Families, policy and the law

Selected essays on contemporary issues for Australia
Collection – May 2014

Contents

28. Social science and family law: From fallacies and fads to the facts of the matter

By Alan Hayes

Download as printable PDF (518 KB)

It would be tempting in a chapter on this topic to focus on some of the current controversies bubbling and boiling in family law circles surrounding the uses and abuses of social science “evidence”. Rather, I have assumed a dispassionate and detached perspective that is usually associated with the scholar, scientist or others who daily exercise the Wisdom of Solomon! I will examine some of the fallacies and fads regarding social science “evidence” that can get in the way of determining the facts of the matter. As such, it bears on the broader question of how social science “evidence” is to be used in family law matters. I will address:

  • the historically contextualised and ever-changing nature of knowledge;
  • some myths of uniformity and common misinterpretations of developmental science; and
  • the primacy of discernment and judgement when assessing the facts of the matter, including the weight to be placed on social science evidence.

The belief that a contemporary perspective represents the highest point of knowledge in any field carries a certain conceit. On the one hand, it can be argued that most topics in contemporary social science, including in my own field of developmental psychology, have a long ancestry, though they are often presented as if only recently “discovered”. On the other hand, some ideas that would have been regarded as “facts” in their day now appear ridiculous to us. And some ideas remain enshrined in social knowledge, even though they have long passed their scientific use-by date!

Science, like all knowledge, is historically contextualised

Yesterday’s facts can become today’s fallacies

Among many that might have been chosen, two examples from the distant past are mentioned briefly.

Dr John Langdon Down, whose name has been lent to the syndrome, concluded that “mongolism”, as it was labelled when first described in 1866, was likely caused by tuberculosis (O’Connor, 2008). This incorrect conclusion was based on his observation of one mother who had the condition, and that the incidence of tuberculosis in children with the syndrome, suggested a possible congenital link (Ward, 1999). Others, however, were quick to associate the condition with the widely held belief that, like other examples of “feeblemindedness”, mongolism was most likely caused by the deleterious effects of education on women. Down did not accept this idea and was actually a champion for the provision of educational opportunities to women (Wiedermann, 1992). We now know, of course, that the condition actually involves errors in cell division that result in a range of chromosomal abnormalities, including the most common: Trisomy 21. While the precise cause still eludes us, we do know that a strong correlate is maternal cellular age, with some associated paternal cellular age contribution also having recently been described. The link to education may be coincidental, given that better educated women may tend to have children later in life. Additionally, social class differences in health and access to health services such as amniocentesis and medically indicated terminations may actually result in a lower rate of the condition in the children of better educated women. How inconvenient.

A related example now seems similarly ludicrous. Prior to the American Civil War, it was concluded that brain size is related to race, gender and intelligence. This was heavily influenced by the work of Dr Samuel George Morton who, in 1820, began collecting an amazing array of Egyptian, Indigenous Australian Aboriginal, African, Asian and Caucasian skulls from around the globe. He amassed so many that friends and colleagues jovially referred to his home as the “American Golgotha” (Gould, 1981). Morton’s conclusions were based on an impressive range of measures of cranial volume (craniometry) that were conveniently optimised with the aim of providing irrefutable scientific evidence of the superiority of white, male brains. On Morton’s death, in 1851, the New York Tribune stated that “probably no scientific man in America enjoyed a higher reputation among scholars throughout the world” (as cited in Gould, 1981, p. 51). Unfortunately for Morton’s place in history, Gould (1981) re-analysed the data and found that Morton’s findings resulted from a “patchwork of fudging and finagling in the clear interest of controlling a priori convictions” (p. 54). Scientific fame can be short-lived and built on fragile foundations.

Three contemporary examples of the changing state of knowledge

Those two examples can be dismissed as fatuous anachronisms. But some of today’s “scientific evidence” can be similarly open to question, if not ridicule. Fad and fashion can inflate the significance of particular research and lead us to ignore the issue of the validity of single studies. As such, assertion is too easily mistaken for evidence.

Three contemporary examples, again among many, show that the changing nature of knowledge is not only a problem of the distant past. A first example relates to our knowledge of the brain and its development. Until relatively recently, it was thought that we had a fixed number of neurones at birth and that these could not be replaced. The ravages of time and, dare I say, lifestyle factors were thought to ensure that neurologically it could only be downhill (the pace of decline was found to occur at a faster rate for men than women!).

