Research

Our research is organized mainly along the two following themes:

Chicken and egg: causal inference in mental health
Psychopathology is a major public health concern and the leading contributor for years lived with disability worldwide. Identifying early risk factors that are causally related to psychopathology is crucial for designing effective evidence-based social policies and interventions. However, identifying true causal risk factors is extremely difficult due to problems like environmental and genetic confounding or reverse causation (i.e. chicken and egg). For example, is alcohol use causing depression or are depressed people more likely to drink as a consequence of their depression. As a result, even well-established risk estimates can simply be a consistent measure of bias. In our lab, we aim to use statistical innovation and genetically informative designs in order to strengthen causal inference. For example, we use the twin differences design to better establish the role of childhood bullying victimisation on mental health in adolescence. We are also currently involved in studies using Mendelian randomisation, a technique that use DNA information to make better causal inference. In addition, in collaboration with national and international colleagues, we look at mechanisms that could explain how these risk factors “get under the skin” and explain later mental health difficulties (see collaborations).

Developmental genetics and the externalizing spectrum
A lot of our research focuses on the so-called ‘externalizing spectrum’ including behaviours such as ADHD, aggression and substance use. For example, we have demonstrated the importance of individual differences in the developmental course of these externalizing behaviours on a range of long-term outcomes including criminality and substance abuse. We also look at the reasons behind these individual differences in the developmental course. For example, applying for the first time developmental techniques to ADHD (biometric decomposition of latent growth models), we have showed that genetic factors explained most of the individual differences in the developmental course of symptoms. In other words, developmental genetic factors seemed to largely explain persistence versus remission in ADHD. Most interestingly, these genetic factors were largely different from those explaining the baseline levels in ADHD symptoms pointing towards a specific set of developmental genes. These studies also highlighted the importance of “developmental genetic effects”, i.e. the fact that genetic influences largely explained why some children had persistent or rising levels of behavioural problems with age, whereas symptoms declined in other children. In addition, his research showed that the effects of shared environmental influences (e.g. family socioeconomic status) were largely short-term. These findings contrast with the common belief that the effects of genes are ‘fixed‘ throughout development and that changes in symptoms can be explained mainly by environmental factors (e.g. changes in family circumstances) and have profound implications regarding our understanding of how environmental risk and resilience operate throughout childhood.

We are grateful to the following present and past funders: