Living in an urbanized environment undeniably leads to more exposure to urban environmental exposures. Previous studies conducted on urban health were mostly focused on air pollution, while the urban environment is also characterized by its built environment and access to natural spaces. Recently, there is a surging interest to better understand the interplay of different environmental factors that define the urban environment and its effect on children health. Living in a more urbanized environment has been associated with greater adiposity and higher blood pressure in children. Importantly, child cardiometabolic health parameters were mostly investigated individually, while they are intercorrelated. Two approaches have been used to study child cardiometabolic health, a clustering method and a risk score.

How children develop both emotionally and physically may be shaped by their social experiences. Studies investigating adverse experiences in early life suggest that such experiences may have long-term negative effects on mental wellbeing and stress that continue into adulthood. Furthermore, experiencing chronic stress can have physical effects on the body – for example, increased levels of the stress hormone cortisol can elevate inflammation. Over the long term, these effects may increase the risk of diseases such as heart disease and diabetes. This evidence establishes the role of a “psychosocial pathway” linking our social experiences to mental and physical health.

In contrast, social relationships research suggests that positive, supportive social connections confer a psychological benefit, that promotes wellbeing in children and adults and may improve resilience in face of stressful events. This may be achieved by providing a sense of belonging and attachment to others – in other words, social connectedness. Children may experience social connectedness to a range of people across different social contexts, for example within their family; their school; their peers; and their community.

Unpinning the functional aspects of social connections that foster this may therefore identify opportunities to promote mental and physical health and development. However, to date, there has been limited research exploring the physiological effects of social connectedness, and how these may be mediated via stress and its downstream effects, such as inflammation. Epigenetic modification of stress-response genes may underpin long-term effects, however there has been limited research investigating these pathways using birth cohort data. Furthermore, few studies exploring these associations in childhood have included or compared multiple social contexts. Lastly, there is limited research utilising longitudinal data to explore how associations between social connectedness, mental health, stress and inflammation may change over time.

This project aims to address these research gaps by investigating the associations between early life social connectedness, mental health and biological indicators of stress and inflammation across different social contexts – namely, family, school, friends, and community. This project will investigate how these social experiences may establish longitudinal trends in mental health and stress across childhood and into early adulthood. To investigate one potential mechanism that may underpin long-term physical effects, this project will assess the relationship between social connectedness and epigenetic modification of stress-response genes.

According to life-history theory, any organism will strategically divide resources toward growth, maintenance and reproduction (Ellis, 2004). In a harsh environment, humans might mature earlier to enable earlier reproduction – to secure the transmission of one’s own genes in the next generations (Belsky et al., 1991). Previous research has indeed indicated that harsh family environments, such as chaotic life environments or rejecting, inconsistent parental behavior, and severe stressors can lead to earlier pubertal maturation (in girls) (Belsky et al., 2010; Belsky, Steinberg, et al., 2007; Ellis et al., 1999; Holdsworth & Appleton, 2020; Sheppard et al., 2016). Recently, a two-hit model of accelerated aging has been proposed (Belsky & Shalev 2016), specifying that early adversity does not necessarily lead to earlier sexual reproduction even though it has been found to predict pubertal maturation. Belsky and Shalev hypothesized that a supportive environment during puberty can act as a buffer against early sexual reproduction. Moreover, they hypothesized a potential biological mechanism, wherein early childhood adversity may result in epigenetic changes (i.e. advanced biological age compared to chronological age measured via epigenetic clocks) which might result in earlier pubertal maturation and (in case of a non-supportive environment) in earlier sexual reproduction.
Some previous proposals have looked at parts of this model (e.g. B878, B897, B2760, B2883, B3077, B3690), but we will be the first to combine these parts, such as relation between father absence and puberty or the relation between pubertal development and sexual risky behaviors into one overarching model of the life history theory.

We propose research to advance precision in predicting individual prognostic trajectory and individual response to intervention for three common and debilitating categories of mental disorders in childhood: (1) Depressive Disorders, (2) Anxiety Disorders, and (3) Attention Deficit Hyperactivity Disorder. Our research will advance this precision by elucidating the etiologic heterogeneity of samples of children within these three diagnostic groups and determining clinical signatures corresponding to such heterogeneity. Such signatures will guide the development of a set of assessment and clinical decision-support tools that we will evaluate – integrating behavioral tests/measures – for classifying children with depression, anxiety disorders, and ADHD into sub-groups strongly informing on individual prognosis and probable responsiveness to specific categories of intervention.

