The UK Office for National Statistics estimates that in 50 years’ time, there will be an additional 8.6 million people aged 65 years and over. Longer lifespan has clear benefits, but when it is associated with an increased proportion of the population suffering from age-related diseases, it can pose a burden to individual sufferers and to the economy.

Telomeres are ‘DNA tails’ at the end of chromosomes that shorten as we age, in accordance with the number of cell divisions. The rate at which telomeres shorten is also affected by genetic, environmental and pharmacological factors, which is important because premature telomere shortening is hypothesized to predispose to multiple age-related diseases, including coronary artery disease and rheumatoid arthritis. This is because cells with very short telomere lengths are less able to divide, leading to the accumulation of old, damaged or unhealthy cells within a tissue, and subsequently an increased risk of disease. A deeper understanding of which specific factors affect rates of telomere shortening might allow us to identify who is most at risk for premature telomere shortening and what sort of interventions may be effective at preventing age-related diseases.

This project will use the rich phenotype data within ALSPAC to define genetic, environmental and pharmacological factors associated with telomere length and its rate of attrition.

We want to find out in what way everyday habits and behaviours actually can change how people with a severe mental illness experience this illness, and, by finding that out, how we can possibly advise people, GPs, and the government in helping people feel better and live a better life they enjoy more in the long term. To do that, we are collecting information on how active a person with one of three specific mental illnesses keeps; how often they spend time outside, like in a garden, park or forest; how well and how much they sleep; whether they smoke or drink alcohol, and if so how much and when or when not; and how resilient they are personally to the bad or sad things that can happen in life, like having to move or losing their job or a loved one dying. We then try to find out how likely for example a highly active person with for example bipolar disorder is to also spend a lot of time outside in a park or garden, and how likely they are to sleep better and more hours during the night, and whether they smoke or drink alcohol (a lot) or not. And then we check whether them being so active changes how bad they feel with regards to their mental illness, and how their mental illness affects them. And we do the same thing for people with schizophrenia and severe depression. The idea behind it is that all these habits and behaviours make another habit or behaviour more or less likely to happen, so a person who is highly active would technically also be less likely to smoke a lot. And smoking a lot makes it very likely that if you have depression, you don't feel very good and experience a lot of negative feelings, more so than a person with depression who doesn't smoke. We'll be working on this for three years, building a blueprint-model on this collection of information, and then test how strong this model is on other datasets. And if we're right and we can find a strong model of influencing behaviours and habits, then we can use this model to help councils and the government give out better information on how to help make people live a healthier and better life for themselves.

Adverse childhood experiences have been associated with unfavorable health behaviours, somatic and psychological complaints in pregnancy. Beyond pregnancy experiences, a large body of research highlights intergenerational effects of maternal history of early trauma on their offspring. Given the growing interest on early adversity consequences during the perinatal phase, we aim to examine the associations between traumatic childhood events and pregnancy health behaviour, psychological symptoms, birth outcomes, sociodemographics and breastfeeding. For this we intend to include mother-infant pairs from the Avon Longitudinal Study of Parents and Children. Adverse childhood events consist of abuse (e.g. emotional, physical and sexual), neglect, (e.g. emotional and physical) and household dysfunction (e.g. parental mental illness, divorce or incarceration). We measure pregnancy health behaviour (e.g. exercise, smoking, alcohol, BMI), psychological symptoms (e.g. anxiety and depressive symptoms), sociodemographics (e.g. education, social class) and breastfeeding (e.g.initiation and duration).

Animal experiments suggest that exposure to toxins such as found in cigarette smoke may impact respiratory health across generations. Studies in humans are however limited. In this study, we ask if gene activity differs in children whose fathers smoked prior to them being conceived. Differences have been observed in participants of the RHINESSA study. Here we ask if similar differences are observed in ALSPAC participants.

