Proposal summaries
B4668 - Impacts of being on an elective waitlist - 05/08/2024
We have unprecedented numbers of patients on elective waitlists, with many waiting longer for treatment than ever before. It would be useful to more fully understand the consequences of long waits for treatments, on: the patient, the health and care system, the wider economy and society.
Initial work, using BNSSG data, has investigated the effects on NHS care settings, such as primary, secondary, community and mental health services.
(https://bmchealthservres.biomedcentral.com/articles/10.1186/s12913-024-1...).
This essentially involved a ‘case-control’ study, in which the healthcare activity of the ‘case’ group (those on a waitlist) was compared to the ‘control’ group (those not on a waitlist). Results showed an increase in activity in many NHS care settings, indicating additional resources to manage these patients up to the point of treatment, and possible harms for the patient.
The ALSPAC data has a greater coverage of other variables, aside from NHS care activity.
B4666 - Elucidating the biological pathways involved in scarring through the use of integromics and mouse and zebrafish models - 31/07/2024
Repair of adult tissues involves a complex interplay of several key cell lineages and inevitably leads to formation of a fibrotic collagenous scar, whereas embryonic tissues heal perfectly without any resulting scar deposition. This dramatic difference in repair efficiency between embryonic versus neonatal/adult tissues has been instrumental is guiding us towards potential causes of scarring. Indeed, we now believe that one major driver of scarring is the wound inflammatory response which doesn't initiate until a transition period in foetal development which, in turn, coincides with the developmental onset of tissue scarring. This insight has led us towards further mechanistic cell and molecular studies in model organisms, such as mouse and zebrafish, which help us better understand the scarring process and how one might modulate the wound inflammatory response in order to improve or prevent scarring.
Whilst these approaches, motivated by comparing embryonic versus adult healing, have been fruitful, it is clear that scarring is a complex, multifactorial response likely driven by a number of interacting mechanisms. We would like to use a conceptually similar comparative approach to gain further insights into the fundamental cell and molecular mechanisms of scarring by analysing differences in degree of scarring, not between embryo and adult, but rather across human adult populations since we know there is a range of “scarring phenotypes” from “minimal scarrer” to keloid scarring individuals. This use of human phenotypic variation in a population based, using an integrative approach: genetic variation (genetic association, genomewide association studies – GWAS), gene silencing (methylation, epigenetic association studies - EWAS), gene expression (transcriptomics, transcriptome-wide association studies - TWAS), has the potential not only to yield gene variant correlates of scarring, but also to point towards specific biological contributions to wound healing, both at causative and regulatory and levels.
The use of natural human experiments (e.g. Bacillus Calmette–Guérin (BCG) vaccination wound healing, Caesarean section (C-section) wound scarring and examples of human disease related fibroses) has never before been used for identification of scarring genes, even though the approach has proven to be powerful for discovering genes associated elsewhere with a wide variety of complex health outcomes (www.ebi.ac.uk/gwas/).
Fibrosis and scarring are closely related processes that involve the formation of excess fibrous connective tissue in organs or tissues, typically in response to injury or chronic inflammation. Fibrosis is defined as the accumulation of excess extracellular matrix components, particularly collagen, in and around damaged or inflamed tissues. Scarring is the end result of this process, where fibrous tissue replaces normal, functional tissue. In early stages, fibrosis may be reversible if the underlying cause is treated. However, advanced fibrosis and scarring are often permanent and irreversible. Fibrosis can occur in virtually any organ, including the lungs (pulmonary fibrosis), liver (cirrhosis), kidneys, heart, and skin. Fibrosis can be caused by various factors, including chronic inflammation, autoimmune diseases, infections, toxins, and radiation exposure. In some cases, the cause is unknown (idiopathic).
Furthermore, alongside a growing number of catalogues charting the results of human genetic association studies for health outcomes and intermediates there are tools able to consider (in frameworks of causal analysis) the existence of potentially causal and modifiable relationships between exposures of interest (e.g. inflammation, differential wound repair or scar) and health outcomes (e.g. wound healing, recovery, and disease).
Using human genetic data to help explore the potential of biological pathways contributing to health and disease in applied epidemiological designs is an approach that we have refined and developed and is an integrated approach to health research that has yielded important clinically relevant insights but has also indicated opportunities (e.g. associated signalling pathways for targeting) to unify basic science approaches with human population-based health data.
