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.

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.

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.

Obesity is a significant challenge for individuals, societies, and economies. Whilst behaviours involved in energy balance, such as physical activity and diet, have been a primary focus of obesity research, several psychosocial factors have also shown promising associations. Social connections (such as social support and social networks) are known to be linked to disease and mortality in later life. Research has shown associations between social connections and a reduced risk of obesity, yet there is little known about these associations in earlier life stages including childhood, adolescence, and young adulthood. Taking a lifecourse perspective has the potential to reset health and social trajectories by encouraging a proactive preventative approach, rather than a reactive treatment approach. The specific roles and relative contributions of the different social connection dimensions (structural, functional, and quality) are also unclear, meaning the optimum ways to intervene are unknown.

Understanding the underlying biosocial mechanisms linking social connections to health is important as it can help establish causality and suggest novel interventions. Stress and inflammatory response systems have been individually associated with both social connections and obesity but have not been studied in this relationship. Ultimately, this project aims to provide a comprehensive understanding of the relationship between early life social connections and obesity across the early lifecourse, including the exploration of the potential underlying biological mechanisms.

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.

Maternal-related diseases affect the development of offspring nervous system. However, there are currently some limitations in the research on this topic, such as small sample sizes, short observation periods, lack of long-term follow-up, unconsidered confounding factors and interactions, etc. To overcome these limitations, our study plans to use the large-scale population cohort data in ALSPAC, adopt advanced statistical methods and causal inference methods, systematically analyze the strength of the association and causal effects of maternal-related diseases between neurodevelopmental disorders in offspring, and explore possible mechanisms and intervention measures.

Most research has found a positive association between religious belief and mental health, but these are often in US samples, which may differ from samples in other countries. We have previously examined childhood and adolescent mental health and parental religious belief, which have found results that differ from much of the previous literature. This study seeks to expand upon our previous studies of childhood and adolescent mental health by examining adult mental health, and whether offspring religious belief is associated with it in a large UK cohort study.

Depression and hypertension commonly co-occur. This comorbidity may be explained by HPA axis dysregulation which has associations with both hypertension and depression. Additionally, sleep problems are a known cause of HPA axis dysregulation, therefore, sleep may serve as a transdiagnositic marker, and potentailly intervention point, for both disorders. This research will focus on childhood and adolescence as previous research has only examined this relationships in adults, despite these conditions being prevalent in younger groups. Additionally, adulthood is a time when these conditions are already well-established. Through examining a younger sample, we can study the directionality and mediation of this relationship at a time when both conditions start to emerge.