Intimate Partner Violence (IPV) is defined as any violent behavior within an intimate relationship or any other controlling behavior that is conducted by a current or former partner. It is the most common form of violence in women which constitutes a major public health problem worldwide. The current explanatory theories of IPV perpetration can be summarized as feminist/sociocultural, social learning theory-based intergenerational transmission and psychological/psychosocial. According to the feminist/sociocultural theory, domestic violence is a consequence of “patriarchy”. From this view, violence is used as a form of power and control of women by men. The intergenerational transmission theory asserts that domestic violence is based on the exposure to, or observation of, violence in the family of origin. Psychological theories propose that there are psychological, psychiatric, behavioural and neurological risk factors for domestic violence perpetration. In the study of IPV perpetration, it is important to consider the variables addressed by such theories as a whole and from a developmental perspective and there is no study that simultaneously considers all the variables of these explanatory theories. The general aim of our study is to identify those etiological mechanisms linking risk factors for IPV perpetration across development. This study will be the first one that sheds light on which the origins of IPV perpetration are by knowing how IPV perpetration develops. Implications in terms of prevention and treatment will be of a great relevance for public health.

Asthma remains a major global public health concern. However, asthma prevalence is different in high-income countries (HICs) and low and middle-income countries (LMICs), and what we know about asthma pathology is generally based on studies in HICs. To address this, the World Asthma Phenotypes Study (WASP) study started in 2016 to better understand types of asthma in five centres around the world; the UK (Bristol: ALSPAC), New Zealand, Brazil, Ecuador, and Uganda. The main objective of this specific project (which is part of WASP) is to focus on the association between soluble airway biomarkers, patterns of airway inflammation, and clinical characteristics, to better understand and characterise types of asthma in the different centres.

Individuals with an intellectual disability (ID) may be more likely to suffer from mental health problems than the general population. We aim to investigate the relationship between ID and mental health using data from a longitudinal study of over 14000 children born in the early 90s with ongoing data collection. We will investigate whether specific risk factors such as cognitive ability, sensory impairments and life events such as bullying may influence this relationship and act as modifiable targets for intervention.

If we want to look at the impact of a given exposure on depression outcomes, we commonly require the assumption that the missingness in our depression indicator is "at random". "At random" is something of a misnomer here, and means "random conditional on measured covariates". In the instance that missingness is in fact not at random, i.e. depression itself affects participants likelihood to respond - then common analytical procedures to investigate the impact of exposures on depression may be biased.

We will develop a method to attempt to address this gap, using the effect of smoking on depression at 18 as a question to demonstrate our proposed approach, which will seek to provide testable conditions under which we can falsify the "missing not at random" assumption.

Individuals with attention deficit hyperactivity disorder (ADHD) may undergo different developmental trajectories throughout adolescence. Previous evidence has indicated that neural signatures and genetics could help to distinguish individuals with persistent ADHD symptoms from those remitted. However, little evidence has been provided to demonstrate whether environmental risk factors, such as substance use, could also affect the development of ADHD symptoms.

This proposal is part of LongITools project (B3289).

Blood pressure tracks from childhood to adulthood, and elevated blood pressure in childhood or adolescence is associated with several intermediate markers of cardiovascular disease (CVD) and with CVD events and mortality in adulthood. There is a growing body of evidence showing that ambient environmental exposures, such as air pollution, noise and many characteristics of the built environment are associated with high blood pressure/hypertension in adulthood, and some associations with blood pressure have also been observed in children.

Early-life, especially prenatal and early postnatal, is a period of rapid development and particularly vulnerable to environmental factors, and adverse exposures in this period could lead to long-term health effects, including higher risk of CVD. Some studies have shown associations between prenatal ambient environmental factors and blood pressure in children, including some measures of the built environment (e.g., facility density, facility richness and building density), noise, temperature, and air pollution. Investigating whether early-life ambient environmental factors are also associated with changes in blood pressure in different developmental periods will further contribute to the understanding of the importance of environmental exposures to the risk of hypertension across the life-course.

Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we aim to assess the association of a range of ambient environmental exposures in early-life with changes in systolic (SBP) and diastolic blood pressure (DBP) during three developmental periods: childhood, adolescence, and early adulthood. We will also seek to replicate the associations found in ALSPAC in other independent European cohorts part of the LongITools project (Generation R, EDEN, PANIC and NFBC 1986).

This proposal is part of LongITools (B3289) and LifeCycle projects.

There is inconsistent evidence of an association between prenatal exposure to air pollution and adiposity in childhood. Some studies suggest positive associations, possibly with stronger magnitude in boys, some find no association, and others find inverse associations between prenatal air pollution and adiposity in childhood. Most studies have been relatively small (<3,500 participants) and assess adiposity at a single time point.

The potential mechanisms linking air pollution to adiposity are still uncertain. Maternal exposure to air pollution may affect fetal growth, and intrauterine growth restriction will influence later-life adiposity. Inflammation is another hypothesised mechanism of the association between prenatal air pollution and offspring adiposity, and this might also be part of the fetal growth pathway.

Using data from three birth cohorts (ALSPAC, BiB and Generation R), this project will assess the association of different measures of air pollution (PM10, PM2.5, NO2 and NO) during pregnancy with fetal growth, trajectories of adiposity in childhood, and maternal and offspring inflammation. We will also explore possible sensitive windows by assessing trimester-specific associations, and whether associations differ by sex. If associations of air pollution with fetal growth, inflammation and childhood adiposity are evident, we will explore and quantify possible mediation by fetal growth and inflammation in the association between prenatal air pollution and childhood adiposity.

The change in body weight from infancy to adulthood may impact later cardiometabolic health. In particular, early onset of excess weight gain and long duration of obesity in youth have been associated with an increased risk of cardiometabolic comorbidities in adulthood. High and low birth weight for gestational age, indicating abnormal fetal intrauterine growth, are also associated with an increased risk of cardiometabolic comorbidities in adulthood. There may be an interaction between birth weight and the change in body weight from infancy to adulthood, where the influence of weight gain on cardiometabolic health may depend on birth weight. In the present study, we aim to uncover the independent and combined effects of birth weight and the change in body weight from infancy to early adulthood, on cardiometabolic health in adulthood.

Information can be obtained from ALSPAC (B number folder) or the UK LLC on request