We now know this is not correct. Nor is the concept that our nervous system is hardwired from birth. “There is a diversity of wiring in the brain. Furthermore, this wiring constantly changes in response to biological and environmental influences” (Institute of Medicine and National Research Council, 2012, p. 3). Advances in neuro-imaging and biochemistry have revealed the brain in a very new, complex and dynamic light. The degree of plasticity of brain functioning is far greater than previously thought, as studies of the transfer of functions in those who have suffered brain injuries now show (Doidge, 2007). Neural tissue has “a remarkable capacity for reorganization” and replacement (Garcia-Segura, 2009, p. 9). While suspected for some time (see, for example, Bergland, 1985), evidence is increasingly available that demonstrates the complex hormonal systems that underpin this plasticity and mediate and moderate the effects of experience (Garcia-Segura, 2009). The brain is the largest gland in the body, with the most complex assemblage of nerve cells and interconnected circuits. And yet, simplifications and erroneous ideas about brain development exert enduring influences on present thinking.

A second example relates to Gardner’s (2004) concept of parental alienation syndrome (PAS), in which a child repeatedly denigrates and belittles one parent, without justification. Emery, Otto, and O’Donohue (2005), among others, questioned the scientific status of this concept and concluded “that it is blatantly misleading to call parental alienation a scientifically based ‘syndrome’” (p. 10), especially given Gardner’s admission that he regarded his single study as the only one that had been statistically based. While others may disagree, given the state of the “evidence”, I would err on the side of caution in the use of such a construct and would not use the term “syndrome” when discussing alienation. Clearly, a definitive conclusion on the topic awaits much further research (Warshak, 2001).

The final example I would cite, albeit briefly, takes me closer to the cauldron. It relates to the concept of bonding. Most prominently associated with the work of Klaus and Kennell (1976, 1982, 1983), Eyer (1992) observed that “research on bonding was inspired by the popular belief that women, one and all, are inherently suited for motherhood” (p. 1), and that the time immediately following birth was a particularly sensitive period in relationship formation that was biologically based. Notwithstanding its weak empirical foundations, the focus on bonding did have benefits in changing obstetric and neonatal care. For example, infant feeding regimes were permitted to suit the needs of the mother and child, rather than the needs of the hospital and its routines. Bonding continues, however, to be confused with the concept of attachment, and the two are frequently used as synonyms. As Minde (1986) concluded, however, while the concept of attachment is supported by a voluminous research literature, there is scant evidence to support the concept of bonding as framed by Klaus and Kennell. “Bonding is, in fact, as much an extension of ideology as it is a scientific discovery” (Eyer, p. 2).

Myths of uniformity

Developmental age and stage

Scientific argument becomes the stuff of popular social knowledge that is all too readily detached from the detail and the critical debates within the scientific community. In this process, scientific evidence can be distorted in its meaning and significance. As such, it then takes on the status of an article of faith rather than empirical fact. Fallacies have a way of persisting and fads are remarkably fashionable.

While I support the focus on the early years of childhood, for example, it has become in some ways faddish. In reading the recent early childhood literature one might conclude that this is the only time in life when key brain developments occur. Those researchers who have focused on developmental epochs other than the early years (Blakemore & Choudhury, 2006; Dahl, 2004) have struggled to have their voices heard. While adolescence is of growing interest (Spear, 2004), some developmental eras, such as middle childhood, continue to be overlooked. And adulthood is still too often seen as merely an end point, rather than a time of continuing developmental change in its own right (Smith, 2006).

Adolescence, for example, is a time of interesting paradoxes. On the one hand, there is a quantum leap in the physical strength, intellectual processing speed and capacity, and overall resilience of adolescents. On the other, it is marked by heightened risk, with morbidity and mortality rates doubling over these years (Dahl, 2004). Changes occur to multiple neurological and endocrinological systems and their interactions (Kelley, Schochet, & Landry, 2004), with brain developmental changes preceding and driving the hormonal changes associated with puberty (Dahl, 2004). Changes to myelination and neuronal pruning, especially in the prefrontal cortex, characterise the entry to adolescence (Spear, 2000, 2004). The net effects of these changes are profound and, in part, explain the propensity of adolescents to seek novelty and engage in risky behaviour (Blakemore & Choudhury, 2006; Kelley et al., 2004; Spear, 2000, 2004). Importantly, the neurological changes that occur in adolescence signal changes that continue through life (Blakemore & Choudhury, 2006).

Rather than slavish adherence to age- and stage-based approaches, as conveniently simplifying as these may be, the action in developmental psychology for some decades has been on the life course. Just as there is considerable variation and overlap on most variables between groups, so too there is considerable difference when one measures developmental age in contrast to chronological age. Further, the older one gets, the less important distance from birth becomes than proximity to death!

Developmental outcomes at any age or stage are also influenced by the interpretation of events, and these in turn change over life (Sameroff, 2004). Parents, children, teachers and, dare I say, social scientists and those across the family law system, have differing views of the meaning and import of children’s behaviour. What is reported can be as much a function of the seer as the seen. De Los Reyes and Kazdin (2005) highlighted discrepancies in informants’ ratings of child psychopathology. They went on to say that developmental history “may represent not the past acting on the present but the present reconstructing the past … People act on and create their own lives, including their memories and their futures, through the formation in the present of future goals, desires, and needs” (p. 75).

