Intimate partner violence (IPV) among adolescents and young adults is a growing yet under-explored problem. IPV can include emotional, physical, and sexual abuse between romantic partners, and it can lead to long-lasting harm. Some adolescents and young adults face higher risk of being involved in IPV, either as victims or perpetrators, especially if they have certain personality traits or have experienced difficult circumstances, such as childhood maltreatment. However, there is still a lack of targeted interventions in the UK that aim to prevent IPV in this group accounting for individual and contextual risk profiles. This project will investigate how personality and experiences of childhood maltreatment influence the risk of IPV among adolescents and young adults, and lay the groundwork for the development of a tailored intervention to promote safe relationships in this group.

People with autism and ADHD have a high occurrence of 1) vitamin D deficiency and 2) having a physical inflammatory condition such as rheumatoid arthritis or inflammatory bowel disease. Understanding if there are genetic links between these occurrences may raise awareness in screening for early signs of inflammation in people with autism and ADHD.

In recent years, a number of studies have proposed that vitamin D has connections in inflammatory processes within the body. There are a number of genes that connect vitamin D metabolism with autism and ADHD, vitamin D metabolism with a systemic inflammatory condition and ADHD with a systemic inflammatory condition.

Initial observations from a process called mendelian randomisation suggest that causal link is potentially present. I am therefore asking if individuals that differ in these genes may be at increased risk of developing a physical inflammatory condition such as inflammatory bowel disease or rheumatoid arthritis. I am also interested in finding out whether differences in these genes increase the risk of progression to an intervention being required, such as medicines or hospitalisation for physical health inflammation symptoms.

My project will involve looking at genetic material from people diagnosed with autism and/or ADHD, their vitamin D levels and comparing the frequencies of inflammation conditions of these genes with the frequencies found in the general population. I will also look at whether certain forms of the gene are more prevalent in hospitalised patients, compared to those who are not. The value in this research is that it could help us understand more about the role the role of vitamin D and inflammation signalling pathways in people with autism and/ or ADHD, and identify targets for drug treatment. Importantly, it may help us to identify individuals who should have routine screening for an inflammatory condition to prevent it causing disabilities. As this project will only involve reanalysis of existing data, I expect the project duration to be a period of months.

It has been suggested that parenting (i.e., parenting behaviours directed toward children) is passed through the generations. However, rigorous evaluation of intergenerational (IG) continuity (i.e., similarities/differences in mean levels of parenting behaviours across generations) and stability (i.e., associations between parents and children’s parenting behaviours) of parenting is lacking. Substantial gaps in existing evidence remain regarding which parenting behaviours are transmitted, when in development transmission occurs and what process underly continuity and discontinuity of IG transmission. Furthermore, longitudinal research that examines associations between parenting in one generation (e.g., G0; grandparents), parenting of the next generation (G1; parents) and developmental and mental health in their offspring (G2; grandchildren) is very limited. Insights into these questions are crucial for targeted intervention and prevention programmes to address IG continuity and stability of parenting to improve offspring developmental and mental health outcomes in the next generation.

Existing evidence-base regarding IG transmission of parenting and its role in intergenerational transmission of mental health risks is extremely limited. Most studies are retrospective, while prospective three-generational studies that utilise data from three generations (G0/Grandparents->G1/Parents->G2/Grandchildren) are acutely lacking. Relatedly, most evidence is based on retrospective rather than prospective reports of parenting, which may be prone to recall and reporting bias, particularly in the context of parental depression. IG transmission has been mostly examined in the context of maltreatment and harsh parenting (e.g., aggressive, abusive, highly conflictual), with few studies addressing IG transmission of positive parenting in non-clinical populations (e.g., parental monitoring, warmth and enjoyment, inductive discipline, ‘normative’ levels of conflict). Furthermore, evidence of sex differences in IG transmission of parenting is almost non-existing, with most studies historically focusing on mothers and not fathers, without differentiating between genetic, psychological and contextual factors that may confound IG transmission of parenting. Importantly, it remains unclear through which processes and/or mechanisms parenting is transmitted across generations and the role it plays in offspring mental health and development due to retrospective designs and lack of prospective longitudinal three-generational study on parenting and mental health that enable to infer causality. Understanding processes that underly continuity and stability of IG transmission of parenting (i.e., mediators) and factors that disrupt continuity and stability of IG transmission of parenting (i.e., moderators) is of crucial importance to preventive (e.g., enhancing positive parenting) and targeted intervention programs (e.g., disrupting negative parenting) to break the IG cycle of negative parenting and adverse offspring outcomes.

Although self-reported data on parenting captures parental perceptions and attitudes to parenting, it may be biased by parental mental health status and does not capture the nature and quality of family and parent-child interactions. Specifically, family interactions provide a fundamental context for offspring development. In two-parent families (irrespective of parental sex and gender), children experience dyadic and triadic interactions routinely. Family-systems perspective emphasises importance of family sub-systems, such as mother-child, father-child, parent-parent relationship and co-parenting, as developmentally formative in influencing offspring development. These interactional subsystems are interrelated exerting mutual effects, however, they are not captured by dyadic mother- and father-child interactions. Dyadic interactions provide important insights into individual patterns of parent-child interactions (within sub-systems), which are related yet distinct from interaction patterns within other family sub-systems, including parental relationship and co-parenting sub-systems. Emphasis on dyadic parent-child interactions only obscures important role that family-level interactions play in offspring development because accumulation of individual measures is not equivalent to the whole family measure and parental and child behaviours may not be organised in the same way across dyadic and triadic contexts. Furthermore, children have the capacity to engage in both dyadic and triadic interactions early in infancy, with both parental and child behaviours mutually affecting each other, suggesting the need to consider child interactive behaviours in the context of dyadic and triadic interactions. Despite developmental importance of triadic interactions, there is a distinct lack of studies examining both dyadic and triadic interactions and their impact on offspring developmental and mental health outcomes, particularly in the context of parental depression. This is a substantial limitation given growing evidence supporting the importance of triadic family interactions for offspring developmental and mental health outcomes, as well as important clinical implications. Qualitative meaning of the family interactions to parents is as important as behavioural manifestations, particularly in those families where parents experience mental health difficulties. However, it is rarely captured in research, constituting an important limitation as these meanings have important implications for the development of targeted interventions to improve parental and offspring mental health.

