Studies have suggested that waist (cm)/height (cm) ratio (WC/H) is a useful alternative measure of central adiposity and obesity related metabolic risk in adults and children than body mass index (BMI) (1-3). In practice, BMI has shown poor performance in certain cohorts and does not indicate an individual’s distribution of fat. WC/H focuses on central adiposity, a known cardiometabolic risk factor for adults and children. Furthermore, calculating BMI requires weighing equipment, a calculator and potentially software/charts. WC/H only needs a tape measure, uses a simple calculation and has a pre-defined ratio to define risk across participant types (cited as >0.5).

NICE have recently recommended the use of WC/H alongside BMI to assess and predict weight-related conditions. There is currently a paucity of research describing the life course patterns of WC/H or demonstrating that it provides equal or improved prediction in metabolic health from childhood to adult life compared to BMI. There is also little evidence relating WC/H to outcomes or intermediates related to central adiposity in particular – e.g., hypertension and non-alcoholic fatty liver disease.

This study aims to 1) chart the trajectory of WC/H compared to BMI through ages 7, 11, 15 and 24, 2) examine associations of WC/H or BMI, and blood pressure and liver health at these ages and 3) compare these associations to explore if WC/H is more discriminatory in defining risk. This will provide additional evidence for the recommendation of an easier measure to assess clinical need for weight management interventions across childhood and adolescence.

References
1. Ashwell M, Gibson S. Waist-to-height ratio as an indicator of 'early health risk': simpler and more predictive than using a 'matrix' based on BMI and waist circumference. BMJ Open. 2016 Mar 14;6(3):e010159.
2. Savva SC, Tornaritis M, Savva ME, Kourides Y, Panagi A, Silikiotou N, Georgiou C, Kafatos A. Waist circumference and waist-to-height ratio are better predictors of cardiovascular disease risk factors in children than body mass index. Int J Obes Relat Metab Disord. 2000 Nov;24(11):1453-8.
3. Khoury M, Manlhiot C, McCrindle BW. Role of the waist/height ratio in the cardiometabolic risk assessment of children classified by body mass index. J Am Coll Cardiol. 2013 Aug 20;62(8):742-51.

Previous research has shown association between exposure to long-term air pollution and adverse lipid profiles. Fewer studies have been performed using metabolomics, which identify and quantify small molecules to represent an organism’s metabolic state. A metabolic signature in the blood associated with ambient air pollution exposure is plausible given some ambient air pollutants (ultrafine particles and gaseous air pollution) have been reported to enter the bloodstream directly from the lungs. Most research in this area has focused on adulthood, and little evidence is available in younger ages. This study aims to assess the metabolomic signature of air pollution in childhood.

Most research on youth criminal behaviour and recidivism (the tendency for an offender to reoffend) focuses on risk factors, and the literature often describes protective effects of the lack of a risk factor. However, the absence of a risk factor is not inherently protective and a deeper understanding of protective factors is useful in designing public health interventions. Protective factors explored in the literature are: social and emotional support, family support and connectedness, engagement in religious activities, school connectedness, and educational attainment. While there is some initial evidence suggesting these factors are protective against crime and/or promote desistance, this evidence is limited and much of it comes from adult samples and samples outside the UK. This project will use ALSPAC data to examine the role of early life and educational factors in protecting young people from offending, and in promoting desistance.

The Avon Longitudinal Study of Parents and Children (ALSPAC) is a prospective birth cohort, based in and around Bristol, UK. Maintaining data security and participant anonymity and confidentiality are key principles for the study, hence why data access is restricted to bona fide researchers and ALSPAC data are not openly available. Despite these valid reason for restricting data availability, this position is somewhat in conflict with emerging best scientific practices, which encourage making data openly available to facilitate reproducible and replicable open scientific research.

Given the rich nature of the resource, ALSPAC data may also be valuable as a educational tool, such as for teaching methods such as longitudinal modelling or approaches to modelling missing data. To aid these efforts, we want to assess methods for generating and making openly-available synthesised ALSPAC data; these synthesised datasets are modelled on the original ALSPAC data, thus maintaining variable distributions and relations among variables, while at the same time preserving participant anonymity and confidentiality. We will explore how data can be synthesised using the ‘synthpop’ package in the R statistical programming language, and aim to present a list of guidelines which all researchers wishing to release such synthesised ALSPAC data must follow.