It is important to avoid being trapped by the external standpoint into highlighting assumptions based on the norms of development and what one might expect at a particular age or stage. A focus on individual differences highlights the need to see the world, as far as possible, as each child sees it (Henaghan, 2012). As Parkinson and Cashmore (2008) emphasised, children want to express themselves and have their views heard on the things that are salient in their lives. Henaghan quoted Baroness Hale: that when children are heard, “the court will see the child as a real person, rather than the object of other people’s disputes or concerns” (as cited in Henaghan, 2012, p. 40).

Change, continuity and the problem of prediction

A second myth of uniformity relates to the extent of change, continuity and predictability of development. There is considerable scope for change in development. The longer the time between measurement points, the greater the scope for variability. Stability of relationship and personality variables, over time, tends to be low. As Lewis (2001) concluded, “based on the collective evidence to date—in a multitude of domains, including cognitive, social, emotional, and psychopathological—the best that can be said is that there sometimes is very limited support for the belief that earlier events are connected to later ones” (p. 74). For example, it is a mistake to see attachment as a fixed trait or stable individual characteristic across time. There is, in fact, a lack of continuity from infancy to adolescence and beyond. In the longitudinal study conducted by Lewis and his colleagues, attachment at 18 years was related to family status, whether divorced or intact, but not to attachment in infancy.

In quoting Rutter’s conclusion that, “attachment is not the whole of relationships”, Ludolph and Dale (2012) highlighted the role that other elements of the developing child’s context play in complex interactions with the characteristics of each child and the quality of the processes that connect child to context. As such, they argued that attachment should be but one “additive best-interest factor” rather than “a determinative one” (p. 40). Cashmore and Parkinson (2011) made a similar argument. And yet the notion of the power of earlier events and states to determine what happens later in life is an enduring belief. As Sameroff (2004) observed, “developmental achievements are rarely sole consequences of immediate causes and more rarely sole consequences of earlier events” (p. 9).

Given the diversity of pathways through life, the interplay between change and continuity underscores developmental complexity. This begs the questions, “What drives change?” and “What maintains continuity?” As Brooks-Gunn (2003) argued, the issue is steeped in magical thinking and there is still much to be learned about the processes that operate to sustain developmental continuities. She provided a compelling critique of what might be called the “early childhood error”—the belief that all is evident and active, albeit in some instances in latent form, in early life and therefore remediable then, if only we had the knowledge. What is not clear is what is sustained, as opposed to lost, from early experience. I am reminded of Rutter, Maugham, Mortimer, and Ouston’s (1979) book, Fifteen Thousand Hours, and the limited residue of all that time spent in school. Not everything experienced is retained!

As Clarke and Clarke (1976) observed, “what one does for a child at any age, provided it is maintained, plays a part in shaping his development within the limits imposed by genetic and constitutional factors” (p. 273). I would echo Farran’s (2000) conclusion that “somehow, [we have] to move beyond thinking of the problems of young children as being something someone else fixes at an earlier age or in a different place so that other systems do not have to change. A developmental focus that covers the first 12 to 15 years of life would be a good start” (p. 542).

What might this mean in a family law context? As Sroufe put it, “we cannot definitively say, based on attachment assessment, this child should be with this parent more than with that parent. The major thing that I think a judge would do well to know is that attachment relationships are a lifetime thing” (as cited in Sroufe & McIntosh, 2011, p. 463). Much can and does change over a lifetime!

The dynamic nature of development makes the timing of our actions and interventions to address problems a difficult issue. Problems emerge over time. Difficult temperament, conduct problems and aggressiveness tend to appear early in life, while social withdrawal, difficulties in peer relationships and academic problems tend to manifest themselves in the school years. The outcomes of early vulnerabilities are a function of the number of risks and problems and the presence of factors that catalyse their emergence or ameliorate their effects. In development, difference is the norm, change is the constant and the diversity of development pathways is typical. This makes decision-making based on attempts to predict the future particularly challenging.

Critical consideration of the evidence underpins discernment and judgement

The importance of the long view

Prospective longitudinal studies are essential if we are to tease out the factors that drive developmental outcomes. Such studies follow a sample that is broadly representative of the population, prospectively, rather than identifying a group of interest, such as a clinical sample, and looking retrospectively for the factors that might explain their membership of the group. Prospective longitudinal studies can provide valuable insights into issues of change and continuity of pathways (Masten, 2004). The prospective Life Chances Study has shown the divergence of life paths in ways that are very difficult to foresee (Taylor, 2011).

Werner (2005) highlighted the value of prospective longitudinal research in identifying the factors that lead to successful adaptation and resilience. Prospective studies “have consistently shown that even among children exposed to multiple stressors, only a minority develop serious emotional disturbance or persistent behaviour problems” (p. 4). By way of contrast, a retrospective research strategy “created the impression that a poor developmental outcome is inevitable if a child is exposed to perinatal trauma, poverty, parental psychopathology or chronic family discord, since it examined only the lives of the ‘casualties’ not the lives of successful ‘survivors’” (p. 3).