Understanding fibrosis and scarring is crucial for developing effective treatments for a wide range of chronic diseases. While advanced fibrosis remains a challenging medical problem, early intervention and new therapeutic approaches offer hope for improved outcomes.
In this study, we will use several strategies:
• We will investigate a more comprehensive number of variants in genes, using the topmed reference panel, given its diverse sample population from both Europeans and non-Europeans, with a total of 97,256 high-coverage genomes, to help identifying variants responsible for scarring and fibrosis.
• With a focus on those that are not that frequent in the population (frequency under 1%), we will investigate whole genome and exome sequencing variants, to help identifying variants responsible for scarring and fibrosis phenotypes.
• We will investigate regulation pathways of scarring and fibrosis phenotypes using the information provided by epigenetic and expression arrays.
B4591 - Exploring links between Developmental Language Disorder in childhood and later work outcomes at 27 years - 31/07/2024
Developmental Language Disorder (DLD) and Developmental Dyslexia are common conditions in childhood yet have received relatively little research funding when compared to other neurodevelopmental conditions, and this is particularly so for DLD (Bishop, 2010; McGregor, 2020). An important consequence is that, there is limited research on the long-term impact or support needs when these conditions persist into adulthood. DLD and reading difficulties (RD) can affect educational attainment, lifelong learning and constitute hidden disabilities in the workplace. They frequently co-occur (Snowling, Hulme & Nation, 2020), increasing challenges for diagnosis, management and service provision.
This study is part of a broader PhD which will explore occupational health aspects relating to DLD and reading difficulties that impact on functioning in the workplace, through the experiences of young people and adults with DLD.
Although studies have shown that, on average, people with DLD and reading difficulties are likely to have poorer educational attainment and employment prospects, compared to those without DLD, there is currently limited knowledge of the reasons for such outcomes.
This study acknowledges that the training and employment prospects of young adults with DLD depend on their educational attainments. The analyses will therefore investigate educational and adult outcomes.
Bishop, D.V.M. (2010). ‘Which Neurodevelopmental Disorders Get Researched and Why?’, Plos One, 5(11), Plos One [Online]. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0015112
McGregor, K.K. (2020). How We Fail Children With Developmental Language Disorder. Language, Speech and Hearing Services in School, p.1-12. https://pubs.asha.org/doi/10.1044/2020_LSHSS-20-00003
Snowling, M.J., Hulme, C. & Nation, K. (2020). Defining and understanding dyslexia: past, present and future. Oxford Review of Education, 46(4). https://doi.org/10.1080/03054985.2020.1765756
B4665 - Health state changes over time a cohort and linked NHS data approach - 31/07/2024
• We’ve developed a model which simulated how the health state of our population will evolve over the next two decades (https://realworlddatascience.net/case-studies/posts/2024/05/08/dpm.html).
• This is crucially underpinned by what has happened to the health state of our population in the recent data.
• Essentially, the model ‘baseline scenario’ extrapolates these recent health state changes.
• However, we only have three years of data to determine these health state changes (the key restriction here is the all-important primary care data – other data sources do go back further).
• We are interested to understand how the health state of our population (or ALSPAC cohort thereof) has changed over a longer time period.
• This could help us better shape the ‘baseline scenario’ by extrapolating behaviour from a longer time period (not just the last three years).
• Crucial to this is data on individual attributes over time, which we source from our primary care data (2020+).
• Specifically, we use the individual’s Cambridge Multimorbidity Score (CMS), published here: https://doi.org/10.1503/cmaj.190757.
• This is calculated from 37 chronic conditions, see here: https://www.cmaj.ca/content/cmaj/suppl/2020/01/28/192.5.E107.DC1/190757-....
• Would it be possible to calculate these over time for the ALSPAC cohort, and thus calculate the CMS score for each individual, going back as long as possible?
• Additionally, we’d like to understand (1) inward/outward migration to the cohort, re patient characteristics, and (2) any detectable/inferable delays in diagnoses, re patient characteristics.
• The outputs of this will help us better understand health state changes in our population, and so better inform the ‘baseline scenario’ in our abovementioned simulation model.
