Identifying and understanding predictors of risky behaviour can help to inform prevention and intervention strategies for related outcomes. For example, alcohol consumption may have an influence on risky sexual behaviour, understanding this relationship could inform prevention and interventions for sexually transmitted diseases, unplanned pregnancies, abortions, and general sexual health. Another risk factor is for subsequent risk behaviours is adverse childhood experiences (ACEs). Individuals with histories of multiple ACEs are found to be more likely to engage in risk behaviours such as smoking, excessive drinking, risky sexual behaviour, illicit drug use and suicidal behaviour than those without.
This project will use longitudinal data from the ALSPAC study to identify predictors of risk behaviours in adolescence and early adulthood.

The link between women's reproductive and cardiovascular health is increasingly recognised. Some, but not all studies have shown that women who experience night sweats and/or hot flushes as part of the menopausal transition are more likely to have heart disease. We also know that women who have complications during pregnancy are at greater risk of heart disease later in life. Here we would like to investigate the associations between all of pregnancy complications, menopausal symptoms and cardiovascular health in a general population of women, the ALSPAC mothers. We will also use genetics data to examine whether genetic risk for for more adverse cardiovascular health are associated with pregnancy complications and/or vasomotor symptoms.

Reducing inequalities in child mental health is a public health priority, yet the pathways that link social conditions to mental health outcomes in the early years are unclear. Few studies have compared the social distribution and prevalence of mental health problems across countries, or have compared pathways to any inequalities. Understanding these pathways is critical in order to guide public policy to improve child health and reduce inequalities. In Life Cycle cohort families we aim to assess how early years risk factors mediate the relationship between childhood SECs and subsequent inequalities in child mental health and cognitive development.

Puberty is a time of sweeping biological and social change. Boys and girls who experience early and/or rapid puberty are at elevated risk for psychiatric and physical health problems, including substance use disorders, suicide, polycystic ovary syndrome (in females), and cardiovascular disease. Psychiatric disorders like major depressive disorder also become much more prevalent at puberty and may impede cognitive skill development . Considering the many negative implications of departures from the normal pubertal development, understanding the genetic and environmental regulators of puberty has become a topic of increasing urgency. Our research aims to identify specific and potentially modifiable environmental factors that influence pubertal timing and examine its association with children’s cognitive development and mental health, and we view genetic and epigenetic data as essential tools for accomplishing that goal.

Scientific progress on understanding genetic influences and epigenetic changes (including DNA methylation) at puberty has moved slowly. Previous studies looking at changes in DNA methylation across puberty have been conducted in very small samples; nevertheless, this previous work support the potential to develop an epigenetic clock for pubertal age, analogous to epigenetic clocks that exist for aging. However, generating a clock that is highly accurate and robust requires longitudinal DNA methylation data spanning the pubertal transition. We will substantially improve the rigor and reproducibility of previous research on the epigenetics of pubertal age by using a discovery sample that is substantially better-powered (the Texas Twin project) and by replicating results in an independent sample (ALSPAC). We can then examine potential environmental (e.g., family socioeconomic background) and genetic predictors (e.g., polygenic scores of reproductive phenotypes) of our epigenetic clock for pubertal age, as well as the cognitive and mental health sequelae of advanced epigenetic pubertal age.

Self-harm among adolescents and young adults is a widespread public health problem. Self-harm is often a maladaptive coping strategy used to alleviate severe emotion dysregulation following stressful events. Adolescence is a period of marked development in the realm of social relationships and socio-emotional competencies. However, the developmental associations between social stress and self-harm across the adolescent years are poorly understood. In particular, the mechanisms linking social stress and self-harm are largely understudied. Better knowledge about these processes is urgently needed, in order to identify promising targets for interventions designed to support adolescents with self-harm and help them cease from this self-destructive behavior.

Therefore, the aim of this project is to investigate how social stress and self-harm are interrelated between early adolescence and early adulthood. A particular focus will be on the mechanisms underlying these associations. Candidate mediators are a) biological manifestations of stress (e.g., inflammation) and b) physical health and health behaviors (e.g., sleep patterns). Potential gender differences will also be considered.

