Exposure to air pollution has been associated with poorer cardiovascular health and cardiovascular disease, and inflammation is one of the postulated mechanisms of this relationship. Most studies have investigated the association between air pollution and inflammation using C-reactive protein (CRP), particularly in adulthood. Evidence in younger ages and using other inflammatory markers is limited. This study will explore the association between air pollution and inflammation from childhood to early adulthood using different inflammatory markers.

The Avon Longitudinal Study of Parents and Children (ALSPAC) is a prospective birth cohort, based in and around Bristol, UK. Maintaining data security and participant anonymity and confidentiality are key principles for the study, hence why data access is restricted to bona fide researchers and ALSPAC data are not openly available. Despite these valid reason for restricting data availability, this position is somewhat in conflict with emerging best scientific practices, which encourage making data openly available to facilitate reproducible and replicable open scientific research.

Given the rich nature of the resource, ALSPAC data may also be valuable as a educational tool, such as for teaching methods such as longitudinal modelling or approaches to modelling missing data. To aid these efforts, we want to assess methods for generating and making openly-available synthesised ALSPAC data; these synthesised datasets are modelled on the original ALSPAC data, thus maintaining variable distributions and relations among variables, while at the same time preserving participant anonymity and confidentiality. We will explore how data can be synthesised using the ‘synthpop’ package in the R statistical programming language, and aim to present a list of guidelines which all researchers wishing to release such synthesised ALSPAC data must follow.

Crime in adulthood is a well-established long-term consequence of childhood adversity, but the exact mechanism underlying this process is not well known. One mechanism suggested by research is that childhood adversity results in impaired neurobiology, emotional and executive functioning, and self-regulation. Disrupted emotional processing is linked to behavioural problems such as conduct disorders due to an impaired ability to recognise certain emotions, namely anger and fear, with the latter being linked to increased violence. Impaired executive functioning is hypothesized to lead to decreased inhibitory control and cognitive flexibility, while disrupted self-regulation is linked to increased aggressiveness due to an inability to regulate one’s thoughts, actions, and emotions. These deficiencies and their outcomes have been linked to crime, especially violent crime. However, other factors such as genetics, socioeconomic status and alcohol use can increase the likelihood of experiencing additional adversity while also influencing the nature and extent of these impairments. The resulting differences in cognitive and emotional impairments may result in different types of crimes being committed. We hope that better understanding of the processes mediating adverse childhood experiences (ACEs) in children and crime in adulthood can inform more precise therapy employed by clinicians treating these ACEs, as well as more cost-effective measures for policymakers to target the effects of these ACEs in vulnerable populations.

This project aims to understand growth during and after a pregnancy in which the placenta is faulty and less able to nourish the fetus, and its impact on the key developmental brain function of sleep, via mathematical modelling.

Growth is a crucial part of healthy development. So, it is important to understand what happens when growth is impaired. In some pregnancies, the placenta cannot transfer as much oxygen and sugar to the fetus as required. To deal with this, the fetus prioritises its most important organ - the brain - and directs most oxygen and sugar there. This results in the size of the brain relative to the body being larger than usual.

Sleep is a key developmental brain function, supporting the formation of memories. This is why babies spend up to 97% of their time asleep. Because sleep occurs to help our brain but also the rest of our body, the size of the brain relative to the body explains for how long we need to sleep. We believe that the brain growing too large relative to the body may disorganise sleep, and make it less good at helping to form memories. This could explain why infants who grow like this sometimes have later learning difficulties.

In this project, we are going to collate and collect data which will allow us to mathematically test our theory that faulty growth impairs sleep. The results will help to understand this condition better, and could suggest new ideas for personalised therapies, e.g. that strengthen sleep.

Individuals with Attention deficit hyperactivity disorder (ADHD) may be more likely to suffer from mental health problems than the general population. We aim to investigate the relationship between ADHD and depression using data from a longitudinal study of over 14000 children born in the early 90s with ongoing data collection. We will investigate whether specific risk factors such as bullying and childhood adversity may influence this relationship and act as modifiable targets for intervention.

