Digital technology has become an indispensable aspect of children's lives, providing unparalleled prospects for learning, entertainment, and social interaction. Nonetheless, the excessive and problematic utilization of digital devices has emerged as a prominent global concern. Based on the statement of the American Academy of Paediatrics (AAP), children aged two years or older were recommended to limit the amount of total entertainment screen time to no more than two hours. Excessive screen time may lead to harmful health outcomes among children and adolescents, including mental health problems.
However, whether the link between screen time and mental health is causal is questionable. There may be bidirectional associations, with poor mental health affecting screen time and vice versa. And associations may be affected by gene-environment correlations/genetic confounding.

Extreme heat (> 40°C heat) is becoming more and more commonplace in the UK meanging overheating in homes and buildings is a key risk. It is important to understand how this affects people’s physical and mental health, wellbeing and behaviour during heatwaves so that strategies can be developed to help people adapt.

Most research in the UK related to heat and health is focused on outdoor temperatures and population-scale health outcomes (e.g., mortality in South-West England) rather than people’s experiences and perceptions of heat, which varies between individuals and the buildings they live in.

We will fill these gaps by working with ALSPAC to develop and test a questionnaire that will ask participants about their experience and behaviour during a heatwave. The data collected from this plot will not be linked back to any ofther data but will help us to understand how heat might affect the health and wellbeing ofdifferent people, help to inform the development of early warnings and contribute to a fellowship application leading to more detailed research in ALSPAC.

In 2010, the American Heart Association (AHA) created ‘Life’s Simple 7 (LS7)’ – a risk score aimed at quantifying ideal cardiovascular health behaviours within large populations. This risk score consisted of seven modifiable factors known to influence cardiovascular disease; namely body weight, physical activity, diet, smoking, total cholesterol, glucose, and blood pressure. Over the last 12 years, LS7 has been shown to be effective in predicting a wide-range of future cardiovascular events in older cohorts, as well as the subclinical development of early cardiovascular risk in the young. In 2022, the AHA revised and updated this risk score to become ‘Life’s Essential 8 (LE8)’, adding sleep quality as a new modifiable risk factor for disease and altering definitions of what constitutes ‘ideal behaviours’ in many of the other risk factors. The comparability of this new score to LS7, however, and feasibility of using it in large population datasets to predict outcomes such as early changes in heart and brain health remains unknown.

In 2010, the American Heart Association (AHA) created ‘Life’s Simple 7 (LS7)’ – a risk score aimed at quantifying ideal cardiovascular health behaviours within large populations. This risk score consisted of seven modifiable factors known to influence cardiovascular disease; namely body weight, physical activity, diet, smoking, total cholesterol, glucose, and blood pressure. Over the last 12 years, LS7 has been shown to be effective in predicting a wide-range of future cardiovascular events in older cohorts, as well as the subclinical development of early cardiovascular risk in the young. In 2022, the AHA revised and updated this risk score to become ‘Life’s Essential 8 (LE8)’, adding sleep quality as a new modifiable risk factor for disease and altering definitions of what constitutes ‘ideal behaviours’ in many of the other risk factors. The comparability of this new score to LS7, however, and feasibility of using it in large population datasets to predict outcomes such as early changes in heart and brain health remains unknown.

Repair of adult tissues involves a complex interplay of several key cell lineages and inevitably leads to formation of a fibrotic collagenous scar, whereas embryonic tissues heal perfectly without any resulting scar deposition. This dramatic difference in repair efficiency between embryonic versus neonatal/adult tissues has been instrumental is guiding us towards potential causes of scarring. Indeed, we now believe that one major driver of scarring is the wound inflammatory response which doesn't initiate until a transition period in fetal development which, in turn, coincides with the developmental onset of tissue scarring. This insight has led us towards further mechanistic cell and molecular studies in model organisms, such as mouse and zebrafish, which help us better understand the scarring process and how one might modulate the wound inflammatory response in order to improve or prevent scarring.

Whilst these approaches, motivated by comparing embryonic versus adult healing, have been fruitful, it is clear that scarring is a complex, multifactorial response likely driven by a number of interacting mechanisms. We would like to use a conceptually similar comparative approach to gain further insights into the fundamental cell and molecular mechanisms of scarring by analyzing differences in degree of scarring, not between embryo and adult, but rather across human adult populations since we know there is a range of “scarring phenotypes” from “minimal scarrer” to keloid scarring individuals. This use of human phenotypic variation in a population based, genetic association approach (genomewide association studies – GWAS), has the potential not only to yield gene variant correlates of scarring, but also to point towards specific biological contributions to wound healing. The use of natural human experiments (e.g. Bacillus Calmette–Guérin (BCG) vaccination wound healing, Caesarean section (C-section) wound scarring and examples of human disease related fibroses) has never before been used for identification of scarring genes, even though the approach has proven to be powerful for discovering genes associated elsewhere with a wide variety of complex health outcomes (www.ebi.ac.uk/gwas/). Furthermore, alongside a growing number of catalogues charting the results of human genetic association studies for health outcomes and intermediates there are tools able to consider (in frameworks of causal analysis) the existence of potentially causal and modifiable relationships between exposures of interest (e.g. inflammation, differential wound repair or scar) and health outcomes (e.g. wound healing, recovery, and disease).

Using human genetic data to help explore the potential of biological pathways contributing to health and disease in applied epidemiological designs is an approach that we have refined and developed and is an integrated approach to health research that has yielded important clinically relevant insights, but has also indicated opportunities (e.g. associated signaling pathways for targeting) to unify basic science approaches with human population based health data (see below).

Currently, vascular ill-health appears to be the most preventable component of cognitive decline in older age. There is however very limited understanding about the time at which signs of damage are already present in diseases that take decades to result in symptoms. In this project we will work to identify through imaging the markers that can help us quantify the health status of vessels and associated tissues in the brain. We will also work to better understand their relationship to known risk factors for cardiovascular disease.

There is emerging evidence of high levels of (often undiagnosed) autism within homeless populations, with current estimates of around 12-18% of people receiving support for homelessness meeting criteria for an autism diagnosis. However there is a lack of population-wide studies exploring the co-occurrence of homelessness or insecure housing and autism diagnosis or traits.

Whilst other studies exist elsewhere charting the metabolome of disease or of adult or mid-to-late age participants, there are few examples of longitudinal metabolomic data. ALSPAC does have proton nuclear magnetic resonance spectroscopy data on an extended lipidome and select protein panel (Nightingale), however data do not exist for longitudinal liquid chromatography/mass-spectroscopy derived metabolites. This approach has the potential to substantially expand the metabolite collection in ALSPAC, to allow new association analyses and also to provide a benchmark or longitudinal standard for circulating metabolites across ages. This work proposes to collect new data (from existing samples) under a sampling framework aiming to maximise capture of longitudinal changes in metabolic profile.

Attention deficit hyperactivity disorder is a major neurodevelopmental disorder during childhood, affecting 5% of children across the UK. Mental health difficulties, such as anxiety, stress, and depression, often cooccur with ADHD and can persist from childhood, through adolescence, to adulthood. Separately, ADHD has also been linked to increased levels of obesity and a more sedentary lifestyle. This issue is concerning given that research has shown that participation in exercise and sports provides a range of health-related benefits, including better mental health. Hence, we aim to 1) explore the biological, social, and psychological factors that predict higher sports participation in individuals with ADHD, 2) evaluate whether higher sports participation predicts better mental health in the long-term in individuals with ADHD, and 3) explore whether the longitudinal relationship between sports participation and mental health to be different between individuals with higher and lower symptoms of ADHD.