B4648 - Inference of trait Tail Genetic ArchitectureS - 26/07/2024
Understanding genetic architecture in quantitative traits and complex diseases has been pivotal in biomedical research. Over years of effort and technological advancements, GWASs and sequencing studies have revealed that the genetic architecture of complex traits often comprise of a range of genetic components, including common variant, rare inherited and de novo variants. However, there remains an understudied aspect: the genetic architecture at individuals-level. For instance, individuals in the tails of trait distribution can be predominantly driven by common polygenic variants or by rare/ de novo variants with substantial effects.
B4664 - Search of genetic variants related with lung function a GWAS meta-analysis - 26/07/2024
Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. Recently, over a thousand variants in over 500 genes were associated with lung function. Those variants were involved in different cell functions, providing information that brings us closer to understanding the mechanisms underlying lung function and COPD.
In this study, we will investigate a more comprehensive number of variants in genes, using the TOPMed reference panel, given its diverse sample population from both Europeans and non-Europeans, with a total of 97,256 high-coverage genomes, to help identifying variants responsible for lung function impairment.
B4663 - Development of Picky eating and Avoidant restrictive food intake disorder predictors correlates and longitudinal outcomes - 25/07/2024
Picky eating is a common behaviour in children, that can range from being a normal phase in child development to a severe problem that causes negative physical and psychological consequences for the child and greatly impacts families. In its extreme picky eating can be part of Avoidant restrictive food intake disorder (ARFID); a debilitating feeding and eating disorder characterized by avoidant/restrictive eating by volume and/or variety resulting in important physical, health, and social consequences. As ARFID is a relatively new diagnosis, little is known about its longitudinal course and outcomes. Very little research is available on manifestations of ARFID in the general population.
B4661 - Towards an understanding of social media The effects on health well-being and genetic susceptibilities - 06/08/2024
In 2022, 63% of the world population actively used social media, spending a daily average of 2 hours and 27 minutes on these platforms. Despite its widespread adoption, our understanding of social media's impact on health and well-being remains limited, mostly due to lack of data availability on social media use. This proposal has two objectives. The first aims to study the relationship between social media use and mental health across different stages of life, considering various factors that influence social media exposure. The second investigates whether genetic susceptibilities towards mental disorders explain patterns of social media use. The exploration of these objectives will contribute towards advancing our comprehension of social media.
B4660 - UKLLC Predictors of suicide ideation suicide attempts and self-harm among adolescents in the UK prior to and during/after COV - 05/08/2024
Information can be obtained from ALSPAC (B number folder) or the UK LLC on request
B4659 - Genomics of obesity and overeating and their personality correlates - 19/07/2024
Obesity is the consequence of sustained positive energy balance over time where excess energy intake is the main pathway leading to obesity. Eating behaviors play a significant role in regulating food intake. Commonly used questionnaires measuring eating behaviors exhibit high correlations with each other and have been shown to share an underlying factor varying in severity - uncontrolled eating. Uncontrolled eating is associated with obesity and BMI cross-sectionally and longitudinally. Behavioral genetic models provide evidence that uncontrolled eating is a heritable trait with heritability estimates comparable to those seen in other personality or behavioral traits. Heritable variances of BMI and uncontrolled eating constructs show significant overlap. The genetic overlap between uncontrolled eating and BMI suggests that self-control of food intake may serve as the key mediating mechanism through which genetic factors influence differences in body weight. However, causality in this relationship is not necessarily unidirectional, as higher BMI could also lead to increased levels of uncontrolled eating. Another common construct in eating behaviour is food restriction, or restraint. Together with uncontrolled eating, they explain vast majority of variance in eating behaviour traits. The aim of this study is to investigate the genetic basis of uncontrolled eating and restrictive eating, examine their genetic correlations with various other phenotypes, and assess the causal relationship between uncontrolled eating, restraint and BMI.
B4657 - Investigating the links between bullying and youth violence - 26/07/2024
Successful violence interventions depend on the identification of upstream risk factors, an understanding of their relative importance, and how they relate to each other. The project outlined in this proposal would focus on examining bullying as a potential risk factor. Bullying is a common, worldwide social problem, which tends to peak in early to mid-adolescence as children develop greater independence, form new peer groups, shape their adult identities and behavioural patterns. There can be an overlap between bullying and being bullied – ‘bully-victims’ are those who bully others and who are bullied themselves. The pathway from bullying behaviours in childhood and early adolescence to violent behaviour in young adulthood could be causal, or could reflect common factors that predispose young people to both being a bully or a victim and to later violence, such as abuse, negative peer group influences, low connectedness to school, and poor academic achievement.
