D2K, PEALS, Newcastle University

Understanding Society: METADAC project approvals

Title Plain Language Summary Committee date Applicant Keywords
Institution
Co-Applicants
Funders
FPLD1 and Severe Insulin Resistance GWAS Familial Partial Lipodystrophy Type 1 (FPLD1) is a rare disorder of fat distribution with an extreme phenotype, associated with severe resistance to the glucose lowering effects of insulin. This study aims to investigate whether individuals with this disorder carry an excess of markers for known measures of “metabolic syndrome” risk (insulin and lipid measurements, blood pressure, BMI, waist-hip ratio) when compared to unaffected control participants from UKHLS. It also aims to discover whether these individuals carry any new markers that might contribute to FPLD1 disease risk, again, in comparison with unaffected control UKHLS participants. 01/12/2015 BARROSO, Dr Inês Familial Partial Lipodystrophy, Severe Insulin Resistance, GWAS, genetic risk score
Wellcome Trust Sanger Institute
Felicity PAYNE, Eleanor WHEELER & Allan DALY
Human Genetics Working Group, WT Sanger Institute Core funding
Genomics of social support, personality and cognition and their relation to mental health and cognitive ageing Genes play an important role in shaping the social behaviour and cognition/cognitive ageing as they modulate the brain activity through molecular pathways; therefore, it can be said that genes regulate the expression of behaviour. Social support and cognition are correlated with an individual’s mental health as these social interactions require effective communication and participation. We would like to use information from the 1985 birth cohort to: (1) assess the impact and associations between social behaviour (social support) and cognition in individuals with and without symptoms of depression and anxiety, (2) perform a genetic analysis of social support and cognition within the same population by studying changes in the DNA of individuals, and (3) harmonise these data with data from different cohorts 07/06/2016 NICODEMUS, Dr Kristin Social support, social dysfunction, personality, cognition, GWAS, mental health, cognitive ageing
University of Edinburgh
Elvina GOUNTOUNA, Thalia Perez SUAREZ, Kathy EVANS, Rosie WALKER, Lara Neira GONZALEZ, Daniel McCARTNEY
No outside funding.
Inflammatory cytokines interleukin-6, interleukin-1-beta, and C-reactive protein as causal risk factors for depressive symptoms: A Mendelian randomisation study The purpose of this study is to determine whether poor immune system functioning can cause symptoms of depression. We aim to do this by examining whether genetic variants that are associated with inflammatory factors predict a higher likelihood of having depressive symptoms, a method which reduces several types of bias. First, genetic variants that are known to be associated with specific inflammatory factors (interleukin-6, interleukin-1-beta, and C-reactive protein) would be identified and used to construct a genetic score which represents these inflammatory factors. Data from several other cohort studies including the UK Household Longitudinal Study would then be used to examine causal links between genetic scores for inflammation and depressive symptoms. Confirmation of these causal links may reveal pathways that can be targeted for the prevention and treatment of depression; the absence of causal links may shift the focus of future research onto other targets for therapy. 14/07/2016 CARVALHO, Dr Livia Inflammation; Depressive symptoms; Causality; Mendelian randomisation
University College London
Dr Joshua BELL, Dr Golam KHANDAKER
MRC (ImmunoPsychiatry Consortium)
Assortative mating and genetics This project aims to use socioeconomic and genetic data from the Understanding Society. We will examine variation in spouses’ characteristics to investigate the similarity of partners to one another – this is also called assortative mating. We will examine different characteristics such as socioeconomic status (e.g., educational attainment) and health (e.g., weight and height). Assortative mating may have direct implications for the transmission of socioeconomic status and inequality across generations. Similarities between partners may be due to preferences for specific characteristics or could also capture underlying (unobservable) traits and constraints that people face when forming a relationship. In this project, we will first investigate whether we can use genetic variation (differences in family traits) among partners to better measure the similarity in their attributes. This information will help us to learn whether and how individuals value one or more characteristics in a partner. It will also help us to learn which type of characteristics matter (socioeconomic and/or health ones?). The project will then calculate measures of genetic predisposition (polygenic scores) to assess the degree of assortative mating in the partners’ 27/02/2017 QUINTANA-DOMEQUE, Dr Climent Matching Models, Marriage, Schooling, Exclusion Restriction, Instrumental Variables, Polygenic Scores
University of Oxford and St Edmund Hall
BARBAN, Dr Nicola; DE CAO, Dr Elisabetta; OREFFICE, Dr Sonia
n/a
