Eating disorders are severe psychiatric conditions that often start in adolescence. They present with other serious health problems, have a high mortality rate, and are becoming increasingly prevalent in the UK population. Prevention of eating disorders is the ultimate aim but knowledge of risk factors for eating disorders is limited.

There is no consensus about the relationship between socioeconomic status (SES) and eating disorder incidence in adolescence as current research is based on cross-sectional studies in adults. Different aspects of SES might have different effects on eating disorder symptoms (e.g., parental education and income). SES might have indirect effects on eating disorders via food insecurity, poor dietary patterns, and early mental health problem, however these hypotheses have not been previously tested.

Our proposed research will help identify childhood risk factors for eating disorders and inform future preventative interventions.

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

Early adversity predicts greater disease risk later in life across numerous outcomes; however, biological pathways are incompletely understood. Previous studies have implicated altered immune function in these relationships, specifically chronic inflammation, which is associated with both adversity and multiple health outcomes, including cardiovascular disease (CVD) and all-cause mortality. While these studies have been informative, inflammation is only one component of the immune system, and there is suggestive evidence that adversity might have broader effects besides heightened inflammation that impact later life health. The immune system consists of two subsystems, non-specific innate immunity and specific acquired immunity. Chronic inflammation represents up-regulation of innate immunity, while studies linking adversity to acquired immunity tend to report suppressive effects. Research in evolutionary biology and ecological immunity has suggested that an up-regulation of innate immunity and down-regulation of acquired immunity could be an adaptive “future-discounting” strategy in harsh and unpredictable environments, as innate immune activation can provide short term benefits but comes with long-term costs to health and longevity, while acquired immunity provides less immediate benefits but enhances future defense.

Consistent with the above model, we have recently found evidence that early adversity (e.g., low SES) in the Cebu Longitudinal Health and Nutrition Survey (CLHNS) predicts a lower percentage of circulating acquired immune cells and higher percentage of innate inflammatory cells in young adulthood. Here we propose to expand on this work by testing whether similar associations are found in the ALSPAC cohort, using immune cell composition data derived from both flow cytometry and DNA methylation (DNAm) at multiple ages.

People who exhibit disordered eating behaviours, such as binge eating, restricting, and purging, are at increased risk of problematic alcohol use. It is commonly proposed that this is a partially causal relationship, with behaviours such as binging and restricting actively contributing to the development of problematic alcohol use. This may be because disordered eating behaviours can increase negative affect, reward sensitivity, and impulsivity, which are factors known to contribute to problematic alcohol use.

However, there are also reasons to believe that problematic alcohol use may in turn contribute to the development and maintenance of disordered eating behaviours, through similar mechanisms operating in the opposite direction. Additionally, ‘out of control’ or ‘binge-type’ alcohol use may be particularly distressing for individuals with disordered eating, due to the caloric nature of alcohol, and thus may result in increased compensatory behaviours (i.e., disordered eating behaviours). Longitudinal studies thus far have reported mixed findings regarding the causal direction between disordered eating behaviours and problematic alcohol use and have been hampered either by small sample sizes or poor measures.

Thus, this project aims to investigate and describe the direction(s) of causation between disordered eating behaviours and problematic alcohol use using robust measures and a large sample size.

Furthermore, the literature is unclear on whether purging or bingeing is more related to problematic alcohol use, as many studies have either looked at one or the other, or collapsed them into one category (i.e., ‘bulimic symptoms’). Thus, this study will look to consider the relative magnitude of association of each of these two behaviours, as well as restrictive eating behaviours, and problematic alcohol use.

A rising tide of research and policy interest in Adverse Childhood Experiences (ACEs, e.g. child maltreatment, parental intimate partner violence or substance misuse) has led to substantial financial investment in services to prevent the health consequences of ACEs. These initiatives rest on estimates of the health burden/costs of ACEs. Yet very little research attempts to interrogate the causality of associations between ACEs and health, despite potential confounding by upstream factors such as poverty and genetics. Robust evidence that ACEs causally affect health would strengthen the rationale for investing in interventions that prevent ACEs or seek to mitigate their adverse effects. Yet if some associations are spurious or over-estimates, this risks: costs of ACEs being overstated, scarce public resources being wrongly diverted away from other upstream determinants of health such as poverty, and perpetuating a stigmatising narrative that those exposed to adversity have uniformly poor health.

In BEYOND-ACES, cutting-edge research using prospective longitudinal and genetic data from 6 international cohorts will generate a step-change in evidence about whether ACEs are causally related to health-related behaviours, physical health, and mental health. We will use robust methodologies: difference in difference (DiD) to avoid time-fixed confounding, marginal structural models (MSM) to avoid time-varying confounding, polygenic scores to evaluate gene-environment correlation, and methods to account for genetic confounding. Underpinning this is a cross-cutting programme of methodological innovation: developing DiD and MSM for use with the composite exposures necessary in ACEs research, and evaluating approaches to interrogate whether the health consequences of ACEs differ according to the timing and duration of exposure. BEYOND-ACES will move beyond the current simplistic narrative about ACEs and health, and yield a step change in the quality of research in this field.

It has previously been shown that there is a relationship between age of first intoxication (AFI) and mental health disorders. However, many studies in this area tend to focus on the relationship between the AFI and substance-use disorder, rather than other mental illnesses, or how pre-existing mental disorders predict substance-use in teenagers. Burke et al (1990) found that the hazard rate for developing a substance-use disorder is highest when the AFI is between ages 15 and 19 and found that this risk decreases as the individual ages, which is consistent with other literature. This suggests that teenage years are a vulnerable period for individuals as there is a high potential for the development and maintenance of a substance-use disorder. The impact of pre-existing mental health issues on substance use is demonstrated in a study conducted by Sung et al (2004), which found that girls who struggle with anxiety before the age of 16 have an increased risk of substance-use disorder, and boys with a history of depression in childhood and early adolescence also have an increased risk. Research suggested that substance-use disorders can also be a symptom of mental illnesses, for example, Robins et al (1985) found evidence that implies this disorder is a symptom of antisocial personality disorder. However, there is a lack of investigation into whether the AFI is associated with the onset of psychopathological symptoms.

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.

The aim of this research is to determine the relationship between DNA methylation at the SOCS3 region and both height and mothers social class. Work leading up to this proposal has indicated that SOCS3 methylation may be associated with height and stunting in cohorts based in Lower Middle Income Countries (LMICs). Analysis in ALSPAC will help to answer whether these associations are also present in High Income Countries (HIC) such as the UK. Analysis of genetic data will determine the variance in DNA methylation determined by genetic and/or environment and the causal direction of any associations identified.

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.