children who are bullied. More research, in particular longitudinal research, is needed to understand the short- and long-term physical health, psychosocial, and academic consequences of bullying involvement on the individuals who have a pattern of bullying others, when those individuals are distinguished from children who engage in general aggressive behavior.
Individuals who bully and are also bullied experience a particular combination of consequences that both children who are only perpetrators and children who are only targets also experience, such as comorbidity of both externalizing and internalizing problems, negative perception of self and others, poor social skills, and rejection by the peer group. However, at the same time this combination of roles in bullying is negatively influenced by the peers with whom they are interacting (Cook et al., 2010). After controlling for adjustment problems existing prior to incidents of bullying others or being bullied, a nationally representative cohort study found that young children who have been both perpetrators and targets of bullying tended to develop more pervasive and severe psychological and behavioral outcomes than individuals who were only bullied (Arseneault et al., 2006).
Adolescents who were involved in cyberbullying as both perpetrators and targets have been found to be most at risk for negative mental and physical health consequences, compared to those who were only perpetrators, those who were only targets, or those who only witnessed bullying (Kowalski and Limber, 2013; Nixon, 2014). For example, the results from a study by Kowalski and Limber (2013) that examined the relation between children’s and adolescents’ experiences with cyberbullying or traditional bullying and outcomes of psychological health, physical health, and academic performance showed that students who were both perpetrators and targets had the most negative scores on most measures of psychological health, physical health, and academic performance, when compared to
those who were only perpetrators, only targets, or only witnesses of bullying incidents.
Physical Health Consequences
Wolke and colleagues (2001) examined the association of direct and relational bullying experience with common health problems and found that students ages 6-9 who bullied others and were also bullied by others had more physical health symptoms than children who were only perpetrators or were not involved in bullying behavior. Hunter and colleagues (2014) evaluated whether adolescents who were involved in bullying experienced sleep difficulties more than adolescents who were not involved. They analyzed surveys that were originally collected on behalf of the UK National Health Service and had been completed by adolescents ages 11-17. Controlling for gender, school-stage, socioeconomic status, ethnicity, and other factors known to be associated with sleep difficulties—alcohol consumption, tea or coffee consumption, and illegal drug use—the authors found that individuals who were both perpetrators and targets in bullying incidents were almost three times more likely (OR = 2.90, 95% CI [1.17, 4.92]) to experience these sleep difficulties, compared to uninvolved young people. Additional research is needed to identify the mechanisms underlying short- and long-term physical health outcomes of individuals who bully and are also bullied.
There is evidence that individuals who are both perpetrators and targets of bullying have the poorest psychosocial profile among individuals with any involvement in bullying behavior; their psychosocial maladjustment, peer relationships, and health problems are similar to individuals who are only bullied, while their school bonding and substance use is similar to individuals who are only perpetrators (Graham et al., 2006; Nansel et al., 2001, 2004). Individuals who both bully and are also bullied by others experience a greater variety of both internalizing and externalizing symptoms than those who only bully or those who are only bullied (Kim et al., 2006).
Some meta-analyses have examined the association between involvement in bullying and internalizing problems in the school-age population and concluded that that individuals who are both perpetrators and targets of bullying had a significantly higher risk for psychosomatic problems than individuals who were only perpetrators or who were only targets (Gini
and Pozzoli, 2009; Reijntjes et al., 2010). In their meta-analysis, Gini and Pozzoli (2009) reviewed studies that examined the association between involvement in bullying and psychosomatic complaints in children and adolescents. Analysis of a subgroup of studies (N = 5) that reported analyses for individuals who bully and are also bullied by others showed that these individuals have a significantly higher risk for psychosomatic problems than uninvolved peers (OR = 2.22, 95% CI [1.77, 2.77]).
Studies suggest that individuals who bully and who are also bullied by others are especially at risk for suicidal ideation and behavior, due to increased mental health problems (see Holt et al., 2015, and Box 4-1).
Similar to individuals who bully, individuals who bully and are also bullied by others often demonstrate heightened aggression compared with non-involved peers. Compared to these other groups, they are by far the most socially ostracized by their peers, most likely to display conduct problems, and least engaged in school, compared with those who are either just perpetrators or just targets; they also report elevated levels of depression and loneliness (Juvonen et al., 2003). Additional research is needed that examines the unique consequences of those children and youth characterized as “bully-victims” because often they are not separated out from “pure victims” (those who are bullied only) in studies. School shootings are a violent externalizing behavior that has been associated with consequences of bullying behavior in the popular media (see Box 4-2 for additional detail).
Several studies have examined the associations between bullying involvement in adolescence and mental health problems in adulthood and have found that individuals who have bullied others and have also been bullied had increased risk of high levels of critical symptoms of psychosis compared to non-involved peers (Gini, 2008; Sigurdson et al., 2015). Research is limited in this area, and the topic warrants further investigation.
Bullying cannot be viewed as an isolated phenomenon; it is intertwined within the particular peer ecology that emerges, an ecology constituted of social processes that serve particular functions for the individual and for the group (Rodkin, 2004). Bullying frequently occurs in the presence of children and youth who are bystanders or witnesses. Research indicates that
bullying can have significant adverse effects on these bystanders (Polanin et al., 2012).
Bystanders have reported feelings of anxiety and insecurity (Rigby and Slee, 1993) which stemmed, in part, from fears of retaliation (Musher-Eizenman et al., 2004) and which often prevented bystanders from seeking help (Unnever and Cornell, 2003). In a study to explore the impact of bullying on the mental health of students who witness it, Rivers and colleagues (2009) surveyed 2,002 students, ages 12-16 and attending 14 schools in the United Kingdom, using a questionnaire that included measures of bullying at school, substance abuse, and mental health risk. They found that witnessing bullying significantly predicted elevated mental health risks even after controlling for the effect of also being a perpetrator or victim (range of = .07 to .15). They also found that being a witness to the bullying predicted elevated levels (= .06) of substance use. Rivers and Noret (2013) found
that, compared to students who were not involved in bullying, those who observed bullying reported more symptoms of interpersonal sensitivity (e.g., feelings of being hurt or inferior), helplessness, and potential suicide ideation.
In conclusion, there is very limited research available on the consequences of witnessing bullying for those children and youth who are the bystanders. Studies of bystander behavior have traditionally sought to understand their motives for participation in bullying (Salmivalli, 2010), their roles (Lodge and Frydenberg, 2005; Salmivalli et al., 1996), their behavior (either reinforcing the bully or defending the victim) in bullying situations (Salmivalli et al., 2011), and why observers intervene or do not intervene (Thornberg et al., 2012) from a social dynamic perspective, without exploring the emotional and psychological impact of witnessing bullying. More research is needed to understand these consequences.
One subpopulation of school-aged youth that may be at increased risk for detrimental short- and long-term outcomes associated with bullying victimization is poly-victims. Finkelhor and colleagues (2007) coined the terms “poly-victim” and “poly-victimization” to represent a subset of youth who experience multiple victimizations of different kinds—such as exposure to (1) violent and property crimes (e.g., assault, sexual assault, theft, burglary), (2) child welfare violations (child abuse, family abduction), (3) the violence of warfare and civil disturbances, and (4) being targets of bullying behavior—and who manifest high levels of traumatic symptomatology. The identification of a poly-victim is grounded not only in the frequency of the victimization but also in victimization across multiple contexts and perpetrators (Finkelhor et al., 2007, 2009).
Ford and colleagues (2010) determined that poly-victims were more likely to meet criteria for psychiatric disorder, including being two times more likely to report depressive symptoms, three times more likely to report posttraumatic stress disorder, up to five times more likely to use alcohol or drugs, and up to eight times more likely to have comorbid disorders, compared to youth that did not meet criteria for poly-victimization. Poly-victims often engaged in delinquent behavior, associated with deviant peers (Ford et al., 2010), and were entrenched within the juvenile justice system (Ford et al., 2013). Students who were poly-victims in the juvenile justice system reported higher levels of traumatic symptomatology (Finkelhor et al., 2005). However, it is currently unclear whether being bullied plays a major or minor role in poly-victimization.
In the following sections, the committee describes five potential mechanisms for the psychological effects of bullying behavior for both the children who are bullied and children who bully. These include self-blame, social cognition, emotional dysregulation, genetic predisposition to mental health outcomes and bullying, and telomere erosion.13
13 A telomere is the “segment at the end of each chromosome arm which consists of a series of repeated DNA sequences that regulate chromosomal replication at each cell division.” See http://ghr.nlm.nih.gov/glossary=telomere [December 2015]. Telomeres are associated with “chromosomal stability” and the regulation of “cells’ cellular replicative lifespan” (Kiecolt-Glaser et al., 2011, p. 16).
One important mechanism for the psychological effects of bullying is how the targets of bullying construe the reason for their plight (Graham, 2006). For example, a history of bullying and the perception of being singled out as a target might lead an individual to ask “Why me?” In the absence of disconfirming evidence, some might come to blame themselves for their peer relationship problems. Self-blame and accompanying negative affect can then lead to many negative outcomes, including low self-esteem, anxiety, and depression (Graham and Juvonen, 1998).
The adult rape literature (another form of victimization) highlights a correlation between experiencing rape and self-attributions that imply personal deservingness, labeled characterological self-blame, since they may lead to the person thinking of themselves as chronic victims (Janoff-Bulman, 1979). From an attributional perspective, characterological self-blame is internal and therefore reflects on the self; it is stable and therefore leads to an expectation that harassment will be chronic; and it is uncontrollable, suggesting an inability to prevent future harassment. Attributing negative outcomes to internal, stable, and uncontrollable causes leads individuals to feel both hopeless and helpless (Weiner, 1986). In contrast, behavioral self-blame (e.g., “I was in the wrong place at the wrong time”) implies a cause that is both unstable (the harassment is not expected to occur again) and controllable (there are responses in one’s repertoire to prevent future harassment). Several researchers in the adult literature have documented that individuals who make characterological self-blaming attributions for negative outcomes cope more poorly, feel worse about themselves, and are more depressed than individuals who make attributions to their behavior (see Anderson et al., 1994). Research with early adolescents also revealed that characterological self-blame for academic and social failure resulted in heightened depression (Cole et al., 1996; Tilghman-Osborne et al., 2008).
