Clearly, the onset of depressive symptoms, at any stage of an individual’s life, is a cause for deep concern among loved ones. But the emergence of such problems in young children and adolescents is especially worrisome for parents – and never more so than when it coincides with problems at home.
But what really underpins the link between children’s emotional problems and their home environments – and how does the onset of adolescence change things? These questions are at the heart of our latest piece of research, published this week in the Journal of Child Psychology and Psychiatry.
Unpicking the relationship between children’s emotional and behavioural problems and their early environments can be fiendishly difficult. With children plausibly able to influence and be influenced by their environments in equal measure, the direction of effects in any association is seldom clear-cut. And when the environment in question involves biologically related family members – as, typically, within a child’s home – these problems become even knottier, with genetic and environmental sources of influence intermingling.
In an earlier post on this blog, Tom detailed these issues specifically in relation to intergenerational associations – links between parent and child behaviours. He also outlined some of the methodologies commonly used to investigate intergenerational associations: adoption studies, IVF studies, the children-of-twins design, to name a few. However, data from ‘traditional’ child-based twin studies can also be used to investigate links between the home environment, more broadly, and emerging psychopathology.
In our latest paper, published this week in the Journal of Child Psychology and Psychiatry (JCPP), we make use of data from the Twins Early Development Study (TEDS) to investigate links between children’s depressive symptoms and aspects of their home environments. TEDS is a longitudinal, UK-representative twin sample which has been running since the mid-nineties, and still has over 10,000 actively participating families today.
For those of us interested in the developmental emergence of psychiatric disorders, samples like TEDS are invaluable. The fact that TEDS is composed of a mixture of identical and non-identical twins (and their parents) makes the data genetically-informative. This is useful for far more than simply estimating the heritability of individual behaviours. Having accounted for genetic influences on a given behaviour, we can investigate the nature and influence of environmental factors – to a more accurate degree than in a putatively environmental study that fails to take genes into consideration. If we use this genetically-informative data in models that also capitalise on the longitudinal nature of the sample, we can begin to chip away at the complexity of these problems.
In our JCPP paper, we use data from children and their parents collected when the twins were 9, 12, 14, and 16 years old. The prevalence of depression jumps sharply in adolescence 1, 2, but adolescent depression is linked to earlier emotional difficulties 3. As such, this period – the transition between childhood and adolescence – may be a useful one to study to understand the emergence of depressive symptoms. Since an individual’s home environment remains relatively consistent (in composition, if not, necessarily, in nature) across this period, and has been shown to be associated with depression in adolescence 4, 5, it provides an interesting environmental context to test. Specifically, we wanted to know: what is the nature of the relationship between depressive symptoms and the home environment in middle childhood? Does this change in adolescence? And, if so, why?
To answer these questions, we ran a series of statistical models that were designed to test different explanations of developmental change and stability in the association between depressive symptoms and the home environment. The degree to which differences in symptom scores were associated with differences on measures of the home environment (such as parenting and household chaos) was quite consistent between childhood (9-12 years, r = .44 [.40-.49]) and adolescence (14-16 years, r = .43 [.39-.47]). However, we observed subtle changes in the nature of the association.
In childhood, the link between children’s depressive symptoms and their home environment was mainly (70%) due to shared environmental influences – comprising factors such as parenting and neighbourhood characteristics. This is consistent with an explanation of the home operating as an environmental influence on depression scores. In adolescence, these factors were still important, but genetic influences had grown to account for 40% of the association, while unique environmental factors also became significant, accounting for 12%.
So, what does this mean?
The presence of (child) genetic factors in the association between children’s depressive symptoms and their home environment can be interpreted as evidence of children’s behaviour influencing their environment. This is, essentially, the opposite direction-of-effects to that in an account with children as passive recipients of environmental (including parental) influence. Although such extreme nurture-only accounts are largely outmoded, they do still exist and – in spite of the evidence – are widely popularised. As such, these kinds of findings are worth noting whenever they occur (as they, pretty much ubiquitously 6, 7, tend to do).
“We show that the direction-of-effects within links between environmental factors and behaviours should not be assumed – and nor should the links themselves be assumed to represent the same processes at all developmental stages”
However, we were primarily interested in developmental change. First and foremost, the composition of the association did change across this period when the prevalence of depression begins to rise. The way in which it did so was through the waning of shared environmental influences, and the amplification of genetic and unique environmental influences. This is consistent with the idea that the home environment becomes less of a fixed, uniform context in adolescence, and is more influenced by individuals’ genetic propensities and external factors that enter in – and that its links with children’s depressive symptoms change accordingly.
Overall, I think that the results of this study reaffirm that the transitional period between childhood and adolescence is a crucial one for studying the emergence of problems like depression. We also show that the direction-of-effects within links between environmental factors and behaviours should not be assumed, and nor should the links themselves be assumed to represent the same processes at all developmental stages. Most broadly, I am hopeful that work like this helps to show the use of behavioural genetic tools for studying all kinds of questions, and going far beyond the simple estimation of heritability.
JCPP paper reference:
Hannigan LJ, McAdams TA, & Eley TC (2017). Developmental change in the association between adolescent depressive symptoms and the home environment: results from a longitudinal, genetically informative investigation. Journal of Child Psychology and Psychiatry http://doi.wiley.com/10.1111/jcpp.12689
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2 Costello EJ, Copeland WE, & Angold A (2011). Trends in psychopathology across the adolescent years: What changes when children become adolescents, and when adolescents become adults? Journal of Child Psychology and Psychiatry and Allied Disciplines 52, 1015–1025.
3 Bittner A, Egger HL, Erkanli A, Costello EJ, Foley DL, & Angold A (2007). What do childhood anxiety disorders predict? Journal of Child Psychology and Psychiatry and Allied Disciplines 48, 1174–1183.
4 McLeod BD, Weisz JR, & Wood JJ (2007). Examining the association between parenting and childhood depression: a meta-analysis. Clinical psychology review 27, 986–1003.
5 Sheeber L, Hops H, & Davis B (2001). Family processes in adolescent depression. Clinical Child and Family Psychology Review 4, 19–35.
6 Avinun R, & Knafo A (2014). Parenting as a reaction evoked by children’s genotype: a meta-analysis of children-as-twins studies. Personality and Social Psychology Review 18, 87–102.
7 Knafo A, & Jaffee S (2013). Gene-environment correlation in developmental psychopathology. Development and psychopathology 25, 1–6.