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But there is also more evidence-based stuff. Some children do have serious difficulties mastering spoken language, and there is research demonstrating links between parent talk and child language outcomes. We've known since the influential study of Hart and Risley (1995) that there is massive variation in the amount of language children are exposed to at home, and this is predicted by socio-economic status. There are many subsequent studies showing positive associations between aspects of the language that babies and toddlers hear and the rate and complexity of their language development.
When the Guardian ran a piece last week on the latest of these studies, someone tweeted "do we really need a study to demonstrate that?" – to most people it's blindingly obvious that children's language development will be determined by the language that they hear at home. This assumption is shared by many professionals in the field of language development; for instance, in a recent review, Leffel and Suskind (2013) describe poor attainment of children from disadvantaged homes and unambiguously state: "Parent linguistic input lies at the heart of the problem".
Except that it's not so simple. And the complexities become apparent when we look at the type of evidence that we have, which is mostly correlational. Students learn in Psychology #101 that correlation does not equal causation, yet when a causal interpretation seems so obvious to most people, this can get forgotten. I have lost count of the number of times I've seen a study showing that parent talk predicts child language development, where the conclusion drawn by the authors (and press offices and the media) is that limited parental language causes child language problems. No other explanation is even countenanced. Yet if we were well taught in Psychology #101, we would realise that we need to consider alternative explanations for the observed association. The figure below shows three possible causal models; these are not mutually exclusive and so all could play a role.
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| Different Models to account for association between parent talk and child language |
Model A is the one that is typically assumed by most people: parent talk to children boosts their language development, and accordingly, if a child has poor language skills, this is likely to be caused by inadequate talk from parents.
In Model B, the association goes in the other direction. Poor language in the child leads to less talk from the parent. This could occur if, for instance, parents are discouraged from talking to a child who is unresponsive and appears not to understand. Consider too, this recent study looking at outcomes of infants in a special care baby unit . Children who were exposed to more adult language in hospital had better language outcomes; however, as the authors noted, "It could be that parents and caregivers have more opportunity to talk to infants who are less sick."
Model C explains the association without postulating a direct link from parental talk to child language. Instead it sees both of these as outcomes of some other cause. This could be an environmental factor, such as poor diet, or a genetic risk that is shared by parents and their children.
It is the job of researchers to try and find evidence to establish the relative importance of these different causal routes. In the case of child language, this is not just a theoretical exercise: it potentially makes a difference to the kinds of intervention that are likely to be effective in helping children. In particular, if model A is the main explanation for the association, then we should be able to boost poor child language by encouraging reticent parents to interact more like talkative parents. This is unlikely to be effective if model B explains the association. And if model C applies, then we would need to either modify the third factor (X) itself, or clarify how it operated in order to alter its association with poor outcomes in children.
I am concerned about the near-universal acceptance of model A as the sole explanation, because there are two lines of evidence that go against it. First, we can to some extent disentangle the impact of socioeconomic disadvantage and parental talk if we study children whose parents produce little spoken language input because they have a congenital hearing impairment. Some profoundly deaf parents have children with normal hearing. In the past there was concern about such children: how would they learn spoken language if their parents produced little intelligible speech? In fact, the studies that were done obtained unexpectedly positive results, leading to the conclusion that although young children clearly need some exposure to spoken language in order to learn to speak, they could develop normal language on the basis of exposure to other adults outside the home and language on TV (Schiff-Myers, 1988).
The second line of evidence comes from studies that disentangle genetic and environmental influences by considering language development in twins. If parental talk is an important determinant of child language, then we would expect twins growing up together in the same home to resemble each other. However, if model A is all-important, we would not expect the genetic relationship between the twins to have any effect. But it does make a difference, and on many language measures this effect is quite substantial. So we find that twins do resemble each other in general, but that resemblance is quite a bit higher if the twins are genetically identical (monozygotic) than if they are fraternal (dizygotic, and sharing around half their DNA for genes that vary between people).
I remember being struck when I first did twin studies of children's language difficulties at how different two twins growing up in the same family could be – provided they were non-identical. It was, however, unusual to find identical twin pairs where one had a significant language problem and the other was unaffected. The overall pattern of results tells us that the child's genetic makeup plays a role in determining their language development (Bishop, 2006).