Investigating epigenetic changes in shiftwork – a possible mechanism for its impact on health and the body clock Shift work is a widespread feature of our society, with a third of men and a fifth of women in the UK engaged in it. However, shift work has been linked with a number of poor health outcomes, including obesity, diabetes, heart disease, depression and some types of cancer. The mechanisms by which shift work might lead to these diseases are poorly understood. A major area of interest is the effect shift work, and night shift work in particular, has on altering a person’s body clock. There is information available on shift work patterns at multiple time points in Understanding Society. The availability of blood samples for some study participants provides an opportunity to look at biological changes associated with shift work, including the impact shift work might have on epigenetic modifications, which influence how our genes are turned on or off . This work will help us better understand how the occupational exposure of working shifts might become embodied in human biology, with the potential for long term health consequences. 25/05/2017 Prof Caroline RELTON Shift work, sleep, DNA methylation, circadian
SSCM, University of Bristol
Dr Rebecca RICHMOND, Prof George DAVEY SMITH, Prof Meena KUMARI
MRC IEU, Bristol
Impact of economic conditions in year of birth on DNA methylation age acceleration Studies have found that being born in a good or bad year for the national economy can have long term effects on one’s health. For example, those born in an economic downturn experience greater risk of dying from cardiovascular disease. The social and biological mechanisms of this effect are poorly understood. One possisble explanation is that a poor economy at birth may contribute to factors (e.g. malnutrition, stress, etc.) impacting regulatory features of cells, called DNA methylation, increasing the chances of aging more rapidly. Understanding Society is ideally suited to address this knowledge gap: having DNA methylation from many adults born before 1960, when this effect is likely most powerful. We propose to investigate whether poor economic conditions at birth are related to altered DNA methylation in adults, and in particular to a measure of one’s ‘DNA methylation age’ to determine if this contributes to accelerated biological aging. 25/05/2017 Prof Caroline RELTON DNA methylation, age acceleration, business cycle
SSCM, University of Bristol
Dr Paul YOUSEFI, Prof Gerard vAN dEN BERG, Dr Matthew SUDERMAN
ESRC and BBSRC
Investigating the genetic relationships between anxiety, depression, stressful life outcomes,  and cardiovascular risk factors and disease. This study aims to use cardiovascular risk measurements and diagnosis, together with questionnaire data on mental and physical health in Understanding Society in two ways: 1- To discover and validate previous findings from large psychiatric genetics studies. These studies identified inherited genetic changes which may increase risk of depression. 2- To investigate shared genetic factors affecting mental and cardiovascular health (heart disease), as these conditions often occur together.
The ultimate aim is to uncover biological pathways underlying the relationship between cardiovascular disease and depression. The proposed work will be achieved through analysis of genetic and health data, using existing methods. This research will assist in risk prediction, informing treatment, and forming a better understanding of the shared genetics between traits.
03/07/2017 Prof Cathryn LEWIS depression, polygenic risk scores, cardiovascular disease risk, pleiotropy
King’s College London
Delilah ZABENEH, Karen HODGSON, Saskia HAGENAARS, Gerome BREEN, Paul O’REILLY
NIHR Maudsley Biomedical Centre
Family background, genetics and educational achievement. A follow-up study. A number of studies have found big differences in educational achievement between individuals from high and low income backgrounds. Narrowing this achievement gap has now become an issue of great public policy concern. The presumption by many policymakers is that such differences in educational achievement are driven simply by the different quality and quantity of resources (e.g. books, schools, tutoring) that high and low income families can provide. However, an alternative explanation is that at least part of this achievement gap is due to genetic differences.
I will explore this issue using UKHLS data. There are almost 100 genetic variants associated with educational achievement. I will consider whether parts of the DNA code which have been shown to be related to educational achievement differ between high and low income groups. I will then investigate the extent that accounting for these genetic differences can explain variation in educational achievement between individuals from high and low income backgrounds.
12/09/2017 Prof John JERRIM Educational achievement, socio-economic gaps
UCL
n/a
Understanding the genetics of neurodevelopmental disorders We are studying a large group of children with severe intellectual disability, referred from genetics clinics across the UK, in order to find the genes that cause their disorders. We have found evidence that genetic variants (differences in DNA sequence between people) that are common in the healthy population also influence risk of having severe intellectual disability. Some of this common variation is also known to affect educational attainment, i.e. how many years of school someone attends. We want to use the genetic data from people in Understanding Society with information about their educational attainment to compare this to our group of children with intellectual disability. Our eventual goal is to improve our understanding of the biology underlying severe intellectual disability, and to improve our ability to predict the chance that parents with one affected child might have another. 12/09/2017 Jeffrey BARRETT genetics, intellectual disability
The Wellcome Trust Sanger Institute
n/a
Wellcome Trust / Dept. of Health

Last updated with approved projects 3/10/2017

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