You may ask why I want to explain it. Why does the understanding of development require a relational concept of causality? Well, I suggest you grab a coffee because this post is a bit long. But hopefully by the end you will understand why relational causality is the best way of explaining development.
Often when analysing problems simple linear causality (deterministic relation/epigenesis) is used, meaning that one event or property is the cause and it directly leads to one effect (outcome) in unidirectional manner. However, modern scientists do not perceive cause and effect in such a simplistic way. Therefore, the focus is the relationship between two events; it is the bi-directional relationship between the two that ’causes’ the event, as the ’cause’ is not due to only one of the events. In this way of explaining causality, relational causality, the effect is caused by the relationship, and no single variable, system, process, or event is the cause by itself (Gottlieb, 1997). The concept of a simple, single cause of development or developmental disorder appears attractive, mainly due to its simplicity, it is however, reductionist. Moreover, such concept is a misleading one as it implies deterministic mechanism rather than the probabilistic processes that are much more common.
The concept of relational causality has been employed by Gilbert Gottlieb in the study of development. For current purposes development is understood as the growth and change of humans across the entire lifespan, from conception to death. This includes all aspects of human growth and change, including physical, emotional, intellectual, linguistic, social, perceptual and personality development.
It has been argued that understanding of development demands a relational or coactive concept of causality; rather than assuming singular causes, the way it is done in simple linear causality. That is because development often is non linear, for example semantic and episodic memory development (Gottlieb & Halpern, 2002; Baddeley, 1999). Relational concept of causality aims to heal the split of biological and socio-cultural categories that describe the development and suggest integration of action (Lerner, 2001). For example, the environment influences biology and biology influences environment. Relational causality emphasises that development is a bit random and interactive. The promoted view is that development comes about as a result of dynamic and emergent interactions between genes, structural brain changes, behaviour, and the environment rather than those variables making separate contributions to the outcome (Gottlieb, 2007). Gottlieb offered a concept called probabilistic of epigenesis that constitutes an alternative not only to the nature-nurture concept of development but also many developmental theorists such as Vygotsky and Piaget who propsed stage-like development.
The Probabilistic Epigenesis framework emphasises the reciprocity of influences within and between levels of an organism’s developmental manifold (genetic activity, neural activity, behaviour, and the physical, social, and cultural influences of the external environment) and the ubiquity of gene–environment interaction in the realisation of all phenotypes (Gottlieb, 1998). Probabilistic epigenesis defies the central dogma persistent in sciences such as biology and psychology that genes and environments make identifiable separate contributions to the phenotype outcomes of development (Gottlieb, 1998).
It has been argued that relational concept of causality has more to offer to understanding of development and abnormal development than any other explanation or model separately. For example, developmental disorders are usually recognised during early childhood. Therefore, with probabilistic epigenesis in mind, it is expected to find performance deficits spread across different performance domains rather than one particular domain.
And there is support for this expectation, research into Williams Syndrome (WS) and autism has shown that domain-specific explanatory theories are not well supported, and that impairments in both, Williams syndrome and autism are more widespread than previously appreciated (Elsabbagh & Johnson, 2007; Karmiloff-Smith, 2007). For example, a common approach in autism research is to seek a primary cause of autism and perceiving other deficits as peripheral to the primary cause, however, no one deficit can be proposed to be a core one since the deficits co-occur at the same time during early life stages. No models that involve a single core deficit in autism have yet explained the range of data available. And it should not be necessarily assumed that there will be a unitary developmental cause of this kind (Elsabbagh & Johnson. 2007). Especially, as certain deficits, such as disengagement, occur in various developmental disorders and are not specific to autism alone (Elsabbagh & Johnson, 2007). Developmental disorders should not be explained in terms of impaired and intact domains, as this approach ignores the probabilistic dynamics of gene expression during embryogenesis upon the neurochemistry and of progressive brain development during postnatal growth (Karmiloff-Smith, 1998). Therefore, understanding development requires relational causality explanation as the alternative, linear causality, is simply reductionist.
Same applies to genetic causality, claims that imply a directness of genetic effects (‘genes for’) do not agree with the evidence that genetic pathways are much more indirect. Genetic influences are indeed all-pervasive and extremely important but they are frequently indirect. The evidence that certain gene is implicated in the liability to develop depression, an eating disorder, to behave antisocially, or even developing conditions such as autism or schizophrenia, does not mean that the gene causes these outcomes. The evidence suggests that the gene products operate via one or more biochemical pathways that only indirectly lead to normal or abnormal outcomes. Therefore, development is much more complex than implied by statements that genes lead to any kind of disorder (Rutter, 2006; Collier and Treasure, 2004). As further argued by Rutter (2006) the main effect may be on a specific part of the brain that is responsible for a key psychological function, on neurotransmitter functions, on some aspect of cognition or on some aspect of neuroendocrine operation.