So what has this to do with models A, B and C? Quite simply, the twin data support a version of model C: given that genes affect language development, we expect parents (who share around half their genes with their children) to resemble their children. We already know that parents of children with language impairments are more likely than other parents to have some kind of language or literacy problem themselves (Barry et al, 2007). This doesn't affect everyone: of course there are many literate and articulate parents whose children have language difficulties. But on balance, these kinds of difficulties run through generations, and we therefore expect to see an association between limited language ability in parents and language difficulties in their children. Note that a genetic account will also predict that language difficulties in children will predominate among those of lower social-economic status: parents who themselves are language-impaired are likely to have low levels of educational attainment and poor occupational prospects.
This kind of genetic explanation for parent-child similarities has a lot of evidential support, but people are very reluctant to accept it. If you propose that genes may play a role in children's developmental difficulties, people will tend to assume that you have a political agenda aligned with the Third Reich, with a goal of identifying a genetic underclass who should not be helped because they are just 'made that way'. This reflects a wrong-headed genetic determinism that is at odds with contemporary understanding of how genes work. Genes do not determine your fate: their impact is likely to vary according to the environment, and by modifying environments we may alter outcomes. Unlike in model A, though, model C predicts that sensitivity to specific environments may depend on one's genes. The arguments have been cogently put in a recent book by Asbury and Plomin (2013), who lament the way in which genetic influences on children's development have been ignored in favour of a political stance that blames educational and developmental difficulties on either poor parenting or poor teaching. If, as has been repeatedly shown, there is evidence that genes are important in influencing children's language development, then we may be squandering our intervention resources by ignoring this fact.
The bottom line is that we need more research. Well-conducted randomized controlled trials on the impact of modifying parent input have been thin on the ground to date, and have not generated impressive evidence of efficacy (see my earlier blogpost) . Obviously, it's early days, and I'd cheer on others who are attempting such research. Results may depend on the nature of the intervention, the aspects of language that are assessed, and the type of population the intervention is used with. My suggestion is that rather than denying the reality of genetic effects, we should be conducting research to find out what kinds of input are most effective for children who are at genetic risk. It is possible that rather than more language input, they may do best with a different kind of language input, specifically tailored to take into account their cognitive strengths and weaknesses. We are a long way from understanding how best to do this, and meanwhile, ingenious and dedicated practitioners are working hard to tackle the very real problems that some children experience. My message is simply that to lay the blame for these difficulties at the door of parents, and to anticipate that problems can be readily overcome by encouraging parents to talk more to their children may be oversimplistic.
To finish, I cannot resist adding my favourite quote from Richard Dawkins, which focuses on mathematics rather than language learning, but gets to the nub of inappropriate concerns about genetic explanations:
People seem to have little difficulty in accepting the modifiability of "environmental" effects on human development. If a child has had bad teaching in mathematics, it is accepted that the resulting deficiency can be remedied by extra good teaching the following year. But any suggestion that the child's mathematical deficiency might have a genetic origin is likely to be greeted with something approaching despair: if it is in the genes "it is written", it is "determined" and nothing can be done about it: you might as well give up attempting to teach the child mathematics. This is pernicious rubbish on an almost astrological scale ..... What did genes do to deserve their sinister juggernaut-like reputation? Why do we not make a similar bogey out of, say, nursery education or confirmation classes? Why are genes thought to be so much more fixed and inescapable in their effects than television, nuns, or books?
Richard Dawkins (1982) The extended phenotype, Oxford University Press (p. 13)
References
Asbury, K., & Plomin, R. (2013). G is for genes: The impact of genetics on education and achievement. Chichester: Wiley Blackwell.
Barry, J. G., Yasin, I., & Bishop, D. V. M. (2007). Heritable risk factors associated with language impairments. Genes, Brain and Behavior, 6, 66-76.
Bishop, D. V. M. (2006). What causes specific language impairment in children? Current Directions in Psychological Science, 15, 217-221.
Caskey, M., Stephens, B., Tucker, R., & Vohr, B. (2014). Adult talk in the NICU with preterm infants and developmental outcomes Pediatrics DOI: 10.1542/peds.2013-0104
Hart, B., & Risley, T. R. (1995). Meaningful differences in the everyday experience of young American children. Baltimore, MD: Paul H. Brookes Publishing Co.
Leffel, K., & Suskind, D. (2013). Parent-directed approaches to enrich the early language environments of children living in poverty. Seminars in Speech and Language, 34(4), 267-277. doi: 10.1055/s-0033-1353443
Schiff-Myers, N. (1988). Hearing children of deaf parents. In D. Bishop & K. Mogford (Eds.), Language development in exceptional circumstances (pp. 47-61). Edinburgh: Churchill Livingstone.
This article (Figshare version) can be cited as:
Bishop, Dorothy V M (2014): Parent talk and child language. figshare.
http://dx.doi.org/10.6084/m9.figshare.1030407