Depression is one of the most important risk factors for suicide. Almost 60% of people who die by suicide experienced depression at some point in their life. Yet, it remains unclear why only certain people with depression eventually become suicidal. Recent evidence suggests there are sensitive periods in development when life experiences, such as depression, can have stronger effects on mental illness. It is also well documented that suicidality results from both life experiences and genetic risk.
However, most studies of genetic risk for suicide, depression, and subsequent suicidal suicidality focus on people measured at a single timepoint. This limitation prevents us from 1) identifying people who are at the highest risk for future suicidal behaviours and 2) developing timely and effective interventions that prevent suicide in people with depression. As such, this project will use longitudinal data from two birth studies to determine when and how genetic risk and experiences of depression during childhood and adolescence influence suicide risk in early adulthood.
First, we will identify the specific ages and patterns of depression during childhood and adolescence that most predispose young adults to suicide. These results will help us build and implement interventions that are positioned at the best possible time to prevent suicide risk among youth affected by depression.
Second, we will determine whether children and adolescents with increased genetic risk for suicide or mental illness are more likely to become suicidal after experiencing depression at specific ages. These findings will improve our ability to identify youth who are at greater risk for suicide and provide insight into the genetic pathways leading to suicide.
Third, we will identify biological mechanisms that explain the link between depression and suicide. We will focus on epigenetic changes, as they are linked to human health and are thought to reflect both life experiences and genetics. Thus, they may represent a biological pathway through which suicide risk can become “molecularly programmed”. Identifying epigenetic changes that link depression to suicide risk will help guide the development of biomarkers that will allow us to identify at-risk youth quickly and effectively.
In sum, this project will highlight key periods and biological targets that can be used to predict and prevent suicidality among childhood and adolescents who experience depression. These will ultimately catalyse better interventions that prevent suicide in young adults.

I am interested in the ways in which eating disorders were being discussed (both popularly and amongst academics/practitioners) and researched in the late 20th/early 21st century. I’m especially interested in ALSPAC because of the specific interest in the impact on eating disorders on maternity (a relatively unusual approach at the time.) I am only interested in material on the eating disorder research components of ALSPAC

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

Cannabis use in youth is an important public health concern, especially as it often starts in young teens and in light of recent changes in Canadian legislation. The possible effects of cannabis (marijuana, weed, etc.) use on mental health are poorly understood. Cannabis is known to be associated with later psychosis. But what about more common mental health problems like depression, anxiety, and suicidal thoughts or attempts? Our first objective is to clarify the associations, if any, between cannabis use and later anxiety, depression, and suicidality, and whether they are causal or simply associative. Our second objective is to test the genetics-environment link – whether youth with pre-existing vulnerability to mental health problems are more at risk of depression, anxiety, and suicidality if they use cannabis, while the risk remains low for others. We will use data from the ALSPAC population-based longitudinal cohort. Participants had been asked at various times whether, how often, and when they started using, as well as questions on their mental health. Data will be analyzed by robust approaches to provide strong evidence in support (or not) of the links between cannabis use and later depression, anxiety, and suicidality. Clinically relevant patterns of cannabis use will be examined: a) ever used, b) age at onset, and c) intensity. Our findings will allow clinicians, researchers, and policymakers to develop better prevention and treatment programs to avoid mental health consequences of cannabis use in young people.

Previous research has established the effects of maternal mental health on children and adolescents MH but there is limited evidence on the association between maternal mental health and risky behaviours in adolescence, such as substance use (Campbell et al., 2009; Pearson et al., 2013). Studies have demonstrated that depressed parents played a significant part in offspring’s MH and substance use in adolescence and adulthood (Weissman et al., 2006). These results have been replicated by Flouri and Ioakeimidi (2008) finding that adolescents, particularly male, engaged in more risky behaviours, including alcohol use, when their mothers had chronically high or increased depressive symptoms, compared to those that their mothers never experienced depression. Wickham and colleagues (2015) also showed that adolescents who were exposed to maternal depressive symptoms in middle childhood showed a stronger association with using common substances (alcohol, cigarettes, and marijuana) and earlier engagement in such behaviours, including hallucinogenic use. This project aims to extend the evidence and look at different maternal mental health conditions and their relationship with substance use in adolescence using the ALSPAC data.