Social cognition has been hypothesised to be important in the development of PTSD (1). Previous research has shown that individuals with PTSD have a variety of social cognitive deficits (2), but whether these existed prior to the development of PTSD has not yet been determined. Furthermore, it is not clear whether social cognitive deficits increase risk of trauma exposure, whether trauma causes social cognitive deficits, and whether social cognitive deficits mediate or moderate the relationship between trauma and PTSD

Metabolites are the ultimate end-point of a biological process and are therefore seen as a link between genotype and phenotype. Assigning individual metabolite changes to diseases is difficult because of the complexity of their interrelationships. Prior to analysis quality control of metabolomics data is required. We have developed a package that automates these quality control steps. We will use the raw metabolomic data as a use case for our package.

Body composition is known to affect metabolite concentrations. These changes may be implicated in disease development. Following quality control we will use the metabolomic data to investigate the relationship between metabolites and different body composition traits.

using same principle of pediatric asthma risk scores to predict asthma in childhood I have created risk factors to predict asthma at age 18 and 26 years old

There has been remarkably little research on women's experience of menstruation from a population health perspective, despite menstruation and pre-menstrual symptoms having wide-reaching consequences for women's physical and mental health. We need a better understanding of the biological (e.g. hormone levels, epigenetics) and lifestyle factors (e.g. smoking, alcohol, diet) that might predict and/or causally affect menstrual experiences (e.g. cycle length, heaviness, regularity, pain and premenstrual mood). This better understanding could inform ways to predict who is at risk of poor experiences, and develop strategies to prevent or improve those experiences. We also need a better understanding of the impact of different menstrual experiences on women's physical and mental health (e.g. fatigue, depression, life satisfaction). Again, this could inform strategies to predict which women are at risk of poor outcomes and help develop preventative interventions.

Social withdrawal (SocW) – defined as reduced social interaction – is a key feature of psychotic disorders and multiple other psychiatric outcomes. Despite growing recognition of its negative consequences, SocW remains one of the least studied human traits, and its underlying mechanisms remain subject of wide speculation. The overall goal of this project is to examine elucidate the role of SocW in the development of psychosis.

By combining clinical data with increasingly powerful ‘genetic risk scores’ (i.e. the sum of risk genes that have shown to be associated with a behavioral trait), we are now able to test whether SocW is a cause or merely a consequence of symptoms in psychosis development. Using the UK Biobank we will create a powerful genetic risk score for SocW, and use this score to examine the role of SocW in psychosis in two large developmental cohorts: The Avon Longitudinal Study of Parents and Children (ALSPAC) and Philadelphia Neurodevelopmental Cohort (PNC). Jointly, these studies followed nearly 16,000 young individuals from childhood to young adulthood, through ages encompassing typical onset of and peak onset age of psychosis. In ALSPAC, we will also test the association between changes in psychotic symptoms and changes in SocW behaviorally, and explore the effects of SocW and established environmental risk in the path to psychosis.

Overall, we aspire to better understand the well-established association between SocW and psychosis, determine critical windows during which individuals may be more or less prone to the influence of SocW, and facilitate much-needed preventive targeted therapies.

Cannabis is widely used for recreational and medical purposes with usage increasing rapidly following its legalization in parts of the world[1]. While there are well-documented effects of cannabis on the users themselves, the impact of its consumption during pregnancy on offspring is much less clear. Previous studies have reported that maternal cannabis usage during pregnancy is associated with lower birth weight and there is the suggestion of impaired neurodevelopment in both observational cohorts in humans and experimental studies in animal models[2-7]. However, how maternal cannabis exposure leads to these adverse health outcomes in offspring remains unclear.
Epigenetic mechanisms play an important role in regulating gene expression and cell homeostasis. Previous experimental studies showed that DNA methylation in offspring could be modified by maternal cannabis exposure[8-10]. In some cases this leads to dysregulation of the immune system of the fetus[11-13]. However, no human studies have yet been conducted, and no specific epigenetic signatures have been identified related to cannabis exposures. We hypothesize that maternal cannabis exposure during pregnancy alters the epigenetic profiles and leads to a specific epigenetic signature of the fetus through in utero exposure, and the epigenetic alterations can then lead to impaired neurodevelopment in the offspring. Therefore, we propose to investigate the association of maternal cannabis exposure around the time of pregnancy with DNA methylation profiles in offspring at birth in the ALSPC cohort.

Studies investigating the influence of early-life pet exposures on the risk of childhood asthma have been inconsistent: some studies have observed a decreased risk whilst others have observed no effect or even an increased risk of asthma following early-life pet exposure. This study aims to use data from several longitudinal studies to investigate how exposure to pets during pregnancy or early-life influences the likelihood of: a) the immune system recognising allergens (allergic sensitisation); b) developing asthma. The study will also investigated the relative influence of type (dogs vs. cats), timing (pregnancy, early life, never) and degree (number) of pet exposures on allergic sensitisation and asthma.

Cardiovascular disease, a frontline cause of death worldwide, has some risk factors such as obesity, poor cardiorespiratory fitness (CRF), and vascular dysfunction whose primordial signs exist in childhood. Evidence suggests that excess body fat and poor CRF predict increased cardiometabolic risk and the progression of atherosclerosis. However, the mechanisms underlying vascular dysfunction with respect to predictors such as CRF, body fat, and lean mass in the young remains poorly understood.

It is unclear whether CRF in childhood and adolescence impact arterial structure and function in later life. Although several studies have assessed the influence of childhood CRF on early and or later arterial health, they are either of cross-sectional or short-term longitudinal design. Most of these studies have focused on a specific period (e.g. early or late childhood) and are restricted to a one-time measure of CRF. Moreover, inappropriate scaling measure of CRF such as not accounting for the confounding effect of body fat makes interpretation of existing evidence difficult.

Similarly, accumulation of body fat and lean mass during childhood through adolescence may significantly impact arterial health in early adulthood. But, studies that describe the physiological adaptation of vascular structure through adolescence to young adulthood in relation to increased body fat and lean mass are few. A repeated measure of CRF, body fat and lean mass is essential to determining critical periods of early life during which these factors implicate later arterial health. Evidence on suitable target ages for cardiovascular intervention, alongside unraveling the cryptic mechanisms by which CRF, body fat and lean mass relate to arterial health could be achieved. We would, therefore, assess the importance of early life exposures (e.g. CRF, body fat, lean mass, and/or endothelial function) from childhood through adolescence on vascular phenotypes between ages 9 to 24.

The consequences of childhood obesity remain one of the biggest public health burdens in the UK. 1 in 3 children are already overweight or obese by age 10 years. This is especially problematic because obesity has been linked to many health conditions, such as diabetes, cancer and depression. There is now substantive evidence that obesity runs in families, but genetics alone cannot explain the current rise of obesity in the population. So environmental factors have been proposed to be causal for this development. It is this dual determination, that remains paradoxical:
How is it possible that obesity is explained by both genes and environments and what does this complexity mean for public health interventions?
For childhood obesity, we already know that genetic and environmental factors are
important. However, it is not known how environmental factors might be protective of genetic
liability.
The main questions are:
1. Do parental feeding practices, such as offering food to soothe, enhance or buffer the
association between genetic liability and later childhood BMI, and what could be
achieved if we changed parental feeding strategies?
2. Does the child’s physical activity mediate the association between childhood genetic
liability and later BMI, and what would happen if levels of physical activity increased?
3. Can maternal genetic risk influence the child’s body size, even though the genetic liability
are not passed on?
4. What is the association between genetic liability and the built environment of the family
home, such as access to green spaces and public transport?