Globally, increasing prevalence of obesity has been observed, not just amongst adults but also in children. Studies have suggested that early development of obesity in childhood is associated with obesity in adulthood and development of chronic illnesses. It is thus important that factors associated with the rising prevalence of obesity amongst children are investigated, so that early interventions can be put in place to address the issue. While the causes contributing to obesity are complex, healthy eating is one of the most important and modifiable risk factors to address this issue. Traditionally, studies have been conducted to understand specific food group or nutrient and the association with obesity. However, in recent decades, food systems have undergone major changes that have led to a rising availability of ultra-processed foods globally. Under the NOVA food processing classification, ultra-processed foods are defined as industrial products made with many ingredients not accessible in domestic kitchen and typically contain a myriad of artificial additives. While there are growing evidence that the consumption of ultra-processed foods are linked to obesity in adults, this has not been examined in children except for few cohort studies with short follow up time. Therefore, this project aims to investigate the link between childhood consumption of ultra-processed foods and the development of overweight and obesity from childhood to early adulthood in the ALSPAC birth cohort. The results of this study will address an important gap in literature and also provide valuable insights to help shape future policies in tackling childhood obesity.

Research using data from the AVON Study has found developmental stability of language development (Bornstein et al., 2018, Science Advances). Children whose language ability ranks low at 6 months are likely to continue to rank low when they are 15 years old. The results are group-level results revealing group tendencies, rather than pinpointing whether a particular infant will likely to develop better or poorer language in later childhood. We would like to examine whether a more precise analytical approach can be adopted so that we will be in a better position to forecast language development at the individual-child level.

Problematic alcohol use is a major public health burden. It is important to understand how to best predict individuals most at risk for alcohol problems so they can be targeted for early prevention efforts. This project will explore whether combining polygenic risk scores can enhance the prediction of alcohol problems.

This project will investigate how speech sounds develop in the first 8 years of life in children born prematurely. Preterm children are at increased risk of impaired neurodevelopment, which can include problems with acquisition of speech and speech disorder. Speech sound disorder can impact their learning, mental health, and life chances in adulthood. This study will provide information on how prematurity impacts speech development and how this compares with full-term children. This will help health professionals in the early identification and intervention of preterm children requiring support.

The study comprises five workstreams. 1) a full systematic review of the literature to determine the characteristics associated with speech sound development in preterm children; 2) examination of data from the ALSPAC dataset to explore the characteristics and outcomes of speech development in preterm children in the first 8 years of life compared with full term children; 3) examination of data from the National Neonatal Audit Programme (NNAP) to explore how the degree of prematurity impacts speech development in preterm children; 4) collection of new data from a clinical sample of preterm children recruited from NHS neonatal services in Bristol and Cardiff; 5) a UK-wide online survey will determine the role of Speech and Language Therapists in NHS neurodevelopmental assessments for preterm children in the first 3 years of life.

This projects seeks to deepen our understanding of how the timing of puberty affects adult health outcomes, specifically, risk of cardiovascular disease (CVD). The age at which a girl gets her first menstrual period (age at menarche, or AAM) has a peculiar relationship with CVD: both earlier and later AAM are associated with increased risk of CVD in adulthood.

In preliminary work focusing on later AAM, we applied human genetic techniques to distinguish the effects of common genetic changes on AAM from the effects of other, yet-to-be-identified factors. We were surprised to find that the relationship between later AAM and CVD depends on the underlying cause of later AAM. If caused by common genetic changes, later AAM is actually associated with _lower_ risk of cardiovascular disease. In contrast, if caused by other factors, later AAM is associated with _increased_ risk of cardiovascular disease.

The broad goals of this project are 1) to better understand how common genetic changes affect AAM by subgrouping common genetic variants based on their effects on childhood factors known to affect AAM, and 2) to identify factors other than common genetic changes that influence AAM.