Particular uncertainties in psychology research provide even more support for probabilistic epigenesis approach to development. For example, Caspi et al. (2002) found that a functional polymorphism in the gene encoding the neurotransmitter-metabolizing enzyme monoamine oxidase A (MAOA) was found to moderate the effect of maltreatment in childhood. Maltreated children with a genotype conferring high levels of MAOA expression were less likely to develop antisocial problems. Therefore, Gottlieb (2007) concluded that the study supports probabilistic epigenesis, because children with the short form of the MAOA polymorphism reared under conditions of no maltreatment, probable maltreatment, or severe maltreatment, it is only the latter group in which a substantial number exhibit some form of aggression. Alternatively, having the long form of the genotype significantly reduces the probability of the development of antisocial behaviour even under conditions of severe maltreatment, therefore the association between genes and the aggressive behaviour outcome remains inconclusive (Gottlieb, 2007, Caspi et al. 2002). It is argued that factors other than genes, such as life experiences are crucial to understanding outcomes such as personality development, making the importance of relational causality even clearer. Therefore, the context of development must always been taken into account, as there are further relationships, where it is clear that the interaction of factors is necessary for the observed effects to occur. This becomes very clear in the study of certain psychological issues, i.e eating disorders. Research findings suggest variations of dopamine or serotonin to be associated with issues such as eating disorders, depression, anxiety or above mentioned aggression. However, the associations, do not imply simple causality but rather developmental-relational causality (Gottlieb, 2007; Bulik, 2005). In the case of development of eating disorders, even though there is no doubt that certain biological susceptibilities or socio-cultural or familial factors play a role in the development, it is broadly agreed that no single one ’causes’ a certain eating disorder and that individual context should be taken into account (Bulik, 2005; Scalf-McIver & Thompson, 1989). The importance of context becomes very apparent in the study of eating disorders. Twin studies suggest relationships where both MZ twins are more likely to develop an ED than DZ twin pairs, giving a great argument for the genetic influence, however, the environment in which the twins grow up is also broadly shared and current literature lacks data on separated twins with eating disorders (Hamilton, 2007). It is apparent that in the case of eating disorders there are many vulnerability factors, no single one ’causes’ the disorder, and an interplay of the factors is needed for the disorder to develop.
Furthermore, approaches based on probabilistic epigenesis principles, have been developed in specific areas of psychology. Johnson (2000) developed Interactive Specialisation approach to cognitive brain development. Interactive specialization explains cognitive development as back-propagated interactions between genetics, brain, body and environment (Johnson, 2000). Cognitive functions are perceived as the emergent product of interactions between different brain regions. Development is therefore seen as constant interaction of the components, rather than strictly following pre-specified genetic template. Furthermore, this view suggest that a reorganisation of interactions between different brain structures and areas as a result of new skill acquirement. Relatively recent magnetic resonance imaging (MRI) studies suggest that both progressive and regressive processes, as opposed to simple linear patterns of change, underlie changes in cognitive abilities, supporting the above proposed models of development (Amso & Casey, 2004).
Conclusions
As discussed above, understanding development requires the acceptance of the coactive relational causality explanation of development. Focusing on only one part of the relationship will lead to losing important parts of the process, and this is the most important reason why relational causality needs to be employed in understanding and study of development. It is more fruitful to approach development with the focus on interactions between variables within each individual placed in a particular context. Such approach must be employed from early infancy, and simultaneously at multiple levels: genetic, neural, cognitive, environmental and behavioural, with subcategories of physical, social and cultural influences; with particular stress on the bi-directionality of the influences and interactions. This is because all these dynamics of development are crucial to a hollistic understanding of development and developmental disorders.
The complex dynamics of both normal and abnormal development indicate that relational causality might be the most viable theoretical framework within which to explore normal and abnormal development, and developmental disorders in particular; as the systems should be explored as whole. The influences and effects of gene-neural-environment-behaviour correlations and interactions, are all of crucial importance, e.g. through biochemical epigenetic effects the environment influences the functioning of genes (Rutter, 2006).
Finally, probabilistic epigenesis has more to offer in terms of progress. If employed, this framework, has the potential to facilitate bringing research and practice closer together. However, if viewed through the relational causality framework, the causes, categorisation, and diagnostic tools for developmental disorders would be challenged.