Attention-Deficit Hyperactivity Disorder (ADHD) has symptoms of inattention, hyperactivity, or both. However, patients with ADHD often experience symptoms of other disorders such as autism spectrum disorder (ASD), epilepsy, conduct disorder, or anxiety symptoms. Previously, it was reported that there are shared heritability and cognitive process across the conditions, implying that there are common underlying biopsychological factors that have not been identified.Epigenetic biomarkers, especially blood DNA methylation (DNAm) became significantly important in understanding neurodevelopmental disorders such as ADHD. Even though the associations between DNAm and each condition were investigated, there is a limited amount of research on DNAm biomarkers across ADHD-related phenotypes (ADHD and co-occurring symptoms). We hypothesized that the underlying biological factors would be specific to clusters of conditions and could be used as a diagnosis factor for children. Therefore, we propose to investigate the relationships between each of the individual traits linked to ADHD and DNAm to reveal their epigenetic similarities and differences. The epigenetic similarities and differences will give in-depth insight to understand ADHD. We will use a series of computational methods including EWAS and machine learning to investigate the DNAm biomarkers of complex ADHD-related phenotypes from around 1500 participants from the Avon Longitudinal Study of Parents and Children.

Previous research has found partial evidence for a role of personality traits in mental health outcomes. However, many of these studies do not examine all of the big 5 personality traits simultaneously, examine mental health generally, or a small number of mental health symptoms. These studies also tend to examine participants cross-sectionally, without examining the way in which personality traits may influence mental health longitudinally, after controlling for confounders. This study aims to overcome the previous patchwork coverage of this topic by combining a range of exposure and outcome variables in a prospective cohort study.

Eating Disorders (ED) (full and partial syndrome anorexia nervosa and bulimia nervosa and binge eating disorder) are life- threatening illnesses that start in adolescence and affect between one and two in ten adolescents and young adults. There is a lack in our understanding of why eating disorders develop, which affects our ability to develop treatment and adequately prevent eating disorders. This project builds on our previous studies in ALSPAC, showing that metabolism and growth might play a role in the development of eating disorders. We aim to combine metabolic function, body composition, blood and inflammatory markers, as well as genetic information to understand progression and development of eating disorders and related symptoms in the 3 generations of ALSPAC participants. This study will be fundamental in understanding how eating disorders develop and progress across the life span.

Depersonalisation disorder (DPD) is a distressing condition that typically emerges in young adulthood, characterised by detachment from one’s body and self, and/or one’s environment. Individuals with DPD retrospectively report adverse childhood experiences (ACEs) and are objectively evidenced to have a dysfunctional biological stress system. However, no research has looked at the biological mechanisms that translate ACEs into DPD later in life. Using self-report and biological data of parent-child dyads from the Avon Longitudinal Study of Parents and Children (ALSPAC), I aim to fulfil this research gap. Within the ALSPAC data, instances of childhood sexual, emotional, and physical abuse, emotional neglect and family dysfunction are reported separately by both parents (during annual assessment of the child’s development), and by the child (later in life), which can be combined, creating a measure of ACEs that doesn’t rely solely on retrospective reports. Stress system dysfunction is measured by cortisol (a stress hormone) level, interleukin-6 and C-reactive protein (measures of inflammation). At ages 12 (N = 6832), 17 (N = 5217) and 24 (N = 4021), symptoms of DPD were assessed. Using statistical modelling, I am examining whether the accumulation and the timing of childhood abuse translates into DPD symptoms, mediated by abnormal cortisol and inflammation levels. Additionally, factors with potential to provide risk for, or resilience against, developing DPD symptoms are also being evaluated to provide a comprehensive representation of how DPD symptoms may develop. These include sleep, drug use, attachment, maladaptive cognitions and social position.