In the first attribution study focused specifically on bullying, Graham and Juvonen (1998) documented that sixth grade students with reputations as targets made more characterological self-blaming attributions for harassment than behavioral self-blaming attributions. Characterological self-blame, in turn, partly mediated the relationship between victim status and psychological maladjustment as measured by depression and social anxiety. Many studies since then have documented the relation between being targets of bullying, characterological self-blame, and maladjustment (Graham et al., 2006, 2009; Perren et al., 2012; Prinstein et al., 2005). Furthermore, bullied youth who endorsed characterological self-blame were likely to develop negative expectations about the future, which may also increase risk for continued bullying. For example, Schacter and colleagues (2014) reported that characterological self-blame endorsed in the fall of
sixth grade predicted increases in reports of being bullied in the spring of sixth grade. Self-blame can then instigate psychological distress over time as well as increases in experiences of being bullied.
Such findings have implications for interventions targeted at bullied youth. The goal would be to change targets’ maladaptive thoughts about the causes of their plight. For example, one could seek more adaptive attributions that could replace characterological self-blame. In some cases, change efforts might target behavioral explanations for being bullied (e.g., “I was in the wrong place at the wrong time”). In such cases, the goal would be to help targeted youth recognize that they have responses in their repertoire to prevent future encounters with harassing peers—that is, the cause is unstable and controllable (Graham and Bellmore, 2007). External attributions also can be adaptive because they protect self-esteem (Weiner, 1986). Knowing that others are also victims or that there are some aggressive youth who randomly single out unsuspecting targets can help lessen the tendency to self-blame (Graham and Bellmore, 2007; Nishina and Juvonen, 2005). This approach of altering dysfunctional thoughts about oneself to produce changes in affect and behavior has produced a rich empirical literature on attribution therapy in educational and clinical settings (see Wilson et al., 2002). The guiding assumption of that research can be applied to alleviating the plight of targets of bullying.
The most commonly cited models of social cognitive processes often connect back to work by Bandura (1973), as well as to more recent conceptualizations by Crick and Dodge (1994). These models have been applied to understanding aggressive behavior, but there has been less research applying these models to bullying behavior specifically. Related research by Anderson and Bushman (2002) on their general aggression model allows for a more focused understanding of the thoughts, feelings, and behaviors that contribute to the development of the negative outcome. This framework characterizes the inputs, the routes, the proximal processes, and the outcomes associated with aggressive behavior and either being targeted by or perpetrating bullying behavior (Kowalski and Limber, 2013; Vannucci et al., 2012). Although these theories pertain to aggressive behavior more broadly, given that bullying is considered by most researchers to be a specific form of aggressive behavior, these broader theories may also improve understanding of the etiology and development of bullying. For example, research on hostile attribution bias suggests that aggressive youth are particularly sensitive to ambiguous and potentially hostile peer behaviors. Similar hypersensitivity to threat is also likely present in youth who bully.
Another particular element of social cognitive processes that has been
linked with aggressive behavior is normative beliefs about aggressive retaliation (Crick and Dodge, 1994; Huesmann and Guerra, 1997). Such beliefs include the belief that aggressive retaliation is normative, acceptable, or justified, given the context of provocation. There has been exploration of links between these beliefs and both reactive and proactive aggression. However, there has been relatively limited research specifically focused on bullying behavior. Yet, the available literature suggests that although it may seem as if targets of bullying would most likely endorse such attitudes, it is the perpetrators of bullying, including those who are involved in bullying as both a perpetrator and a target, who are mostly likely to support aggressive retaliation (Bradshaw et al., 2009, 2013; O’Brennan et al., 2009).
Attempts to identify mechanisms linking bullying to adverse outcomes have largely focused on social-cognitive processes (Dodge et al., 1990) as described above. More recently, researchers have begun to examine emotion dysregulation as an additional mechanism that explains associations between peer victimization and adverse outcomes. Emotion regulation refers to the strategies that people use to “increase, maintain, or decrease one or more components of an emotional response” (Gross, 2001, p. 215). One’s choices among such strategies have implications not only for how robustly one responds to a stressor but also for how quickly one can recover from a stressful experience. Several studies have shown that emotion regulation difficulties—also called emotion dysregulation—increase youths’ risk of exposure to peer victimization (Hanish et al., 200414) and to bullying (Mahady Wilton et al., 2000). However, it is important to understand whether peer victimization itself causes emotion regulation difficulties, which in turn predict the adverse outcomes that result from peer victimization (e.g., depression, aggressive behaviors).
Several lines of evidence support the hypothesis that emotion dysregulation may account for the relationship between peer victimization and adverse outcomes among adolescents. First, constructs that are related to peer victimization—including social exclusion (Baumeister et al., 2005) and stigma (Inzlicht et al., 2006)—impair self-regulation. Second, chronic stress during childhood and adolescence leads to deficits in emotion regulation (Repetti et al., 2002). Bullying has been conceptualized as a chronic stressor for children who are the perpetrators and the targets (Swearer and Hymel, 2015), which in turn may disrupt emotion regulation processes. Third, laboratory-based studies have indicated that peer victimization is associated
with emotion dysregulation (e.g., self-directed negative emotion, emotional arousal and reactivity) in the context of a novel peer interaction (Rudolph et al., 2009) and in a contrived play-group procedure (Schwartz et al., 1993). Over time, the effort required to manage the increased arousal and negative affect associated with peer victimization15 may eventually diminish individuals’ coping resources and therefore their ability to understand and adaptively manage their emotions, leaving them more vulnerable to adverse outcomes (McLaughlin et al., 2009).