The work of Sampson and Laub (2005; Laub & Sampson, 2003) underscores the scope for developmental change and the factors that alter negative pathways and maintain positive ones. In considering young men with a history of juvenile offending, they cited the evidence for the world of work, with its regularities and routines, and close personal relationships as two salient sets of influences that alter negative pathways and sustain more adaptive life trajectories. The presence or absence of connections to work and relationships, explain the patterns of desistance or persistence they observed in the life courses of the juvenile offenders. Of those who offend as juveniles, only a very small percentage goes on to a career in crime.

In reflecting on the Kauai Longitudinal Study—arguably the groundbreaking study of resilience—Werner (2005) extended the list of influences:

Among the most potent forces for positive changes for high-risk youth who had a record of delinquency and/or mental health problems in adolescence, and for teenage mothers, were continuing education at community colleges; educational and vocational skills acquired during voluntary service in the Armed Forces; marriage to a stable partner; conversion to a religion that required active participation in a “community of faith”; recovery from a life threatening illness or accident that required a lengthy hospitalisation; and occasionally psychotherapy. (p. 7)

The Australian Temperament Project (ATP) also provides valuable insights, via the lens of early temperament and its relationships to a range of outcomes (Hayes, Smart, Toumbourou, & Sanson, 2004; Smart & Vassallo, 2005). The study commenced in 1983, when the 2,443 participants were aged between 4 and 8 months. They are now young adults.

Of particular relevance to the present discussion is the evidence that the ATP provides of the variation in the time when pathways became noticeable. The pathway to multiple substance use at the age of 15 to 16 years, for example, was discernible in infancy. Those who went on to be involved in substance abuse in adolescence were, on parental report, less rhythmic as infants; less persistent and less cooperative as toddlers; less shy from 3 to 4 years on; more aggressive from 5 to 6 years on; and from primary school on showed greater inflexibility, poorer peer relations, more depressiveness but lower anxiety and fearfulness. A wide range of indicators, any one of which is unlikely to be predictive!

In contrast, the pathway to persistent antisocial behaviour in adolescence only became noticeable in the primary school years. Those who showed problems of antisocial behaviour had noticeably higher levels of acting out, aggression, hyperactivity, attention problems and volatility that became apparent in the primary school years. In turn, they had lower levels of cooperation, self-control and relationship with parents. At least in terms of temperament, however, there were no significant associations with parental reports of their characteristics in infancy.

The ATP provides an example of a pathway that was evident early in life for boys but not until middle childhood for girls. Boys who went on to show anxiety in adolescence were noticeably more anxious and more likely to be considered to be shy by the age of 3. For girls, their higher anxiety, parent relationship factors and externalising problems only became noticeable at 11 to 12 years of age.

So pathways may be differentiated by key sub-group characteristics such as, in this case, gender, as the work of Edwards (2006) also showed in relation to the greater effects of disadvantage on the early development of boys. Finally, prediction of outcomes is likely to be difficult (Hayes, 1990), given the wider representation in the population of the indicators of any problem. Again, this reinforces the need for longitudinal studies designed to trace the various pathways people follow through life (France & Utting, 2005). It again demonstrates the perils of prediction in individual instances. Often, what is presented as predictive evidence is actually better characterised as “retro-diction”. That is, the correlations are calculated retrospectively rather than from analyses of a truly prospective prediction study, where one would analyse the extent to which the predicted outcome actually came to pass; neither an easy nor an impossible exercise.

Genetic and environmental influences

So what else drives continuity? Is it the stability of the environment or are there genetic underpinnings that interact with experience? In considering the continuity of personality characteristics, Caspi and Roberts (2001) concluded that there is modest continuity:

Although the environment is often put forward as a reason for continuity in personality, there is little evidence to support the hypothesis. The genetic underpinnings of continuity are just now beginning to be reported in longitudinal behaviour genetics studies and the early evidence is provocative. (pp. 61–62)

As such, the sources of individual differences are complex. If one considers aggressive behaviour, a topic of considerable contemporary interest—especially for the Australian Government—there is accumulating evidence of the influence of genes and environments. The genetic influences underpin differences in neurotransmitters (such as serotonin) that underpin impulsivity and the propensity to aggressive reactivity (Pihl & Benkelfat, 2005; Rhee & Waldman, 2011) and hormones, including testosterone or the stress-related hormone cortisol (van Goozen, 2005). While the biological contributors to aggression are progressively becoming better understood, there is still much more to be learned about the complex interplay of genetic and environmental factors (Rhee & Waldman, 2011).

