Poor mental health affects all domains of life, including work, relationships and physical health. Prevalence of mental illness in the UK is increasing, with 1 in 6 people experiencing mental health problems each week. One way of tackling this mental illness epidemic is through prevention. We can achieve this by maintaining and improving people's general mental health and wellbeing, before they reach a clinical diagnosis of mental illness. In this project we are interested in identifying behaviours in ones life that can be modified to improve mental health and wellbeing.

One possible predictor of mental health is our health behaviours. For example, our diet, how much physical activity we do, how much alcohol we consume and whether or not we smoke. While this may seem intuitive, there are many gaps in the research literature. First, it is commonly thought that these behaviours influence our mental health and wellbeing, but little research has been done to assess whether this is a causal effect rather than just a correlation. In order to identify effective intervention targets, it is critically important to ensure that these are causal. We will use complementary methods, allowing us to approach our research question through a number of different lenses. If we can draw consistent results, then we will be able to obtain the strongest and most informative evidence. Second, there is little research that has looked at the nuances of these health behaviours. For example, does the length or intensity of physical activity matter when considering its effect on mental health? We will use the wealth of secondary data available to us to untangle these specific details. Third, these health behaviours do not occur in isolation, therefore, we will investigate how they work together to affect
mental health. And finally, early intervention (i.e. in childhood) is an important aspect of prevention. We will use novel methods to understand how parental health behaviours influence the child's mental health. This can inform us about whether it is better to intervene on the parents or on the child's health behaviours.

Eczema is an itchy skin condition that is caused by a combination of genetics – our DNA – and environmental effects, eg allergens and irritants. Eczema and other allergic conditions often run in families, showing that the effects of our DNA are important, but we are not sure which specific genes are responsible for causing eczema. If we could understand genetic mechanisms we may be able to use this knowledge to develop better treatments.
Studies carried out in large populations (including ALSPAC participants) have shown which regions of DNA may contribute to causing eczema. We have tested these regions in the lab and shown, using skin samples grown in an incubator, that genes which are switched on or off in skin can cause eczema or protect against eczema. We now need to explore whether these findings are important in childhood, comparing children with and without eczema. We would like to do this using the results of analyses from blood and skin samples collected in ALSPAC.
We hope that the results of our work will give valuable clues to how an individual’s DNA contributes to their risk of suffering from eczema.

The negative health risks of exposure to cigarette smoke are well known; including personal, second-hand and foetal exposure during pregnancy.
These health risks, in addition to a high prevalence in the UK and worldwide, make accurate measurement of smoking status an important factor in most epidemiological studies.

DNA methylation appears to provide reliable and long-term markers of tobacco smoke exposure. In fact, it is possible to use combinations of methylation levels at smoking-associated CpG sites to not only differentiate among current, former and never smokers but to also detect smoking intensity, number of smoking years and time since cessation. These aspects of smoking aren't necessarily captured in questionnaire-based responses for a given study. Even if they were, they might not be reliable and may even be misreported. For example, saying you smoke 20 cigarettes a day doesn't say how deep you inhale those cigarettes or whether the brand matters. Moreover, you might be a current smoker but say you're not a smoker out of guilt. Methylation provides a continuous measure (0-100%) in response to various aspects of smoking (rather than "yes/no"), and objectively shows a response to smoking, so can overcome these issues.

Recently, a study by Leffondre found a comprehensive measure of smoking history that incorporated intensity, duration, and time since cessation (including the half-life of the effect of stopping smoking). We will use ARIES DNA methylation data to develop predictors of smoking behaviour using this index, which we will compare against self-reported smoking behaviour from questionnaires and ALSPAC cotinine data. We hope to derive a comprehensive prediction model of smoking which can be applied to other cohorts. Methylation may be able to be used in the absence of self-report data, or more importantly, help improve prediction of diseases which are caused by smoking.

Prenatal depression has been reported to have associations with adverse pregnancy/ birth outcomes in previous observational studies. However, due to residual confounding, the causal effect of prenatal depression on these outcomes still remain unclear. Mendelian randomisation works well as a novel causal inference approach with utilising genetic variants as instrument variables. This aim of this project is to conduct genome wide association studies (GWAS) of prenatal depression to facilitate Mendelian randomisation studies in perinatal epidemiology area.