Several studies have provided empirical support for emotion dysregulation as a mediator of the association between peer victimization and adverse outcomes among adolescents. In one of the first longitudinal demonstrations of mediation, McLaughlin and colleagues (2009), using data from a large, prospective study of adolescents (ages 11-14), showed that peer victimization at baseline predicted increases in emotion dysregulation four months later, controlling for initial levels of emotion dysregulation. In turn, emotion dysregulation predicted subsequent psychological distress (depressive and anxious symptoms), thereby mediating the prospective relationship between peer victimization (relational and reputational forms) and internalizing symptoms (McLaughlin et al., 2009). Subsequent research from this same sample of adolescents showed that emotion dysregulation also mediated the prospective relationship between peer victimization and subsequent aggressive behavior (Herts et al., 2012).
There is also emerging evidence that emotion regulation mediates relationships between bullying and adverse outcomes. In one example of this work, Cosma et al. (2012) examined associations between bullying and several emotion regulation strategies, including rumination, catastrophizing, and other-blaming, in a sample of adolescents. Although bullying was predictive for each of these emotion regulation strategies, only one (catastrophizing) mediated the relationship between being a target of bullying and subsequent emotional problems. Thus, while more research is needed, existing evidence suggests that both social-cognitive and emotion regulation processes may be important targets for preventive interventions among youths exposed to peer victimization and bullying.
Genetic Predisposition to Mental Health Outcomes and Bullying
Longitudinal research suggests that being the victim or perpetrator of bullying does not lead to the same pathological or nonpathological outcomes in every person (McDougall and Vaillancourt, 2015). There are many factors that contribute to how a person responds to the experience
of being victimized, with very strong links already established with life experiences, as reviewed above. Most studies examining heterogeneity in outcomes associated with bullying have focused on environmental characteristics, such as individual, family, and school-level features to explain why some individuals fare better or worse when involved with bullying (Vaillancourt et al., in press). For example, the moderating role of the family has been examined with results indicating that bullied children and youth with better home environments tend to fare better than those living with more complicated families (Flouri and Buchanan, 2003; also see Chapter 3 of this report). Far fewer studies have examined the role of potential genetic influences as mediators between life experiences such as bullying and mental health outcomes. Identifying potential genetic influences is critical for improving understanding of the rich behavioral and epidemiological data already gathered. At the present time, evidence-based understanding of physiology and neuroscience is very limited, and insufficient data have been gathered to produce informed hypothesis testing.
There is a growing body of literature examining the relative role of genes’ interaction with the environment in relation to experiences with trauma. However, there are fewer studies exploring potential relations between genes and being the target or perpetrator of bullying. At first glance these studies may appear to suggest that a person’s involvement with bullying is predetermined based on his/her genetic profile. Yet, it is important to bear in mind that heritable factors are also associated with specific environments—meaning it is difficult to separate genetic effects from environmental effects. This is a phenomenon termed gene-environment correlations, abbreviated as rGE (Brendgen, 2012; Plomin et al., 1977; Scarr and McCartney, 1983). For example, aggression, which is highly heritable (Niv et al., 2013), can be linked to the selection of environments in different ways (for review, see Brendgen, 2012). Aggressive children may choose friends who are similar in their genetically influenced behavioral characteristic of being aggressive, and this type of selection influences the characteristics of their peer group (Brendgen, 2012, p. 420). This is an example of selective rGE. A child’s genetically influenced characteristic to be aggressive can also produce a negative reaction from others, such as being disliked. This environmental variable of being rejected now “becomes correlated with the aggressive genotype” (Brendgen, 2012, p. 421). This is an example of evocative rGE. Another way that a person’s genetic predisposition can be correlated with their environment is through a more passive process, called a passive rGE (Brendgen, 2012). For example, aggressive parents may be more likely to live in high-crime neighborhoods, which influence the probability that their child will be associating with antisocial peers. These important rGE processes and confounds of interaction notwithstanding, it is worth mentioning that the research on the genetics of being a target or perpetrator of bullying
is still in its infancy, and caution is needed when evaluating the results, as replication is much needed in this area. Before considering these studies, the committee first reviews the concept of how genetic differences influence behavior because it is important to clarify new concepts in this burgeoning area of science (see Box 4-3).
With this backdrop in mind, the committee focused on twin studies of familial (family environment) versus genetic influence, gene by environment interaction, and a newer area of inquiry, epigenetics: the study of cellular
and physiological phenotypic trait variations caused by external or environmental factors.
Twin studies are routinely used to examine the relative influence of genetics and the environment on a particular phenomenon, such as being the target or perpetrator of bullying. In these studies, the causes of phenotypic variation (for example the variation in being a target or perpetrator of bullying) is separated into three components: (1) the additive genetic component or the heritable factor; (2) the shared environment component or the aspect of the environment twins share such as poor family functioning; and (3) the nonshared environment component or the aspect of the environment that is unique to each twin, such as the classroom if twins are in different classes.
