Abstract
For fifteen years, Kids Company has been working to provide invaluable support to children who have been the victims of abuse and deprivation of various kinds. Many of these children have social, emotional and behavioural problems, which Kids Company seeks to address in a loving, supportive environment. Like my own clinical and theoretical work, the efforts of this important organization draw inspiration from attachment theory — particularly the idea that the quality of early child–caregiver relationships has a crucial impact on children's development in all domains of life.
Based on its foundations in attachment theory and its collective years of clinical experience, Kids Company has recently put forward a bold hypothesis that is also a call to action. According to the organization, many of the children they serve show a ‘violence adapting syndrome’ that involves persistent states of increased arousal. Although its extensive work lends strong to support to such a hypothesis, Kids Company wants to develop this further: it has nobly called for empirical researchers to take up and test its clinical insights in an attempt to offer them greater scientific validity. The resulting evidence-base could help shape the mental health and social care fields to ultimately deliver better care for, and increase the life chances of, our most at-risk children.
To this end, Kids Company has initiated a dialogue between psychiatrists, researchers, doctors and field workers. The three articles in this series are important contributions to that dialogue. Each illuminates, and helps deepen, Kids Company's hypothesis in important ways.
In their article on the neuroscience and genetics of psychopathology, McCrory and colleagues 1 review a number of studies that support the idea that abuse leads to prolonged—and developmentally detrimental—hyper-arousal in children. In this scholarly review of the neuroscience of child abuse, the authors highlight the complexity of findings and the inadequacy of our current understanding. They draw attention to differential patterns of stress response in children and adults with a history of maltreatment, and suggest that patterns of response reflect different strategies that the individual might adopt to cope with chronic adversity. Both hypo-activity and hyperactivity may be indicators of psychopathology but they should also be seen as adaptations.
McCrory and colleagues carefully chart current evidence from magnetic resonance imaging studies of brain structure. Structures implied in learning and memory functions and emotion processing show anomalies in adults with histories of early adversity. The picture they paint is a complex one: It is probable that the age when traumatized and the brain regions implicated, probably subtly interact. There are some clear indicators of this, including cerebellar and corpus callosal atrophy linking social-emotional and cognitive impairments to structural anomalies, particularly anomalies of connectivity in the brain. Functional imaging studies, although smaller in number, confirm amygdala anomalies and point to impaired cognitive control in maltreated youth. In line with the general approach taken by Kids Company, McCrory and colleagues see the child as not merely a victim but as an active agent who attempts to use available social and emotional resources optimally in a challenging environment. This behavioural response is supported by neurobiological systems honed by evolution to adjust to a hostile environment and match its demands as far as possible.
At this point, genetics, the primary mediator of evolution, must enter the scene. Species-wide variability ensures that some children will meet certain types of environmental challenges more readily than others. As McCrory and colleagues indicate, there are intriguing suggestions that some single nucleotide polymorphisms mark a vulnerability to stressful life events on the one hand, and to the positive influence of maternal sensitivity on the other. 2 Accumulating evidence supports the view that the inefficient S allele of 5-HTTLPR in combination with secure attachment increases the likelihood of agreeable yet autonomous social behaviour in adolescents. 3 The same polymorphism, in combination with insecure parenting, predicts poor self-regulation 4 and impulsiveness in response to threats to autonomy. 3 The challenging suggestion is that certain apparent genetic vulnerabilities are retained in the gene pool because under favourable circumstances they enhance social sensitivity, potentially making a child both more and less pro-social, depending on their social environment. It may be interesting to note that ‘collectivistic’ nations, such as Korea or China, appear to have a higher prevalence of S-allele carriers than nations, such as most western countries, where individualism is more highly valued. 5
Cultural differences may also arise in relation to the major contribution which Viding et al. 6 have made with respect to the heterogeneity of the category of anti-social behavioural problems. The work of this group has highlighted the categorical distinction between those young people who commit antisocial acts and appear to feel no guilt or fear and those who lack callous and unemotional (CU) traits. They point to twin studies that suggest that CU traits have high heritability. In turn, children with high levels of CU traits are ‘highly likely to display high levels of conduct problems’. In CU children, these problems are often ‘resistant to some forms of traditional strategies’ for treatment. Thus, the authors' review lends support to the idea that some particularly intractable conduct problems have a genetic basis.
Their paper offers strong justification for the distinction, suggesting that the former group have profound problems with mentalizing in relation to feeling what others feel. The French philosopher Pierre Jacob describes this in his critique of a direct perception model of empathy. 7,8 He proposes a simulation model of empathy, expanding the views of de Vignemont 9 and Singer. 10 This model may be of great value in understanding the distinction between children whose background provides an adequate explanation for their antisocial behaviour (such as the children who are the focus of Kids Company's work), and those to whom Viding et al. draw attention. Jacob identifies four conditions that define empathetic experience, differentiating it from a range of overlapping constructs such as sympathy, contagious emotional experience and standard or cognitive mindreading. In combination, these four criteria define empathy and point to the ‘gap’ in the experience of those who Viding et al. label AB/CU+.
