<\/p>\n
What works for which children\u2014and why\u2014remains an unresolved question.<\/p>\n
At first sight, the impacts of parent training<\/a> and other interventions seem modest at best, when viewed across the general population. But we are beginning to understand that such across-the-board observations may obscure comparatively large effects for some children who turn out to be much more sensitive than others to both skilled interventions and to their absence.<\/p>\n Rather crudely, people sometimes draw an analogy between orchids and dandelions. Orchids are beautiful, but they need a lot of fertile soil and a good gardener even to survive. Given excellent circumstances, they can turn out looking fabulous. But if the soil is poor and the gardener inexpert, they wither away quickly.<\/p>\n On the other hand, consider dandelions. They can adapt to pretty much any environment. They don\u2019t need a brilliant gardener, great soil or fine weather. They manage to survive and look OK in just about any environment. Indeed, improving the soil or hiring a great gardener may make little difference to how they turn out.<\/p>\n This analogy, although crude, illustrates the difference that research is finding between \u201corchids\u201d \u2014children whose well-being is more susceptible to environmental conditions\u2014and \u201cdandelions\u201d \u2014those whose outcomes are more constant, regardless of circumstances that might either seriously set back or transform the development of the orchids.<\/p>\n \u201cTo label people as intrinsically \u2018at risk\u2019 is dangerous because the characteristics that seem to make them vulnerable may be the very characteristics that offer them optimal development, provided they can find supportive environments.\u201d<\/strong><\/p><\/blockquote>\n Part of the explanation may lie in the role that genes play in child development<\/a>.<\/p>\n Children with certain, less efficient dopamine-related genes do worse in negative environments than children without this genotype. However, at least as interesting is the finding that the group with this \u201cgenetic risk\u201d also profits most from positive environments.<\/p>\n A good example of this phenomenon is children who have a specific variant of the dopamine receptor gene. This gene is said to predict attention deficit disorder so it has a bad reputation in the psychological literature.<\/p>\n But, in a randomised controlled trial, we found that if you bring carriers of this risky genotype into a supportive environment, where they have to focus their attention closely in a series of games, they outperform those who don\u2019t carry this genotype.<\/p>\n They seem more able to learn, provided the environment is structured in a way that is motivating and that helps these children, who were at risk of attention problems, to focus better. Such children might need an environment that\u2019s different from a classroom<\/a>, which can be too noisy and chaotic for them.<\/p>\n Classrooms require them to divide their attention in too many different ways. However, placed in the right environment\u2014focused on a game\u2014they learn better than do their peers.<\/p>\n These findings offer great hope in the search for interventions that can benefit children facing difficulties. They suggest that the children who may appear to be most at risk might be the very ones most likely to benefit from interventions. This observation holds the promise that we might achieve a better fit between interventions and groups of children, which might then result in a more cost-effective<\/a> use of resources.<\/p>\n Genotyping children may not be practical or ethically desirable. However, it might not be necessary. We know that certain genotypes can be associated with specific personality traits, such as a \u201creactive\u201d temperament or elevated biological stress reactivity.<\/p>\n Spotting these indicators can tell us that a child might particularly benefit from a certain intervention, or lose out if it isn\u2019t available. All of this can make it easier to screen children to optimize the fit between child and treatment.<\/p>\n For example, we did a series of studies with children aged 3 and 4, where we used video feedback of interactions to show parents which of their interventions were of really high quality. This helped them hone their skills in responding<\/a> and playing with the children.<\/p>\n We found that this guidance was particularly good at reducing aggressive behaviour<\/a> by children with more reactive, difficult temperaments. These more irritable children, with their more vulnerable temperaments, benefited most in terms of less aggressive behaviour when they experienced quick, sensitive, positive parental interactions<\/a> during periods of distress. The impact was much less pronounced for children with less reactive temperaments.<\/p>\n These observations are not an argument for withholding interventions from less susceptible children.<\/p>\n First, for reasons of equity, there cannot be a difference in eligibility for intervention between children with the same needs; second, apparently less susceptible children may simply be less responsive to the interventions that have been tried or tested so far. They may need different types of intervention.<\/p>\n Ideally, differential susceptibility should lead not to inequity but to differential, sensitive interventions<\/a> and thus more effective treatment.<\/p>\n Our findings should also make us more careful about labelling children as \u2018at risk\u2019 because of their constitution, genetic makeup<\/a>, or temperamental features.<\/p>\n We have shown that, in many cases, the problem is not with them but with the environment in which they find themselves. To label people intrinsically as \u2018at risk\u2019 is dangerous because the characteristics that seem to make them vulnerable may be the very ones that offer them optimal development, provided they can find supportive environments.<\/p>\n \u00a0Bakermans-Kranenburg MJ & van IJzendoorn MH (2011), Differential susceptibility to rearing environment depending on dopamine-related genes: New evidence and a meta-analysis<\/a>, Development and Psychopathology, 23.1<\/em><\/p>\nReferences<\/h4>\n