Studies that decompose the unique effects of the environment and genetics on bullying behavior are best illustrated by two examples. Using data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a study of high-risk16 British twins reared together and apart, Ball and colleagues (2008) examined children’s involvement in bullying and the genetic versus environmental contributions associated with their involvement. The twins in this study were assessed at ages 7 and 10 on their experiences with bullying, using teacher and parent reports. Results indicated that 73 percent of the variation in being the target of bullying and 61 percent of the variation in bullying perpetration were accounted for by genetic factors. In another study of Canadian twins reared together and assessed at age 7, using teacher and peer reports to assess peer victimization and aggression, Brendgen and colleagues (2008) found that for girls, 60 percent of the variation in aggression was accounted for by genetic factors and for boys, the variation estimate was 66 percent. For peer victimization, the Canadian study found that genetics did not play a role in the prediction of being targeted by peers. In fact, almost all of the variance was accounted for by environmental factors—29 percent of the variance in peer victimization was from the shared environment and 71 percent from the nonshared environment. The authors concluded that “genetic modeling showed that peer victimization is an environmentally driven variable that is unrelated to children’s genetic disposition” (Brendgen et al., 2008, p. 455).
These two studies address the role genetics might play in the expression of aggressive behavior but conflict on the heritability of being a target of bullying. Most studies examining the heritability of externalizing problems,
which includes studies on perpetrating aggression and bullying, report high heritability estimates. In fact, a recent meta-analysis found that aggression and rule-breaking were highly influenced by genetics, estimating the heritability rate at 41 percent (Niv et al., 2013). Moreover, studies have found that the heritability estimates tend to be higher for more serious forms of antisocial behavior. For example, the heritability of psychopathy in 7-year-old British twin children reared together and apart and studied in the Twins Early Development Study was reported to be 81 percent (Viding et al., 2005). However, estimates of the heritability of peer victimization vary across studies, as illustrated by the above results from Ball and colleagues (2008) contrasted with those from Brendgen and colleagues (2008), and even within studies (Brendgen et al., 2008, 2013).
Brendgen and colleagues have since revised their assessment about the role genetics play in the prediction of being the target of bullying. In a more recent study, following the same children highlighted in the 2008 paper (Brendgen et al., 2008) across three assessment periods (kindergarten, grade 1, and grade 4), Boivin and colleagues (2013) reported that at each grade, among twins who were reared together and apart, genetic factors accounted for a notable percentage of the variance in children’s difficulties with peers. Peer difficulties were assessed as a latent factor derived from self-, teacher-, and peer-reports of peer victimization17 and peer rejection. Specifically, in kindergarten and grade 1, 73 percent of the variance was accounted by genetic factors and in grade 4, genetic factors account for 94 percent of the variance in peer rejection and victimization.
There are several reasons for discrepancies between and within studies of the genetic contribution to bullying behavior. One reason is related to how peer victimization is assessed. Parent-, teacher-, peer-, and self-reports of bullying victimization have been shown to vary considerably across reporters (Ostrov and Kamper, 2015; Patton et al., 2015; Shakoor et al., 2011); thus, the method used to assess involvement with bullying may lead to different results. Another reason for the differences may be related to development. The influence of the environment is expected to change as children age. Young children are particularly sensitive to family influences, while the influence of peers tends to matter more during adolescence (Harris, 1995). Moreover, the type of environment a person is exposed to (i.e., harsh or nurturing) interacts with genes to produce a brain that is tailored to deal with the particular demands of that environment.
Taken together, the genetic studies reviewed suggest that aggression, which characterizes the perpetrator role in bullying (Vaillancourt et al.,
17 Peer victimization was assessed through teacher, peer, and self-ratings. Children were asked to circle photographs of two classmates who get called names by other children and who are often pushed or hit by other children.
2008), might have heritable components, but the findings on being the target of bullying or other aggressive behavior are mixed. Thus, the role of genetic influences on both perpetrating and being a target of bullying requires more empirical attention before conclusions can be drawn.
Researchers also question whether specific genotypic markers of vulnerability (e.g., candidate genes) influence developmental outcomes in the face of adversity (i.e., environment). Importantly, there is some indication that genetics influences the mental health issues related to bullying highlighted above, such as depression and heightened aggression. For example, in gene-environment studies, candidate genes have been examined as moderators of the exposure to a toxic stressor such as child maltreatment and health outcomes such as depression. When the body experiences repeated bouts of stress that fail to resolve quickly, the heightened state of vigilance and preparedness depletes it of resources and the stress hormone cortisol begins to produce adverse effects. Specifically, prolonged stress disrupts brain functions and results in compromised decision making, faulty cognitive assessment, compromised learning and memory, and a heightened sense of threat that alters behavior (Lupien et al., 2005; McEwen, 2014). There is evidence that the impact of changes in cortisol (either too high or too low) on learning may contribute, in part, to bullied children’s decline in academic performance (Vaillancourt et al., 2011), overeating/metabolic disorder, or emotional dysregulation, but this research is relatively new and needs to be explicitly explored within the context of bullying (McEwen, 2014).