B4654 - Height-GaP a quantitative index of human growth conditions deployable at any age - 12/07/2024
Adverse exposures and events during the period of early-life growth are increasingly recognized as important to later-life disease risk. For example, up to 50% of chronic obstructive pulmonary disease (COPD) has been linked to impaired lung growth early in life. A challenge to understanding and exploiting this knowledge is the lack of a simple method to quantify the cumulative impact of adverse early-life growth conditions among adults. This amendment proposes to validate a novel quantitative index of early-life growth conditions that can be deployed across the lifespan.
A recent genome-wide association study of 5.4M adults reported a saturated map of genetic variants associated with height that accounts for over 90% of trait heritability and explains up to 45% of trait variance.5 Since human height is determined in part by genetics and in part by early-life growth conditions, it follows that the difference between measured height and genotype-predicted height (height-GaP) may represent a quantitative and cumulative index of adverse early-life growth conditions. In support of this hypothesis, analysis of UKBiobank data demonstrated that a larger height-GaP deficit was associated with several retrospectively ascertained early-life factors known to adversely affect growth, as well as subsequent all-cause and respiratory mortality.
Retrospective assessment of early-life growth conditions limit the strength of inferences that can made from these UKBiobank observations and motivate this amendment to our current ALSPAC proposal, which is already examining a genotype-based index and lung function.
B4655 - Picky eating in adults causes and consequences in a longitudinal UK birth cohort - 31/07/2024
CONTEXT
Picky eating is very common children, with up to 50% being picky at some point. There is no single widely accepted definition of picky eating (also known as fussy, faddy or choosy eating), although most include refusing familiar foods, sometimes combined with refusal of new foods.
Picky eating in children reaches a peak at about 3-5 years old, usually with a gradual tailing off during early school years. In this way, picky eating in children can be regarded almost as a ‘normal’ part of child development that disappears without the need for help from healthcare professionals. In some children, however, it continues into adulthood. Adult picky eating is thought to be more common in those who were picky eaters as a child, particularly those who experienced pressure from parents to eat particular foods or had an upsetting event involving a food, such as choking.
CHALLENGE
We don’t know very much about how picky eating affects the lives of adults, but it is likely to be a secretive and distressing experience causing social isolation and loneliness. We also know very little about it affects the quality of their diet as an adult and in turn how that influences long-term health. The diets of children who are picky eaters have been well studied, showing restriction of the variety and quality of foods eaten, with concern about effects on children’s growth and development. Again we know very little about the diets of adult picky eaters: studies in the USA have found they ate fewer and less variety of fruits and vegetables, were less likely to have a healthy dietary style.
B4653 - Integrating social science and genetics to better understand transmission of social inequality - 16/07/2024
Social inequalities exist across a range of social and health outcomes.3,4 They are harmful to individuals and have been exacerbated by the Covid-19 pandemic and cost-of-living crisis.5,6 The UK is one of the most unequal developed nations,7 where inequalities cost an estimated £106bn a year8 and are a largely agreed national policy priority (e.g., All Our Health; Levelling Up). Previous research has largely focussed on social or genetic influences in isolation, ignoring one of two truths; that population level social and cultural factors impacts individual outcomes, and that biology has an impact on human behaviour. This project will address the urgent issue of social inequality by examining how (dis)advantage is transmitted from parents to children. It will draw on methods from population genetics to improve evidence and complement existing social scientific research into the formation of inequalities.
B4644 - Risk perception of extreme weather and tick-borne disease in cities - 04/07/2024
This is part of a work package in the team's UKRI funding proposal entitled "CIVIC: Climate Impacts on Vectors in Cities". With a warming climate and increasing number of extreme weather events such as heatwaves, the risk of tick-borne diseases in the UK is expected to increase. CIVIC will investigate climate-mediated changes in vector-borne disease risk in urban green spaces and evaluate best approaches to increasing public understanding of risk and adaptation. This ALSPAC project will be important to achieve the objectives of CIVIC through understanding the cohort's perception, lived experience and behavioral adaptation to heatwaves and tick exposure.