The environmental influences on aggression are similarly complex and multiple. Parental behaviour, especially harsh and inconsistent parenting, and a range of other factors—from maternal alcohol, tobacco and other drug misuse prior to birth to perinatal complications and peer influences in childhood and adolescence—have been linked to an elevated propensity for aggression (Tremblay & Nagin, 2005). A link between witnessing interparental violence and subsequent violent behaviour in intimate relationships in early adulthood has been observed (Cui, Durtschi, Donellan, Lorenz, & Conger, 2010; Uslucan & Fuhrer, 2009), though the relationship is at best modest (Black, Sussman, & Unger, 2010). Analysis of prospective longitudinal birth cohort data from the Christchurch Health and Development Study also showed weak linkages between witnessing interparental violence and subsequent relationship violence perpetrated by young adults, once socio-demographic context factors had been controlled (Fergusson, Boden, & Horwood, 2006). Exposure to violent behaviour, in and of itself, does not necessarily portend a life of violence. Exposure to abuse or neglect early in life, however, can lead to neurological and endocrinological changes that influence reactivity and responsiveness; though, again, these are not necessarily immutable effects. Environmental risk is not destiny.

Nor is DNA destiny. Rather, there is an interplay between environmental factors and genetic pre-dispositions that is much more complex than nature versus nurture. Some of these interactions are epigenetic (literally, “above the genome”). The groundbreaking new field of epigenetics highlights the importance of environmental influences on the expression of genes. Such influences can span generations, as indicated by research that shows how famine in one generation followed by abundance of food in the next can influence the risk of obesity and heart disease across generations (Pembrey et al., 2006). To that extent, you are what your grandparents and parents ate. The marks of experience of previous generations are written on the genome and act to influence the expression of genes. But for each individual, current experience and lifestyle throws the genetic switch. To that extent, you are what you eat.

Differential susceptibility

Susceptibility to intricately interacting genetic and environmental influences is a complex process. Like epigenetics, differential susceptibility is a rapidly developing field of research, with wide implications across several disciplines. Susceptibility to environmental influences varies considerably among children. Those with difficult temperaments, for example, have been shown to exhibit more behaviour problems when experiencing low-quality child care and fewer problems when high-quality care is available (Pluess & Belsky, 2009, 2010). As such, they are more likely to be influenced for good or ill depending on the quality of their developmental context. Children with difficult temperaments have also been shown to be more susceptible to negative maternal discipline and to show fewer externalising behavioural problems if exposed to positive maternal discipline (van Zeijl et al., 2007). Bakermans-Kranenburg and van IJzendoorn (2007) also provided support for the differential susceptibility hypothesis in a study of attachment security, with those children who show insecurity, distress and avoidance (characteristic of disorganised attachment) being more susceptible to unfavourable care environments but responding positively to favourable ones. Their study demonstrates the link between the genetic substrate and differential susceptibility to environmental experiences. Again, prediction is problematic if one only has partial information about the behaviour but not the genes!

A relationship has also been established between a specific gene that underpins differential susceptibility to childhood maltreatment and the propensity to move from being a victim to a victimiser (Caspi et al., 2002). Those with high levels of expression of the monoamine oxidase A (MAO-A) gene were shown to be less likely to victimise others than those with low levels, despite both groups having experienced maltreatment. In part, this illustrates the value of differential susceptibility in explaining why risk is not destiny.

A focus on differential susceptibility also moves the discussion beyond the simplistic binary consideration of whether, for example, particular care-time arrangements have developmental effects, irrespective of other factors. Like many other public health problems, combinations of factors complexly cause developmental outcomes related to health and wellbeing as well as to behaviours such as aggression and violence.

Beyond myths of uniformity

The very term “development” is not a unitary construct. As Lerner, Lewin-Brizan, and Warren (2011) observed, it “continues to engage scholars in philosophical and theoretical debate” (p. 19). Dualisms abound! There are norms versus individual differences and their translation to normative versus ipsative research approaches. There is a continuing interplay of biology and experience and the tension between continuity and change, person and environment, and the competing systems of the individual and the embedding social systems, as well as single sources of influence and the multiple determinants of outcomes, and finally, the ongoing tension between the vulnerability and resilience of each one of us. And yet, development is too often treated as a unitary given.

Social science is also far from a unitary entity. This is yet another of the myths of uniformity that can mislead. As Rathus (2012) stated, or should I say understated, “there is not usually just one social science view about an issue, so reference to any article (or even a set of articles) by a judge will necessarily be selective” (p. 83).

Uncritical acceptance of social science evidence is a clear and present danger for the family law system. King and Piper (1995) cited Tuebner’s observation that:

far from making law more responsive to the demands of other discourses, bringing it closer to the taken-for-granted world which is widely accepted as ‘social reality’ these attempts to incorporate ‘social knowledge’ within law have tended to produce ‘hybrid artifacts of ambiguous epistemic status’. This means that constructs which started out, for example, in the social sciences cannot be transferred unchanged into legal discourse. (p. 33)

Further, the limits of social science must be acknowledged when presented as briefs in family law matters (Kelly & Ramsey, 2009). These limits ought to be framed in terms of the selection criteria for the studies reviewed and synthesised, the theoretical frame and methods, the manner in which effect sizes are assessed, as well as the extent of acceptance by the scientific community. As such, the norms of science should be applied not only to the research, itself, but to the way it is used!