A paradigmatic example of this type of study is one by Caspi and colleagues (2003), in which the moderating role of a functional polymorphism in the promoter region of the serotonin transporter gene 5-HTTLPR was examined in relation to exposure to maltreatment in childhood and depression in adulthood. Results indicated that depression rates were far greater among abused individuals if they had two copies of the short allele.18 Among individuals with a long allele, depression rates were lower, suggesting that the long allele was protective, while the short allele was a risk factor for depression in the face of adversity. Although the exact role of this serotonin-related gene has been a subject of controversy, a meta-analysis concluded that overall, the results are consistent across studies (Karg et al., 2011). Nevertheless, skepticism and controversy remain regarding studies of gene-environment interactions (Dick et al., 2015; Duncan, 2013; Duncan and Keller, 2011; Duncan et al., 2014). This important debate notwith-
18 An allele is an alternate form of the same gene. Except for the XY chromosomes in males, human chromosomes are paired, so a cell’s genome usually has two alleles for each gene.
standing, there is evidence that variations in genotype might moderate the relation between exposure to being bullied and health outcomes. For example, Sugden and colleagues (2010) found that bullied children who carried two short versions of the 5-HTTLPR gene were more likely to develop emotional problems than bullied children who carried the long allele. Importantly, this moderating effect was present even when pre-victimization emotional problems were accounted for statistically. In addition to this study, three other studies have demonstrated the moderating effect of the 5-HTTLPR gene in the bullying-health link (Banny et al., 2013; Benjet et al., 2010; Iyer et al., 2013), with depression being worse for carriers of the short/short genotype (both alleles are the short version) than carriers of the short/long and long/long genotypes.
Although the evidence suggests that genotypes moderate the relation between being a target of bullying and poorer mental health functioning like depression, it is important to acknowledge that this relation is more complex. Indeed, some individuals may be particularly biologically sensitive to negative environmental influences such as being bullied, but this genetic vulnerability can also be linked to better outcomes in the context of a more supportive and enriched environment (see Vaillancourt et al., in press). This phenomenon is termed differential susceptibility (Belsky and Pluess, 2009; Boyce and Ellis, 2005). For example, in their study of 5 and 6-year old children, Obradovic and colleagues (2010) found that high stress reactivity as measured using respiratory sinus arrhythmia and salivary cortisol was linked to poorer socioemotional behavior in the context of being in an environment that was high in family adversity. In a context characterized by lower adversity, high stress-reactive children had more adaptive outcomes.
To the committee’s knowledge, there are no studies that have examined bullying perpetration in relation to serotonin transporter polymorphisms, although there are studies that have examined this polymorphism in aggressive and non-aggressive children. For example, Beitchman et al. (2006) examined 5-HTTLPR in clinically referred children between the ages of 5 and 15 and found a positive association between the short/short genotype and aggression. In other studies, the short allele has been associated with problems with impulse control that includes the use of aggression (Retz et al., 2004).
The moderating role of different candidate genes has also been examined in relation to exposure to childhood adversity and poorer developmental outcomes (see review by Vaillancourt et al., in press). With respect to bullying, only a few studies have examined gene-environment interactions. In one study by Whelan and colleagues (2014), harsh parenting was associated with increased peer victimization and perpetration, but this effect was
not moderated by the Monoamine Oxidase A (MAOA) genotype.19 In another longitudinal study, Kretschmer and colleagues (2013) found that carriers of the 4-repeat homozygous variant of the dopamine receptor D4 gene were more susceptible to the effects of peer victimization20 on delinquency later in adolescence than noncarriers of this allele. Finally, in a large sample of post-institutionalized children from 25 countries, VanZomeren-Dohm and colleagues (2015) examined the moderating role of FKBP5 rs136078021 in the relation between peer victimization22 and depression symptoms. In this study, gender was also found to be a moderator. Specifically, girls who had the minor genotype (TT or CT) were more depressed at higher levels of peer victimization, but less depressed at lower level of peer victimization than girls who had CC genotype. For boys, the CC genotype was associated with more symptoms of depression than girls with the same CC genotype who had been bullied.
It is clear that genetics influences how experiences contribute to mental and physical well-being, although the specifics of these gene-environment interactions are complex and not completely understood. Even though genes appear to modulate humans’ response to being a target or a perpetrator of bullying behavior, it is still unclear what aspects of these experiences are interacting with genes and which genes are implicated to produce the variability in outcomes. Human genes and environment interact in a very complex manner: what biological events a particular gene influences can change at different stages of development. That gene therefore interacts with the environment in unique ways across the development timeline. These gene-environment interactions can be subtle and are under constant flux (Lake and Chan, 2015). Knowing both the genes involved and the specific environment conditions is critically important to understanding these interactions; a simplistic view of either the genetic or environmental component, especially when considered in isolation from the behavioral literature, is unlikely to be productive.
22VanZomeren-Dohm and colleagues (2015 measured peer victimization using the MacArthur Health and Behavior Questionnaire Parent-Form, version 2.1, in which parents reported on their children’s experiences of overt peer victimization.
It is clear from the research reviewed here that there are a variety of pathways leading to adaptive and maladaptive endpoints and that these pathways can also vary within the “system” along with other conditions and attributes (McDougall and Vaillancourt, 2015, p. 300), including a person’s genetic susceptibility. In this section, the committee focuses on studies examining how genetic susceptibility can make certain individuals more sensitive to negative environmental influences.