Jacob's vital suggestion is that the vicarious component of empathy is provided by enactive imagination (e-imagination) which he ascribes to the off-line functioning of the visual system. We know that inputs from memory generate visual images comparable to those which are generated by standard perception. 9 In addition, neuroimaging studies have demonstrated the activation of comparable networks of the brain whether a person is exposed to a painful experience or observes a loved one having the same experience. 10 It is assumed that e-imagination generates from internal inputs some aspects of the external experience. In empathy, part of the same brain systems that operate during direct experience run ‘off-line’ (based on memory images). The experience of pain has a sensory motor and an affective component. In empathic pain only the affective component of the pain system is operating. We normally ‘feel’ the pain of the person (‘the target’) but only at the emotional level generated by e-imagination. The pain then is more like a sense of an emotional disarray which is given meaning by the observing of the target. As we suspect that in AB/CU+ individuals the affective component of enactive imagination may be compromised by a combination of genetic and early environmental factors, their capacity for e-imagination is impaired. This would explain why they have trouble ‘feeling the other's pain’.
But genetic differences do not operate in a vacuum: as McCrory and colleagues highlight, gene–environment interactions mediate risk and resilience for adult psychiatric outcomes. Furthermore, some childhood disorders are highly correlated to environmental adversity. An e-imagination deficit could be constitutional or acquired. More specifically, we presume that the experience of trauma may have direct impact on the capacity for e-imagination, thus only some of the apparently CU+ children come to experience AB for primarily constitutional reasons.
We have suggested elsewhere 11 that traumatic experiences appear to interfere directly with the processing of emotional experience. The anxiety created in relation to the actual experience of emotional or physical pain disrupts the E-imagination. For victims of childhood trauma, generating a memory that would activate the affective component of pain (necessary for empathy) may be too excessively imbued with anxiety (associated with helplessness or other overwhelming negative affect at the time of the traumatic experience). As a result, these individuals will understandably resist undertaking the creation of the internal inputs necessary to ‘run off-line’ the emotional components necessary to feel empathy. In this case, the distinction between CU+ and CU− children may be conceptualized less in terms of the phenomenology and more in terms of the aetiology of this clinically highly significant distinction.
The key issue of treatment in both instances may then be similar: the activation of e-imagination (the affective component of the relevant perceptual systems). The relative success of restorative justice, 12 which involves confronting the offender with the victim in ways that optimize the chance of E-imagination ‘kicking in’— through face-to-face conferences, victim-offender mediation, restitution, reparation payment, etc.—leads to offenders committing fewer repeat crimes (11%–37%). Intriguingly, restorative justice reduces repeat offending more consistently with violent crimes than with less serious crimes. As Viding et al. point out, antisocial behaviour in children without CU traits ‘appears to be driven primarily by environmental influences’. The authors suggest that any intervention targeted at this population ‘should include a consideration of systemic factors such as parenting and broader social functioning’. This is precisely the sort of work in which Kids Company is engaged.
There is a general consensus that the victims of childhood abuse and deprivation—including those suffering from conduct disorder problems or other forerunners of severe psychopathology—need sensitive interventions if they are to have the best possible life chances. In her review, Blakemore 13 presents an interesting case for delivering such interventions throughout childhood and adolescence into early adulthood. She points to structural and functional brain studies and original research on cognitive perspective-taking tasks to argue convincingly that capacities for mentalization continue to develop from infancy throughout the teenage years. The extent of the reorganization that the brain undergoes in adolescence is not yet known, nor is the degree to which capacities for mentalization can be developed or hindered by environmental factors in this period. But Blakemore's suggestion—that interventions aimed at increasing mentalization can positively impact the lives of adolescents—fits well with the results of our own clinical work.
An interesting challenge is raised by Viding et al., who point out that antisocial behaviour is not linked with difficulties in mentalizing in either CU or non-CU children. As indicated above, we should probably avoid considering mentalizing as a unidimensional construct given (a) its complex links to brain activity across a number of brain areas and (b) its cross-situational variability in most of us, directly related to the level of arousal. 14 Thus, mentalizing conceived of as a capacity to adopt cognitive or emotional perspectives associated with mental states, may be vulnerable under conditions of emotional arousal in these individuals, even if they appear to be able adequately to perform perspective-taking cognitive experimental tasks in the laboratory.
Taken together, the articles in this series have three major implications for the work of Kids Company, for research into early trauma, and for the hope of intervening successfully to improve children's lives. Firstly, the articles demonstrate the potential for clinical and research insights to inform one another productively and for the latter to guide and direct the former in more specific directions, avoiding the all inclusive, ‘scatter gun’ approach that many clinical interventions have taken in the past. 15 Secondly, they further our scientific understanding of the potential neurological consequences of psychosocial adversity and the ways in which combinations of genetic and environmental factors could generate mechanisms of psychopathology. Focusing on genetic vulnerability should never be juxtaposed with appropriate concern when ensuring that a child's environment is appropriately safeguarded. Indeed, without taking models of diathesis-stress seriously, without knowing where genetic vulnerabilities may lie, we will never be able to target our slender resources for preventative interventions at those who need them most. 16 Finally, the articles reinforce the need to support and further the work of exemplary organizations like Kids Company, which are constantly learning from and adapting scientific insights in their fight to address the consequences of trauma and to improve children's lives.
DECLARATIONS
Competing interests
None declared
Funding
None
Ethical approval
Not applicable
Guarantor
PF
Contributorship
Peter Fonagy is the sole contributor
Acknowledgments
None