Mental health issues are among the primary contributors to the global disease burden. Chronic systemic inflammation is a major suspected mechanism, as poor mental health has been linked to the elevated production of inflammatory molecules, which may in turn adversely affect health. While mental health is often considered a risk factor of its own, it may also reflect underlying adverse socioeconomic conditions. Studies have highlighted a social gradient in inflammatory biomarkers, showing that individuals with lower income, education, and occupational status are more likely to have elevated systemic inflammation biomarkers.

The precise factors explaining this social gradient in inflammation remain unclear. Poor social circumstances can lead to poor mental health, which might in turn affect biological pathways. Additionally, it is plausible that individuals facing challenging social circumstances may have fewer resources available to manage mental health issues, which can, in turn, affect their physiology. Understanding the interplay between mental health, social circumstances, and inflammation is further complicated by developmental influences, where early life stress and social environment may have a significant impact on health in later life.

To address these gaps, this project will leverage cutting-edge statistical methods, allowing us to draw new insights into how mental health and social circumstances jointly contribute to systemic inflammation across the life course. We will analyse data from three British cohort studies, each covering different age ranges and capturing multiple instances of mental health evaluations, socioeconomic indicators, biomarkers of inflammation, and other influences.

Experiencing mental health issues during pregnancy and after birth can have implications for how womens parenting, including how they feed their children which can impact on child weight outcomes. This research will examine the impact of prenatal mental health (such as anxiety, depression and stress) on women's feelings towards pregnancy and intentions and attitudes to feeding, how they feed their child (in terms of breastfeeding and diet), and child body mass index. These findings can help inform how best to support women and their children.

Although cardiovascular disease (CVD) has traditionally been thought of as a condition that affects older individuals, it is now understood that its origins may begin to develop early in life, during childhood. It is therefore important to identify and promote healthy lifestyle factors in early life stages that may prevent CVD.

Vitamin D has emerged as an important factor in maintaining a healthy cardiovascular system. Low blood levels of vitamin D can lead to inflammation, altered hormone levels, and reduced release of molecules that relax blood vessels. This can in turn raise blood pressure and increase the risk of heart attacks, strokes, and other cardiovascular problems.

Although it is understood that there is an association between vitamin D status and heart health, few studies have explored whether vitamin D concentrations in childhood are related to CVD risk factors and vascular health later in life. To address this gap in the literature, we will use data from the Avon Longitudinal Study of Parents and Children (ALSPAC), which has monitored the health of children from birth into adulthood. Our goal is to determine if higher vitamin D concentrations in the blood during childhood are associated with better vessel function and cardiovascular health indicators – including blood sugar, blood fats, blood pressure, and body fat mass – in adulthood. The goal of this study is to help clarify whether adequate vitamin D concentrations during childhood reduces the risk of developing CVD later in life.

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.

Parents differ in numerous ways, including how they engage verbally and non-verbally with their infants. As the most important source of learning, parents play a key role in teaching critical skills such as language and communication. However, despite the vital role parents play, most research on how children acquire language has focused on identifying general learning mechanisms, often ignoring individual differences among parents. This approach assumes a "one-size-fits-all" model, leading to general recommendations for all parents. In reality, parenting styles vary widely, and more individualised guidance may be more effective.

Our project aims to fill this gap by investigating how individual parenting styles affect language development. Rather than focusing on isolated mechanisms, we propose a data-driven approach to explore how parents function as "language coaches" for their infants. By moving away from idealised, uniform learning models, we seek to uncover how different styles contribute to language acquisition.

Traditionally, research has looked at individual behaviors—such as pitch, speech rate, or vocabulary—separately as predictors of language outcomes. This overlooks how parents combine strategies during interactions. Some parents may rely on prosodic features like varied pitch and slower speech, while others use repetition to reinforce associations between objects and words. Meanwhile, others may provide more varied input, responding rapidly to their child's shifting focus during play. These varied, yet effective approaches highlight the need to understand how different parenting strategies foster language development.

Our project challenges the assumption that all parents should follow the same guidelines to support language development. We will investigate how different combinations of parental behaviours, or "coaching styles," contribute to language learning.

The aim of this project is to investigate the impact of different parental coaching styles on early language development. Specifically, we seek to:

Identify consistent patterns in how parents modify their speech and interaction when engaging with their children.
Examine the connection between these coaching styles and the synchrony observed in parent-infant interactions.

To achieve these goals, we will use cluster analysis, a data-driven method that identifies natural groupings in parental speech and communication behaviours. This allows us to explore how different aspects of speech—such as pitch, speed, and vocabulary—combine with interaction styles, like following or directing a child’s attention.

We will analyse a unique dataset of video recordings from head-mounted cameras worn by both parents and infants during free-play sessions, collected as part of the Avon Longitudinal Study of Parents and Children (ALSPAC). These recordings offer an in-depth, dual-perspective view of parent-infant interactions, capturing the dynamics of communication and engagement in naturalistic settings. By studying this data, we aim to identify clusters of distinct parenting styles and link them to children's language development outcomes. Furthermore, we will explore how parental characteristics, such as anxiety or depression, may influence these parenting styles and their potential impact on language acquisition.

This project will enhance our understanding of diverse parenting strategies, enabling more personalised support, particularly for families with children experiencing language delays. When recommendations feel natural for parents, they are easier to follow, increasing the potential for positive impacts on children's development. Our findings could help shape more effective support programmes for parents, educators, and policymakers by providing practical, tailored advice that reflects individual differences in language coaching styles.

We aim to characterize the associations between environmental exposures and genetics on circulating proteome.

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.

Locus of Control of reinforcement (LOC) has been shown to have far reaching effects in academic and professional achievement, as well as mental and physical health and well-being. In brief, those considered internally controlled (i.e. belief that an outcome is mainly contingent upon their own choices and behaviour) have better outcomes in all areas than those who are more externally controlled (believing what they do makes little difference, and everything is down to luck, chance or powerful others).
Previous research has identified that there is stability in adult LOC over time, however, adolescent LOC is more volatile because of faster and extensive emotional and physical changes.
LOC is important as it has been shown to have an effect almost every aspect of life (on educational achievement, business/employment, financial security, physical and mental health and even mortality (internality predicting better outcomes)). There appears to be no research conducted to date that specifically looks at whether early or late onset of puberty changes an adolescent’s orientation from that at pre- to post-puberty.
LOC was collected from ALSPAC offspring participants at the ages of 8 (n=), 16 (n=) and 27 years (n=). Puberty questionnaires were administered annually between the ages of 8 and 17 years. SITAR calculations of height to derive age at peak height velocity were also available. From the data available we will ascertain the age at which puberty starts and if this has an impact on LOC internality post-puberty.
Aims:
To ascertain whether pubertal timing affects LOC orientation at 16, and whether this remains stable or moves towards internality by age 27.
Are there lasting effects of LOC/pubertal timing on outcomes at age 27+ (including risky behaviours, educational achievement, financial security, criminality, depression and anxiety)?
Why is LOC important in adolescence?
Those children who are external are less likely to do well academically with potentially lasting effects throughout the lifespan. As puberty occurs prior to major educational assessments (GCSEs especially and A levels), it is important to assess if LOC is affected by it. If so, targeted interventions may increase students’ internality at this crucial period in their lives.

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.