Although a person’s DNA is fixed at conception (i.e., nonmalleable), environment can have a strong effect on how some genes are used at each of the stages of development. One way such changes in gene use and expression can occur is through an epigenetic effect, in which environmental events alter the portions of the genome that control when gene replication is turned on or off and what parts of a gene get transcribed (McGowan et al., 2009; Roth, 2014). That is, while an individual’s genetic information is critically important, the environment can help to increase or decrease how some genetic information is used by indirectly turning on or off some genes based on input received by somatic cells from the environment. Such epigenetic alterations have been empirically validated in several animal studies. For example, in one line of epigenetic studies, infant rat pups are raised with either low- or high-nurturing mothers or with mothers that treated the pups harshly. The researchers found that the type of maternal care received in infancy had a notable effect on the rats’ subsequent ability to deal with stress (McGowan et al., 2011; Roth and Sweatt, 2011; Weaver et al., 2004). The behavioral effects were correlated with changes in DNA methylation.23 Epigenetic changes associated with gene-environment interactions is a new and exciting research area that provide a direct link between how our genes are read and is thought to enable us to pass our experiences to the next generations. It is helpful to think of genes as books in a library and epigenetics as placing a barrier in front of a book to decrease the chances it is read or providing easy access to the book. Thus far, research has found that certain epigenetic mechanisms are strongly correlated with different neurobehavioral developmental trajectories, including changes in vulnerability and resilience to psychopathology. How epigenetics relates to individual responses to being a target or perpetrator of bullying is not clear, but the research in related areas of behavior highlights an important emerging area for investigation.
Various epigenetic processes appear to interact with many changes in
23 DNA methylation is a heritable epigenetic mark involving the covalent transfer of a methyl group to the C-5 position of the cytosine ring by DNA methyltransferases (a family of enzymes that act on DNA). Cytosine is one of the four bases that occur in varying sequences to form the “code” carried by strands of DNA (Robertson, 2005).
the brain produced by early life experiences, including not only the number and shape of brain cells but also how these cells connect to one another at synapses (Hanson et al., 2015).
Regarding bullying, the committee identified only one study that has examined epigenetic changes. Specifically, Ouellet-Morin and colleagues (2013) found an increase in DNA methylation of the serotonin transporter gene for children who had been bullied by their peers but not in children who had not been bullied. These researchers also found that children with higher serotonin DNA methylation had a blunted cortisol response to stress, which they had previously shown changes as a consequence of poor treatment by peers (Ouellet-Morin et al., 2011). That is, their 2011 study of twin children assessed at ages 5 and 10 found that being bullied was correlated with a change in how the body responds to stress. Bullied children displayed a blunted cortisol response to a psychosocial stress test. Because the design of the study involved an examination of identical twins who were discordant with respect to their experiences of being bullied (one twin was bullied while the other one was not), Ouellet-Morin and colleagues (2011) concluded that the effect could not be attributed to “variations in either genetic makeup, family environment, or other concomitant factors, nor could they be attributed to the twins’ perceptions of the degree of stress experienced during the task” (Vaillancourt et al., 2013a, p. 243).
In summary, it is important to note that there is no gene for being a perpetrator or a target of bullying behavior. Based on current knowledge of the genetics of complex social behavior, such as bullying, the genetic component of individual response is likely to involve multiple genes that interact with the environment in a complex manner. The current understanding of genetics and complex behaviors is that genes do not cause a behavior; gene-by-environment studies do not use the word “environment” the same way it is used in everyday language or even in traditional social psychology (as in Chapter 3). Rather, it is a construct used in a model to estimate how much variability exists in a given environment. This means that the same gene placed in different environments would yield very different percentages for gene-environment interactions. It is unclear how this information would inform our understanding of bullying.
Telomere Erosion Consequences
Epigenetic research has found that negative life experiences can alter the expression of a gene, which in turn, can confer a risk for poor outcomes. Research also suggests that the experience of being bullied is associated with telomere erosion. The end of each chromatid has been found to shorten as people age; this telomere “tail” also erodes as a function of engaging in unhealthy behavior such as smoking or being obese. Telomere
erosion is also associated with certain illnesses such as cancer, diabetes, and heart disease (Blackburn and Epel, 2012; Kiecolt-Glaser et al., 2011; Vaillancourt et al., 2013a). Given these associations, scientists are now examining telomere erosion as a biomarker of stress exposure (Epel et al., 2004), including the stress of being bullied by peers.
A recent longitudinal study by Shalev and colleagues (2013) examined telomere erosion in relation to children’s exposure to violence,24 a significant early-life stressor that is known to have long-term consequences for health. They found that exposure to violence, including being a target of bullying, was associated with telomere erosion for children assessed at age 5 and again at age 10. The sample for this study included 236 children recruited from the Environmental-Risk Longitudinal Twin Study (Moffitt, 2002), 42 percent of whom had one or more exposures to violence. The study found that cumulative exposure to violence25 is positively associated with accelerated telomere erosion in children, from baseline to follow-up, with potential impact for life-long health (Shalev et al., 2013).