Common errors in the use of social science include:

  • applying evidence from group data to individual instances;
  • holding on to outdated, static models of development that ignore the complex dynamics at play over the life course;
  • grasping, selectively, a single study or a small number of studies while overlooking the caveats and concerns that apply to them;
  • misunderstanding the differences between the concepts of statistical significance, effect sizes and the variance explained by the measures in a study;
  • inflating the weight to be put on a single attribute, variable or outcome when multiple and changing influences impinge on individuals, at the biological, behavioural and social levels of explanation;
  • overstating the capacity to predict likely developmental outcomes and pathways, given the many influences that impinge on lives, by design and accident; and
  • ignoring the complex factors that lead to individual differences, including differential genetic susceptibility.

The way forward is not to eschew the social sciences but to understand the current state of knowledge, across their fields. It is to embrace a more sophisticated and nuanced appreciation of the balance of their strengths and limitations. While they are accumulating valuable insights into developmental processes, the social sciences are certainly not yet in a state to permit formulation of hard and fast rules with predictive powers. And, given the nature of human development, this may never be a realistic possibility. As argued, prediction is problematic. Fortune telling is a fraught enterprise that, more often than not, merely reflects the power of self-fulfilling prophecy. At best, one is left with the balance of probabilities.

When it comes to decisions about lives in the context of individual families, the power to make sound decisions and exercise wise judgements continues to lie in the uniquely human capacity to weigh and evaluate multiple sources of evidence. Having done that, one can only strive to reach a balanced synthesis of the facts of the matter, ever mindful of the historically, culturally and conceptually contextualised nature of knowledge in the social sciences and the family law system.