Crime in adulthood is a well-established long-term consequence of childhood adversity, but the exact mechanism underlying this process is not well known. One mechanism suggested by research is that childhood adversity results in impaired neurobiology, emotional and executive functioning, and self-regulation. Disrupted emotional processing is linked to behavioural problems such as conduct disorders due to an impaired ability to recognise certain emotions, namely anger and fear, with the latter being linked to increased violence. Impaired executive functioning is hypothesized to lead to decreased inhibitory control and cognitive flexibility, while disrupted self-regulation is linked to increased aggressiveness due to an inability to regulate one’s thoughts, actions, and emotions. These deficiencies and their outcomes have been linked to crime, especially violent crime. However, other factors such as genetics, socioeconomic status and alcohol use can increase the likelihood of experiencing additional adversity while also influencing the nature and extent of these impairments. The resulting differences in cognitive and emotional impairments may result in different types of crimes being committed. We hope that better understanding of the processes mediating adverse childhood experiences (ACEs) in children and crime in adulthood can inform more precise therapy employed by clinicians treating these ACEs, as well as more cost-effective measures for policymakers to target the effects of these ACEs in vulnerable populations.

This project aims to understand growth during and after a pregnancy in which the placenta is faulty and less able to nourish the fetus, and its impact on the key developmental brain function of sleep, via mathematical modelling.

Growth is a crucial part of healthy development. So, it is important to understand what happens when growth is impaired. In some pregnancies, the placenta cannot transfer as much oxygen and sugar to the fetus as required. To deal with this, the fetus prioritises its most important organ - the brain - and directs most oxygen and sugar there. This results in the size of the brain relative to the body being larger than usual.

Sleep is a key developmental brain function, supporting the formation of memories. This is why babies spend up to 97% of their time asleep. Because sleep occurs to help our brain but also the rest of our body, the size of the brain relative to the body explains for how long we need to sleep. We believe that the brain growing too large relative to the body may disorganise sleep, and make it less good at helping to form memories. This could explain why infants who grow like this sometimes have later learning difficulties.

In this project, we are going to collate and collect data which will allow us to mathematically test our theory that faulty growth impairs sleep. The results will help to understand this condition better, and could suggest new ideas for personalised therapies, e.g. that strengthen sleep.

There are several studies that have examined the role of personality in pro-environmental attitudes or behaviours. However, they typically investigate either attitudes or behaviours. Environmental attitudes and behaviours have been identified as an area with a significant gap between attitude and behaviour. We wish to address this gap by examining whether personality traits are predictive of both attitude and behaviour, and whether those who have pro-environmental attitudes and perform pro environmental behaviours differ from those who do not. Using the ALSPAC dataset will allow us to examine personality and its role in pro-environmental variables longitudinally.

The National Mental Health Intelligence Network (NMHIN) has been commissioned by NHSE to determine whether an estimate of mental health need for 0–4-year-olds can be produced, with the aim of being able to produce national and local area prevalence estimates for this age group.

This work included an initial feasibility assessment which was advised by an expert reference group (ERG) of experts in the field. The ERG gave a strong steer of using an existing cohort study that assesses the mental health of the children in this age group, considering limited availability of data around the topic which can be generalized at national level.

Currently, we are looking at developing an interim national prevalence that gives an estimate of mental health need among this age group. This will be done by selecting a study sample from ALSPAC, looking at the mental health outcomes of the study group and then applying the prevalence at a national and local level.

The prevalence of multimorbidity increases with age. Therefore, to prevent it and mitigate its impacts, we need to understand how multiple factors at different stages of the life course affect an individual’s health trajectory with ageing.

Currently, an important knowledge gap exists in this area as most research has focused on single life stages and/or single diseases, and often only at adult ages when multimorbidity appears. This overlooks the sequence and dynamic development of comorbidities in the life course.

We will address this gap by creating trajectories of multimorbidity by disease, physiological function and medication usage across all life stages.