This study explores the influence of the ”home obesogenic environment” on childhood obesity and, in particular, the interplay between the environmental and genetic factors. To do so, we generate a latent variable for “home environment” using domains that have been established in the literature as contributing to obesity, generating what we call the “Cultural Risk Score (CRS)”. Using two U.S. datasets, the National Longitudinal Study of Adolescent to Adult Health (Add Health) and the Future of Families and Child Wellbeing Study and one British data set (ALSPAC), we employ Confirmatory Factor Analysis (CFA) and Structural Equation Modeling (SEM) to assess how environmental and genetic factors affect children’s BMI and how different levels of CRS can modulate genetic penetrance. Preliminary findings for the U.S. datasets indicate that dietary factors, physical activity and parental education are the most relevant domains for the home obesogenic environment. Additionally, the model reveals significant variations in genetic effects on BMI across different CRS levels, suggesting important gene-environment interactions. The CRS will be an input in a generalized stable population model and Agent Based Model whose goal is to predict future obesity trajectories.

Adverse childhood experiences (ACEs) are associated with multiple negative health behaviors and consequences including both physical and mental health conditions in adulthood. Previous studies have commonly examined the impact of ACEs on a single outcome. However, recent evidence shows that exposure to ACEs may also increase the risk of multimorbidity such as overweight or obesity in combination with mental health conditions. This project will explore this, and the mechanisms through which the co-occurrence of overweight/obesity and mental health problems might arise.

The causes and consequences of child maltreatment remain highly controversial. Social-psychological and health factors such as parenting stress and child behaviour disorders are often identified as major risk factors for child maltreatment; however, there is limited evidence from existing studies to establish a temporal sequence that confirms a causal relationship. Taking parenting stress as an example, according to the Stress and Coping Model of Child Maltreatment Theory (Hillson & Kuiper, 1994), most research has focused on a unidirectional relationship in which parenting stress leads to child maltreatment. However, emerging evidence suggests a potential vicious cycle in which child maltreatment increases parenting stress through parental guilt and children’s behavioural issues. Verification of these dynamics relies on longitudinal data for bidirectional temporal analysis. This project aims to employ techniques such as cross-lagged panel model to investigate the bidirectional temporal effects between social-psychological or health factors and child maltreatment. By addressing these gaps, this study seeks to enhance understanding of the interplay between parental and child-specific features and child maltreatment, contributing valuable insights to inform prevention and intervention strategies.

Blood traits, such as complete blood count and fetal hemoglobin, are implicated in various physiological and pathological processes. The value of these traits is variable from one individual to another and a significant part of this variation that is due to genetic factors that have been identified. It has been shown in adults that these genetic factors impact patients’ management. However, their impact is poorly known in children. Per example, whether lower white blood count have an impact on infection risk and work up and whether a mildly lower hemoglobin level impairs growth is unclear. Moreover, whether the impact has a causal relationship is unknown. Finally, fetal hemoglobin is a type of hemoglobin specific to fetus that has been selected throughout evolution to favor oxygen delivery to the newborn as it ties more strongly to oxygen than the adult hemoglobin from the mother. As some fetal hemoglobin may persist in adults, the difference between mother and child fetal hemoglobin varies across pregnancies. However, the impact on weight at birth and later in life of this difference remains to be studied. Here, we propose to leverage state-of-the-art genetic approaches to address these two aspects blood traits. We will used the genetic variations known to be associated to blood traits to study their effect throughout childhood without the need of direct measurement. Deciphering the impact of blood traits in children will improve our understanding of their effect and may provide powerful tools to tailor patients’ management toward a personalized, precision medicine.

Observational studies have found evidence that depression, anxiety and neuroticism are prospectively associated with lower urinary tract symptoms (LUTS) in women. Although prospective studies provide evidence of the direction of observed associations, they are limited by unmeasured and residual confounding. Observational studies that rely on self-report questionnaires to assess depression, anxiety and neuroticism exposures are also limited by measurement error. Polygenic risk scores (PRS) can be used estimate an individual’s underlying genetic liability to complex traits such as depression, anxiety and neuroticism. PRS should not be associated with genetic or environmental confounders at a population level, which can bias observational studies.

Previous research has suggested that young people who grew up in homes where their parents were violent or abusive towards each other are more likely to have violent or abusive relationships themselves. We have been looking into this in Children of the 90’s data, to get a better understanding of the relationship between growing up around violence or abuse between parents in the UK, as reported by the parents at the time of the violence or abuse, and being in a violent or abusive relationship as a young adult. However, some participants (both parents and children) will have left the study since being initially recruited, and it is likely that those who are in abusive relationships are more likely to be the ones that leave. In this study, we want to find ways to account for these people that have left, so that our estimates about the risks of being in an abusive relationship are more accurate.