References

  • Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). Genetic vulnerability or differential susceptibility in child development: The case for attachment. Journal of Child Psychology and Psychiatry, 48(12), 1160–1173.
  • Bergland, R. (1985). The fabric of mind. Ringwood, Vic.: Penguin Books.
  • Black, D. S., Sussman, S., & Unger, J. B. (2010). A further look at the intergenerational transmission of violence: Witnessing interparental violence in emerging adulthood. Journal of Interpersonal Violence, 25, 1022–1042.
  • Blakemore, S.- J., & Choudhury, S. (2006). Development of the adolescent brain: Implications for executive function and social cognition. Journal of Child Psychology and Psychiatry, 47(3/4), 296–312.
  • Brooks-Gunn, J. (2003). Do you believe in magic? What can we expect from early childhood intervention programs. Social Policy Report, 17(1), 3–15.
  • Cashmore, J., & Parkinson, P. (2011). Parenting arrangements for young children: Messages from research. Australian Journal of Family Law, 25(3), 236–257.
  • Caspi, A., & Roberts, B. W. (2001). Personality development across the life course: The argument for change and continuity. Psychological Inquiry, 12(2), 49–66.
  • Caspi, A., McClay, J., Moffitt, T. E., Mill, J., Martin, J., Craig, I. W. et al. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297, 851–854.
  • Clarke, A. M., & Clarke, A. D. B. (1976). Early experience: Myth and evidence. London: Open Books.
  • Cui, M., Durtschi, J. A., Donnellan, M. B., Lorenz, F. O., & Conger, R. D. (2010). Intergenerational transmission of relationship aggression: A prospective longitudinal study. Journal of Family Psychology, 24(6), 688–697.
  • Dahl, R. E. (2004). Adolescent brain development: A period of vulnerabilities and opportunities. In R. E. Dahl, & L. P. Spear (Eds.), Adolescent brain development: Vulnerabilities and opportunities (Annals of the New York Academy of Science No. 1021; pp. 1–22). New York: New York Academy of Science.
  • De Los Reyes, A., & Kazdin, A. E. (2005). Informant discrepancies in the assessment of childhood psychopathology: A critical review, theoretical framework, and recommendations for further study. Psychological Bulletin, 31(4), 483–509.
  • Doidge, N. (2007). The brain that changes itself: Stories of personal triumph from the frontiers of brain science. New York: Viking Penguin.
  • Edwards, B. (2006). Does it take a village? An investigation of neighbourhood effects on Australian children’s development. Family Matters, 72, 36–43.
  • Emery, R. E., Otto, R. K., & O’Donohue, W. T. (2005). A critical assessment of child custody evaluations: Limited science and a flawed system. Psychological Science in the Public Interest, 6(1), 1–29.
  • Eyer, D. E. (1992). Mother-infant bonding: A scientific fiction. New Haven, CN: Yale University Press.
  • Farran, D. C. (2000). Another decade of early intervention for children who are low income or disabled: What do we know now? In J. P. Shonkoff, & S. J. Meisels (Eds.), Handbook of early intervention (2nd ed.; pp. 510–548). Cambridge: Cambridge University Press.
  • Fergusson, D. M., Boden, J. M., & Horwood, L. J. (2006). Examining the intergenerational transmission of violence in a New Zealand cohort. Child Abuse & Neglect, 30, 89–108.
  • France, A., & Utting, D. (2005). The paradigm of “risk and protection focused prevention” and its impact on services for children and families. Children and Society, 19(2), 144–157.
  • Garcia-Segura, L. M. (2009). Hormones and brain plasticity. New York: Oxford University Press.
  • Gardner, R. A (2004). Commentary on Kelly and Johnston’s “The Alienated Child: A Reformulation of Parental Alienation Syndrome”. Family Court Review, 42(4), 611–621.
  • Gould, S. J. (1981). The mismeasure of man. New York: W. W. Norton & Company.
  • Hayes, A. (1990). Developmental psychology, education and the need to move beyond typological thinking. Australian Journal of Education, 34(3), 235–241.
  • Hayes, L., Smart, D., Toumbourou, J., & Sanson, A. V. (2004). Parenting influences on adolescent alcohol use. Melbourne: Australian Institute of Family Studies.
  • Henaghan, M. (2012). Why judges need to know and understand childhood studies. In M. Freeman (Ed.), Law and childhood studies (pp. 39–54). Oxford: Oxford University Press.
  • Institute of Medicine, & National Research Council. (2012). From neurons to neighborhoods: An update. Workshop summary. Washington, DC: National Academies Press.
  • Kelley, A. E., Schochet, T., & Landry, C. F. (2004). Risk taking and novelty seeking in adolescence: Introduction to Part I. In R. E. Dahl, & L. P. Spear (Eds.), Adolescent brain development: Vulnerabilities and opportunities (Annals of the New York Academy of Science No. 1021; pp. 27–32). New York: New York Academy of Science.
  • Kelly, R. F. & Ramsey, S. H. (2009). Standards for social science amicus briefs in family and child law cases. The Journal of Gender, Race and Justice, 13, 81–103.
  • King, M., & Piper, C. (1995). How the law thinks about children (2nd ed.). Aldershot: Arena.
  • Klaus, M., & Kennell. J. (1976). Maternal-infant bonding: The impact of early separation and loss on family development. St Louis: Mosby.
  • Klaus, M., & Kennell. J. (1982). Parent-infant bonding. St Louis, MO: Mosby.
  • Klaus, M., & Kennell. J. (1983). Parent-infant bonding: Setting the record straight. Journal of Pediatrics, 102(4), 575–576.
  • Laub, J. H., & Sampson, R. J. (2003). Shared beginnings, divergent lives: Delinquent boys to age 70. Cambridge, MA: Harvard University Press.
  • Lerner, R. M., Lewin-Brizan, S., & Warren, A. E. A. (2011). Concepts and theories of human development. In M. E. Lamb, & M. H. Bornstein (Eds.), Social and personality development: An advanced textbook (pp. 19–65). New York: Psychology Press.
  • Lewis, M. (2001). Issue in the study of personality development. Psychological Inquiry, 12(2), 67–83.
