We will use data from ALSPAC to investigate predictors of trajectories of smoking behaviours, and transitions from smoking to vaping in early adulthood. Smoking remains the leading cause of preventable cancer; understanding factors associated with smoking and vaping, particularly during early adulthood (a critical period when transitions out of smoking are likely to begin), will inform future cancer prevention programmes and public health policy. This includes identifying predictors that can be used to tailor these programmes more effectively, as well as establishing causal risk factors where interventions could be targeted.

We are proposing to collect measures of smoking and vaping in the next questionnaire. This would enable us to extend existing work being carried out as part of B3499.

Eating disorders are serious psychiatric conditions that often start in adolescence. Prevalence and burden of eating disorders are rising, they are developing at earlier ages and hospital admissions rising sharply. Currently, there is a lack in our understanding of how sociocultural factors (e.g., food insecurity, racial discrimination) interact with psychobiological factors (e.g., gender) and comorbidities (e.g., depression). This information is vital for informing prevention and early intervention methods for eating disorders in adolescents.

There are different causes for high cholesterol in the blood. Sometimes, it is because of faulty genes that people inherit from their parents. ‘Polygenic hypercholesterolaemia’ is a condition where the cholesterol is raised because of the combined effect of several faulty genes together. ‘Familial hypercholesterolaemia’ is caused by a severe problem with one gene, rather than many. We know that having high cholesterol could cause heart attack or stroke. In this study we will find out to what extent cholesterol deposits in the neck artery of children with polygenic hypercholesterolaemia and how does it compare to children who have familial hypercholesterolaemia and those who don’t have and cholesterol problems. There are currently no data supporting a treatment of children with polygenic high cholesterol.

Urbanisation has a profound effect on respiratory health in children, partly through some of the adverse environmental exposures such as air pollution and loss of biodiversity. However, relatively little is known about how different land use types within a given neighbourhood affect respiratory health in children over the life course. Evidence is scarce regarding the so-called grey space (industrial, transport hub etc) on children respiratory health in the UK. Recent studies have reported health impacts of certain land use types in children respiratory health, such as green and blue spaces, although the evidence is not always consistent. Parts of the reasons were due to the less accurate assessment of multidimensional nature of green space (amount, types, quality, usages) and the use of a crude indicator in statistical models without strong statistical justifications. This project therefore aims to investigate the effects of land use mix (LUM) around the residential environment on children respiratory health, using both conventional and novel statistical techniques.

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.

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.