In this chapter, the committee reviewed and critically analyzed the available research on the physical health, psychosocial, and academic achievement consequences for children and youth who are bullied, for those who bully, for those who are both bullied and bullies, and for those who are bystanders to events of bullying. It also examined the potential mediating mechanisms of, and the genetic predisposition to, mental health outcomes associated with childhood and youth experiences of bullying behavior. Most studies are cross-sectional and thus provide only associations suggestive of a possible causal effect. This problem is most acute for studies based on anonymous self-report, in which both the independent variable (experience of bullying in one or more roles) and dependent variables (such as emotional adjustment) are data collected at the same time from sources subject to various forms of bias.
The limited amount of data from longitudinal and experimental research designs limits the ability to draw conclusions with respect to causality. Additional longitudinal studies, for example, could help establish that the negative consequences attributed to bullying were not present before the bullying occurred. But even this does not prove a causal effect, since bullying and the associated impairments might be products of some third
24 Exposure to violence included domestic violence, bullying victimization, and physical abuse by an adult.
25 Cumulative violence exposure was measured by an index that summed each type of violence exposure.
factor. Below, the committee summarizes what is known about associations and consequences and identifies key conclusions that can be drawn from this evidence base.
Finding 4.1: Individuals who both bully and are also bullied by others experience a greater variety of both internalizing and externalizing symptoms than those who only bully or are only bullied.
Finding 4.2: Individuals who bully others are likely to experience negative emotional, behavioral, and mental health outcomes, though most research has not distinguished perpetration of bullying from other forms of peer aggression.
Finding 4.3: A large body of research indicates that individuals who have been bullied are at increased risk of subsequent mental, emotional, and behavioral problems, especially internalizing problems.
Finding 4.4: Studies of bystander behavior in bullying have rarely examined the emotional and psychological impact of witnessing bullying.
Finding 4.5: Children and youth who are bullied subsequently experience a range of somatic disturbances.
Finding 4.6: Social-cognitive factors (e.g., self-blame) and unsuccessful emotion regulation (i.e., emotion dysregulation) mediate relationships between bullying and adverse outcomes.
Finding 4.7: There is evidence that stressful events, such as might occur with experiences of being bullied, alter emotional brain circuits. This potential outcome is critically in need of further investigation.
Finding 4.8: Genetics influences how experiences contribute to mental and physical well-being, although the nature of this relationship is complex and not completely understood.
Finding 4.9: Emerging evidence suggests that repeated exposure to bullying may produce a neural signature that could underlie some of the behavioral outcomes associated with being bullied.
Finding 4.10: There are limited data on the physical health consequence of bullying for those individuals who are involved in bullying as targets, perpetrators, as both targets and perpetrators, and as bystanders.
Finding 4.11: Poly-victims (individuals who are targets of multiple types of aggression) are more likely to experience negative emotional, behavioral, and mental health outcomes than individuals targeted with only one form of aggression.
Finding 4.12: The long-term consequences of being bullied extend into adulthood and the effects can be more severe than other forms of being maltreated as a child.
Finding 4.13: Individuals who are involved in bullying (as perpetrators, targets, or both) in any capacity are significantly more likely to contemplate or attempt suicide, compared to children who are not involved in bullying. It is not known whether bystanders are at increased risk of suicidal ideation or suicide attempts.
Finding 4.14: There is not enough evidence to date to conclude that being the target of bullying is a causal factor for multiple-homicide targeted school shootings, nor is there clear evidence on how experience as a target or perpetrator of bullying, or the mental health and behavior issues related to such experiences, contribute to school shootings.
Conclusion 4.1: Further research is needed to obtain more in-depth evidence on the physical health consequences of being the target of bullying including neural consequences.
Conclusion 4.2: Additional research is needed to examine mediators of short- and long-term physical health outcomes of individuals who are bullied. Evidence is also needed regarding how these outcomes vary over time for different groups of children and youth, why individuals with similar experiences of being bullied might have different physical health outcomes, and how physical and emotional health outcomes intersect over time.
Conclusion 4.3: Although the effects of being bullied on the brain are not yet fully understood, there are changes in the stress response systems and in the brain that are associated with increased risk for mental
health problems, cognitive function, self-regulation, and other physical health problems.
Conclusion 4.4: Bullying has significant short- and long-term internalizing and externalizing psychological consequences for the children who are involved in bullying behavior.
Conclusion 4.5: The data are unclear on the role of bullying as one of or a precipitating cause of school shootings.
Conclusion 4.6: Individuals who both bully others and are themselves bullied appear to be at greatest risk for poor psychosocial outcomes, compared to those who only bully or are only bullied and to those who are not bullied.
Conclusion 4.7: While cross-sectional studies indicate that children who are bullied are at increased risk for poor academic achievement relative to those who are not bullied, the results from longitudinal studies are inconsistent and warrant more research.
Conclusion 4.8: Existing evidence suggests that both social-cognitive and emotion regulation processes may mediate the relation between being bullied and adverse mental health outcomes.
Conclusion 4.9: Although genes appear to modulate humans’ response to being either a target or a perpetrator of bullying behavior, it is still unclear what aspects of these experiences are interacting with genes and which genes are implicated to produce the variability in outcomes. Examining the role of genes in bullying in the context of the environment is essential to providing meaningful information on the genetic component of individual differences in outcomes from being a target or a perpetrator of bullying behavior.
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