B4651 - Health behaviours and pregnancy related mental health - 04/07/2024
We know that health behaviours during pregnancy (e.g., diet and physical activity) can impact on health outcomes (e.g., gestational diabetes). However, less is known about the impact of varying health behaviours on mental health outcomes (e.g., perinatal depression), and how the behaviour change of (reducing or increasing) these behaviours may impact perinatal mental health. This project will use traditional and causal epidemiological methods to investigate the impact of alcohol, tobacco and physical activity during pregnancy on maternal mental health using two longitudinal birth cohorts, to highlight pregnancy timepoints to reduce harm.
B4652 - Menopause So what A holistic approach on Hot Flushes Economic Choices Psychological Measurements and Health Conditions - 19/07/2024
Millions undergo yearly biological change, shrouded in misinformation and taboo, with minimal understanding of its impact on their economic decision-making (1). This is how life looks like for menopausal women, who experience a physical, emotional, mental, and social well-being transformation (2). Menopause is 'the permanent cessation of menstruation due to the decline in ovarian follicular activity' (3), broadly also including Peri- and Postmenopause. It causes symptoms like poor cognitive performance (brain fog), hot flushes, low mood, anxiety, and difficulty sleeping (2).
Until now, research focused solely on biology and medicine in the context of menopause, neglecting economic decisions and their complex interplay with hormonal changes, emotions, and biases (see, e.g., (4)). This project is the first to bridge this gap by applying a behavioural economics lens, delving into how menopause influences decision-making besides well-being and health outcomes. With nearly half the global population female (5) and the projected rise of 1.2 billion menopausal women by 2030 (6), understanding the economic implications of menopause matters - for women, society, policymakers, and businesses, as, e.g., menopause reduces women's economic participation (7), the menopause market is expected to be worth $24.4 billion by 2030 (8), and public interest is rising (9).
This project uses economic, psychological, and health data to study holistically how menopause affects women's economic decisions. Understanding economic decisions is fundamental to individuals, institutions, and society, demanding closer examination of underlying biological and psychological factors caused by menopause like hormonal shifts, brain-structure changes, depression, and genetic backgrounds (10; 4; 11). Our project utilises innovative economic experiments by simulating real-world economic scenarios and providing monetary incentives. This method is supplemented by health surveys and genetic data to understand how menopause influences women's economic choices (risk, investment, etc.). The goal is to develop targeted interventions based on our findings to empower menopausal women and improve their lives.
Working with the Avon data is central to our project. We will use the funding we currently apply for to collect data on economic behaviour (a central agenda of the project) and link it to genetic data as well as other health data captured in the Avon database. Understanding how menopausal women make economic choices is especially important, as menopause involves, e.g., financial changes like retirement planning and investment decisions. For example, when it comes to risky behaviour, we hypothesise that menopausal women are more risk-averse due to hormonal changes compared to women during their productive years and men older than 40. We will measure behaviour using the established questions from the preference module and compare the behaviour of menopausal women to people of other age groups and genders.
The preference module is a concise, experimentally validated survey designed to measure risk aversion, time discounting, trust, altruism, and positive and negative reciprocity. These preferences influence individuals' choices across various situations. This module provides standardised measures suitable for all popular data collection methods, making it a valuable tool for numerous applications. Preference measures enhance the prediction of significant economic behaviours and can serve as control variables for identifying causal effects of other factors correlated with preferences.
The development of the preference module is detailed in:
Falk, Armin, et al. "The preference survey module: A validated instrument for measuring risk, time, and social preferences." Management Science 69.4 (2023): 1935-1950.
Menopause and its transition occupy a significant portion of a woman’s life (13). This project offers a timely and cutting-edge approach, promising impactful results that improve lives, inform policy, and empower women to thrive through all stages of their journey.
1. The demography of menopause. Hill, Kenneth. 113-127, : Maturitas, 1996, Vol. 23.2.
2. NHS. NHS. Symptoms Menopause. [Online] 17 May 2022. https://www.nhs.uk/conditions/menopause/symptoms/.
3. WHO. Menopause. World Health Organization. [Online] 17 October 2022. https://www.who.int/news-room/fact-sheets/detail/menopause.
4. Menopause impacts human brain structure, connectivity, energy metabolism, and amyloid-beta deposition. Mosconi, Lisa, Valentina Berti, Jonathan Dyke, Eva Schelbaum, Steven Jett, Lacey Loughlin, Grace Jang et al. 2021, Scientific reports, p. 10867.
5. The World Bank. The World Bank Data. Population, female (% of total population). [Online] 2022. https://data.worldbank.org/indicator/SP.POP.TOTL.FE.ZS.