  • Ludolph, P. S., & Dale, M. D. (2012). Attachment in child custody: An additive factor, not a determinative one. Family Law Quarterly, 46(1), 1–40.
  • Masten, A. S. (2004). Regulatory processes, risk and resilience in adolescent development. In R. E. Dahl, & L. P. Spear (Eds.), Adolescent brain development: Vulnerabilities and opportunities (Annals of the New York Academy of Science No. 1021; pp. 310–319). New York: New York Academy of Science.
  • Minde, K. (1986). Bonding and attachment: Its relevance for the present-day clinician. Developmental Medicine and Child Neurology, 28(6), 803–806.
  • O’Connor, C. (2008). Trisomy 21 causes Down syndrome. Nature Education, 1(1), 1–5.
  • Parkinson, P., & Cashmore, J. (2008). The voice of a child in family law disputes. Sydney: Oxford University Press.
  • Pembrey, M. E., Bygren, L. O., Kaati, G., Edvinsson, S., Northstone, K., Sjöström, M. et al.. (2006). Sex-specific, male-line transgenerational responses in humans. European Journal of Human Genetics, 14, 159–166.
  • Pihl, R. O., & Benkelfat, C. (2005). Neuromodulators in the development and expression of inhibition and aggression. In R. E. Hartup, W.W. Hartup, & J. Archer (Eds.), Developmental origins of aggression (pp. 261–80). New York, NY: The Guilford Press.
  • Pluess, M., & Belsky, J. (2009). Differential susceptibility to rearing experience: The case of childcare. Journal of Child Psychology and Psychiatry, 50(4), 396–404.
  • Pluess, M., & Belsky, J. (2010). Children’s differential susceptibility to effects of parenting. Family Science, 1(1), 14–25.
  • Rathus, Z. (2012). A call for clarity in the use of social science research in family law decision-making. Australian Journal of Family Law, 26, 81–115.
  • Rhee, S. H., & Waldman, I. D. (2011). Genetic and environmental influences on aggression. In P. R. Shaver, & M. Mikulincer (Eds.), Human aggression and violence: Causes, manifestations, and consequences (pp. 143–63). Washington, DC: American Psychological Association.
  • Rutter, M., Maugham, B., Mortimer, P., & Ouston, J. (1979). Fifteen thousand hours. London: Open Books.
  • Sameroff, A. J. (2004). Ports of entry and the dynamics of mother-infant interventions. In A. J. Sameroff, S. C. McDonough, & K. L. Rosenblum (Eds.), Treating parent-infant relationship problems: Strategies for intervention (pp. 3–28). New York: The Guilford Press.
  • Sampson, R. J., & Laub, J. H. (2005). A general age graded theory of crime: Lessons learned and the future of life-course criminology. In D. P. Farrington (Ed.), Integrated developmental and life-course theories of offending (Advances in Criminological Theory No. 14; pp. 165–181). New Brunswick, NJ: Transaction Publishers.
  • Smart, D., & Vassallo, S. (2005). In the driver’s seat: Understanding young adults driving behaviour. Melbourne: Australian Institute of Family Studies.
  • Smith, J. (2006, July). Psychological vitality in old age: A new look at an old concept. Keynote address to the 19th meeting of the International Society for the Study of Behavioral Development, Melbourne.
  • Spear, L. P. (2000). The adolescent brain and age-related behavioural manifestations. Neuroscience and Biobehavioral Reviews, 24, 417–463.
  • Spear, L. P. (2004). Adolescent brain development and animal models. In R. E. Dahl, & L. P. Spear (Eds.), Adolescent brain development: Vulnerabilities and opportunities (Annals of the New York Academy of Science No. 1021; pp. 23–26). New York: New York Academy of Science.
  • Sroufe, A., & McIntosh, J. (2011). Divorce and attachment relationships: The longitudinal journey. Family Court Review, 49(3), 464–473.
  • Taylor, J. (2011). “What happened to the babies?”: Disadvantage and advantage across 18 years. Australasian Journal of Early Childhood, 36(4), 147–152.
  • Tremblay, R. E., & Nagin, D. S. (2005). The developmental origins of physical aggression in humans. In R. E. Hartup, W.W. Hartup, & J. Archer (Eds.), Developmental origins of aggression (pp. 83–106). New York, NY: Guilford Press.
  • Uslucan, H.- H., & Fuhrer, U. (2009). Intergenerational transmission of violence. In U. Schonpflug (Ed.), Cultural transmission: Psychological, developmental, social and methodological aspects (pp. 391–418). New York, NY: Cambridge University Press.
  • van Goozen, S. H. M. (2005). Hormones and the developmental origins of aggression. In R. E. Hartup, W. W. Hartup, & J. Archer (Eds.), Developmental origins of aggression (pp. 281–306). New York: Guildford Press.
  • van Zeijl, J., Mesman, J., Stolk, M. N., Alink, L. R. A., van Ijenendoorn, M. H., Bakermans-Kranenburg, M. J. et al. (2007). Differential susceptibility to discipline: The moderating effect of child temperament on the association between maternal discipline and early childhood externalizing problems. Journal of Family Psychology, 21(4), 626–636.
  • Ward, O. C. (1999). John Langdon Down: The man and the message. Down Syndrome Research and Practice, 6(1), 19–24.
  • Warshak, R. A. (2001). Current controversies regarding parental alienation syndrome. American Journal of Forensic Psychology, 19(3), 29–53.
  • Werner, E. E. (2005). Resilience research: Past, present and future. In R. D. Peters, B. Leadbeater, & R. J. McMahon (Eds.), Resilience in children, families and communities: Linking context to practice and policy (pp. 3–11). New York, NY: Kluwer Academic/Plenum Publishers.
  • Wiedermann, H. R. (1992). The pioneers of pediatric medicine. European Journal of Pediatrics, 151, 317.

Acknowledgements: This chapter is an edited version of a paper presented to the 15th National Family Law Conference, Hobart, on 15 October 2012. I acknowledge the contributions to this presentation of the following colleagues at the Australian Institute of Family Studies: Carole Jean, Lawrie Moloney, Rae Kaspiew, Ruth Weston and Nancy Virgona. Their assistance is greatly appreciated. The views expressed are those of the author and may not reflect the views of the Australian Institute of Family Studies or the Australian Government.