The findings will provide novel insights into the developmental precursors of adolescent self-harm and help improve intervention programs designed to reduce the enormous burden that self-harm can entail for individuals and society.

Social cognition, the ability to understand the mind of other people, is essential for successful social
interaction. Children with emotional and behavioural problems are more likely to have a history of poor
social cognition ability. However, the path from poor social cognition to emotional and behavioural problems
in childhood and adolescence is unclear. The possibility I will explore in this PhD project is that social
cognitive deficits increase stress (i.e., hypothalamus-pituitary-adrenal dysregulation and flattened cortisol
rhythm and/or chronic inflammation), leading to emotional and behavioural problems. Cortisol and
inflammatory cytokines are thought to be promising biomarkers of various stressed-related behavioural and,
particularly, emotional disorders, yet existing evidence in children and adolescents is little and mixed, and
is mostly about clinical disorders. Additionally, it is not known yet how cortisol and inflammatory cytokines
work when facing stress caused by social cognition deficits, especially in the general population. The aim
of the project is to explore the role of these biomarkers in the interplay mechanism of social cognition deficits
and emotional and behavioural problems in children and adolescents, using longitudinal data from a large
general population study, the Avon Longitudinal Study of Parents and Children. Analytically, the project will
explore three relationships: a) the longitudinal association between deficits in core aspects of social
cognition (emotion recognition & theory of mind) and emotional and behavioural problems, b) the role of
cortisol in explaining the association and c) and the role of inflammatory cytokines in explaining the
association. The relationship between inflammation and cortisol is complex so the final analysis exploring
the role of both will consider this complexity fully.

Myopia (short-sightedness) is an eye condition in which distance vision is blurry. People with myopia need to wear glasses or contact lenses, or have laser refractive surgery, to achieve sharp distance vision. When people with myopia get older, they are at a higher-than-average risk of developing permanent sight problems such as macular disease. Myopia typically develops during school age. The reason it develops is not understood, however both genes and lifestyle factors are known to play a role. Children whose parents have myopia inherit a genetic predisposition to develop myopia themselves. In clinical studies, children who are randomly assigned to spend extra time outdoors each day have a lower incidence of myopia, suggesting that spending too little time outdoors is a risk factor. Individuals who spend more years at school also tend to develop a higher level of myopia. Around the world, the prevalence rate of myopia varies widely. This is thought to be related to the variation in the ‘intensity’ of school work and the pressure to do well at school. Myopia has also been linked to mental health problems such as depression and to levels of physical activity. However, for most of these links, it is unclear if myopia is a cause or a consequence of the association.

The ALSPAC cohort is unique in the scale and breadth of the information that has been collected about vision problems in childhood. This includes information about myopia development. In previous studies of ALSPAC participants, our research group has documented the time-course of myopia development and exposure to risk factors or protective factors such as time spent outdoors. For example, children from the ALSPAC cohort who spent relatively less time outdoors than their peers at age 7-years-old were found to have an increased risk of developing myopia by the age of 15. Here, we propose to build on our previous findings. Our primary aim is to discover if myopia is the cause or consequence of its associations with other lifestyle factors and health or wellbeing characteristics. To do this, we will use a technique called Mendelian randomisation, which uses random inheritance of subtle genetic features in a way similar to randomisation of participants in a clinical trial. Usually, Mendelian randomisation studies require very large cohorts of participants – larger than the ALSPAC cohort. However, myopia and many of the related conditions we plan to investigate are highly heritable, which means there is a good prospect of successfully answering our research questions using data collected in a sample the size of the ALSPAC cohort. Our secondary aims are extensions of the primary aim. We will compare the eye characteristics and lifestyle of children growing up in the UK with those of children elsewhere, to investigate if the risks for myopia are similar or different in countries with high or low prevalence rates of myopia. We will also extend our previous studies into the genetics of myopia. The exceptionally high level of detail that the ALSPAC research team has collected about genetics will allow us to test the role of specific genes in conferring a predisposition to myopia, and how this varies depending on the lifestyle risk factors that children are exposed to.