6. Social Determinants of Health in Menopause: An Integrative Review. Namazi, Masoumeh, Sadeghi, Rasoul and Behboodi Moghadam, Zahra. 2019, International journal of women's health, pp. 637-647.
7. Brewis, Joanna, et al. The effects of menopause transition on women’s economic participation in the UK. s.l. : Department for Education, 2027.
8. Grand View Research. Menopause Market Size, Share & Trends Analysis Report By Treatment (Dietary Supplements, OTC Pharma Products), By Region (North America, Europe, Latin America), And Segment Forecasts, 2024 - 2030. [Online] 2024. [Cited: 18 February 2024.] https://www.grandviewresearch.com/industry-analysis/menopause-market#men....
9. Google Trends. Google Trends. Searching "menopause" Worldwide and for the UK. [Online] 15 February 2024. https://trends.google.co.uk/trends/explore?date=today%205-y&q=menopause&....
10. Elevated body temperature is associated with depressive symptoms: results from the TemPredict Study. Mason, Ashley E., et al. 1884, s.l. : Scientific Reports , 2024, Vol. 14.1.
11. An experiment on risk taking and evaluation periods. Gneezy, Uri and Potters, Jan. s.l. : The quarterly journal of economics, 1997, Vols. 112.2, 631-645.
12. National Office for Statistics. Office for National Statistics. National life tables – life expectancy in the UK: 2018 to 2020. [Online] 23 September 2021. https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarri....
13. Brains, hormones, and genes: Introduction to the special issue on the biological foundations of economic decision-making. Fairley, Kim, Fornwagner, Helena and Okbay, Aysu. s.l. : Journal of Economic Psychology, 2023, Vol. 102683.
B4650 - The glue that holds the pieces together Unlocking Cognitive Health in Psychotic Disorders - 15/07/2024
Psychotic disorders like schizophrenia have a strong neurodevelopmental component, yet symptoms often do not emerge until adolescence or early adulthood. Cognitive impairments are among the earliest and most disabling symptoms. Intriguingly, our research reveals that many brain alterations linked to these impairments resemble those associated with premature aging, such as brain atrophy and advanced brain age. Understanding the neurodevelopmental pathways of these cognitive impairments is crucial for creating effective early interventions.
Our aim is to combat cognitive impairment in psychotic disorders as early as possible by:
1) Understanding the developmental features of brain age acceleration in psychotic disorders and what risk factors might exacerbate these, using large-scale neuroimaging datasets and computationally advanced methods;
2) Characterising the neuronal changes associated with advanced brain age, using experimental mouse models for schizophrenia;
3) Identifying treatment targets that could prevent or slow down cognitive impairment in psychotic disorders, using longitudinal proteomic samples (of individuals who later went on to develop psychosis).
Our goal is to unravel advanced brain age at a neuronal level, embed this within a neurodevelopmental framework, and identify effective treatment targets for early intervention against cognitive impairments in psychotic disorders to mitigate cognitive impairments at the earliest stages of the disease.
B4649 - Investigating associations between religion/spiritual beliefs and behaviours and brain MRI variables - 28/06/2024
Religiosity and spirituality are an important factor in the lives of many people. Previous research, using relatively small sample sizes in cross-sectional studies, has found that a high degree of belief in the importance of religion/spirituality was associated with both a thicker cortex and a larger pial surface area in persons at high risk for familial depression. We plan to see if these specific findings replicate in a much larger cohort. We also plan to do an exploratory analysis, where we will look at all of the brain MRI variables measured in ALSPAC to see if any are associated with the religion/spirituality variables measured in ALSPAC.
B4646 - Association between Locus of control and disordered eating - 24/06/2024
Locus of control is described as the way an individual perceives the outcome of events in their life as caused by their own actions (internal) or caused by outside factors uncontrolled by them (external). Research has linked locus of control, particularly external locus of control, with psychopathology, such as depressive symptoms, social anxiety symptoms, and psychotic-like experiences.
There is some evidence indicating that it may also be a risk factor for eating disorders. However, this research is mostly cross-sectional so it can't be ruled out that external locus of control is a consequence of eating disorders. To date, there is a lack of longitudinal research on this association, which limits our understanding of whether there is a causal association.
The present study aims to bridge this gap in the literature by investigating the association between external locus of control in childhood at age 8 and eating disorder symptoms in adolescence at age 16.