Essential hypertension (HTN) is a leading, preventable risk factor for cardiovascular morbidity and mortality. Recent genome-wide association studies (GWAS) have provided major insight into the genetic architecture of blood pressure (BP) traits, in part due to increasingly large sample sizes. Moreover, novel approaches to genetic risk quantification have been shown to improve upon traditional methods by more accurately incorporating the growing number of genetic markers with observable effects on common complex traits into a single construct, leading to greater predictive power and clinical translation. This project aims to derive and validate risk scores for BP traits and assess their predictive power for HTN and related morbidity and mortality.

In high-income countries, underweight is largely ignored in health research, despite a clear link with worse health and higher mortality risk. But in the UK, where changes to welfare policy have been accompanied by an explosion in foodbank use, social differences in underweight must be reassessed. This project will be the first comprehensive investigation of present-day inequalities in low body weight in Britain. Considering adults, children and adolescents, we will describe the extent of inequalities, and identify the most vulnerable groups. We will shed light on causes, by comparing inequalities in present-day UK with inequalities in other policy contexts: the UK in the 1990s and 2000s, and Norway from the 1980s to the present day.
Starkly raised risk of underweight was recently found among British adult jobseekers, and higher risk of thinness among younger disadvantaged children. Reported after substantial changes to welfare policy, it is not clear if such inequalities existed before those changes, if similar patterns are seen in other countries, or which other disadvantaged groups are affected. We will find out when these patterns first emerged in the UK, by comparing data from the 1990s, 2000s and 2010s. To see if they only occur in certain policy contexts – strongly suggesting they are avoidable - we will also use data from Norway, which in the same period had different welfare policies and a lower poverty rate. To identify other vulnerable groups, we will look at underweight among adults in low-income employment, and children and adolescents in households affected by unemployment and low-income employment.
The project therefore fills three urgent needs: to describe the extent of inequalities in low body weight, to identify groups of vulnerable adults and children, and to understand the causes of these inequalities. Policymakers currently do not have the knowledge required to consider inequalities across the full body weight range, and this project will fill that gap.

In the UK 14 million people live in poverty. Four million of these are children. The level of child poverty is rising, and the rate is projected to accelerate in coming years. Growing up in a deprived environment can have a profoundly negative effect on a child’s development. Children from deprived backgrounds are more likely to be placed in special education, fail courses, and complete fewer years of schooling. But the adversities children encounter extend well beyond economic hardship and incorporate multiple familial factors like chaotic home life, poor parental mental and physical health, lack of community support, poor schooling and communication difficulties. These factors have a well-documented impact on multiple child outcomes including educational attainment, mental health, and behaviour. This is a global problem. Up to 50% of children and adolescents growing up worldwide experience at least one episode of childhood adversity in early life: 30% of all mental health problems are attributable to such adversity. The effects are also persistent – early adversity can set a life-long trajectory associated with poor physical and mental well-being and significantly worse occupational and economic outcomes. This results in an inter-generational cycle of disadvantage where deprivation impacts each subsequent generation. Supporting young people who face adversity is one of the major modern challenges for educators, practitioners and policy-makers, as they work to reduce educational under-attainment, poor economic outcomes and address the burgeoning mental health crisis.

Yet not all children who face adversity go on to experience poor outcomes: certain factors appear to insulate children from hardship, such that they demonstrate resilience (broadly defined as succeeding in a particular domain, such as education, despite experiencing adversity). Resilience within mental health is an increasingly recognised phenomenon, but our knowledge about which factors foster resilience across a broader range of outcomes, different populations and in response to diverse sources of adversity is currently limited. Understanding the cross-domain factors that promote resilience is vital to drive the development of interventions that improve the outcomes of child and adolescent victims of adversity. This is the purpose of our project. We want to explore how different environmental factors interact with cognitive and brain development, whether particular features of a child's environment are most strongly linked with these outcomes, and whether some factors foster resilience.