Proposal summaries
B4687 - Investigating the impacts of adverse and protective childhood contexts on violence and health outcomes later in life Analysis o - 05/09/2024
We propose to draw on high-quality longitudinal data about children's lives, including experiences of violence, in three independent cohort studies in Brazil (birth to late childhood), England (birth to adulthood) and Uganda (late childhood to adulthood). The first phase of this project will define and operationalise contextual measures: we theorise that adverse childhood contexts are homes, schools, and neighbourhoods with violence and deprivation, and protective childhood contexts high social connectedness and support. We will use data collected on contexts to operationalise contextual measures specific to each cohort and refine measures based on input from local stakeholders, young people, and researchers in each context. Findings from this phase will highlight new opportunities to apply advanced statistical methods to improve how contexts are measured and defined in violence research.
The second phase will test whether adverse childhood contexts increase the risk of violence later in life and health in early adulthood, and whether protective childhood contexts can mitigate this risk. We aim to conduct causal analyses of longitudinal data to uncover, for example, whether neighbourhood violence and deprivation in childhood could increase interpersonal physical or sexual violence years later - and whether a protective home environment at the same time, or later in life could prevent or interrupt these associations. We will also examine for example, whether adverse childhood contexts are associated with common mental disorders, and cancer and its risk factors. Findings from this phase provide evidence for developing and situating contextual interventions to prevent violence and ill health as children grow up.
The third and final phase of the project will explore how the effects of contexts differ for young people from historically marginalised groups. By applying statistical methods to test if the adverse and protective effects of contexts differ by gender, disability, ethnicity, sexuality, and socioeconomic position, findings will highlight which young people are disproportionately impacted by adverse contexts or less likely to benefit from protective contexts.
B4683 - epigenetic biomarkers for the risk and progression of depression among young adolescents - 02/09/2024
Depression among adolescents is a growing concern, with one in five U.S. teens aged 12-18 experiencing at least one major depressive episode. Early life stress (ELS), which includes experiences of adversity and trauma during childhood, is a major risk factor for developing depression. ELS can cause lasting changes in how genes are expressed, increasing the risk of depression and other health issues later in life. These effects might not show up immediately but can have a significant impact on a person’s quality of life, making it crucial to identify those at risk as early as possible.
Epigenetic changes, such as DNA methylation (DNAm) and microRNAs (miRNAs), are important mechanisms that link ELS to changes in gene expression. Because DNAm levels can change over time, studying these changes provides more accurate predictions about the effects of ELS than single-time-point assessments. Research on animals and some human studies show that miRNAs are also involved in how ELS can lead to depression, and that DNAm might control miRNA expression. While these findings give us important clues about how ELS affects gene expression, research is still limited, often focusing on only a small number of miRNAs. The absence of comprehensive data means we do not have reliable biomarkers to predict who is at risk for depression, making early and effective intervention more challenging.
In this project, we will examine how early life stress influences multiple epigenetic mechanisms and how these mechanically systems interact with each other, contributing synergistically to the risk of developing depression.
B4681 - Use of ALSPAC data for mediation analysis and other statistical method development - 02/09/2024
This project aims to provide training to our PHD students in Division of Biostatistics and Health Data Science. Several projects are proposed, with a focus on developing statistical methods, ranging from gene-by-environment interaction, mediation analysis, and methods to appropriately account for family structure. Ultimately, our goal is to use this information to train the next generation of PHD students who study statistical genetics and genomics.
B4684 - Use of childhood cancer to explore effect of breastmilk on childhood cancer - 02/09/2024
This project aims to improve our understanding of childhood cancer by using a detailed dataset from the Avon Longitudinal Study of Parents and Children (ALSPAC), which contains extensive information about parents and their children. We will also use the ALSPAC data to identify risk factors, particularly related to maternal breastfeeding, and its impact on childhood cancer. Ultimately, our goal is to use this information to train the next generation of PHD students who study statistical genetics and genomics and enhance our knowledge of general health of children and what might increase the risk of cancer in children, helping to inform future research and potentially guide preventative measures.
B4686 - GWAS of breast density in ALSPC - 02/09/2024
Breast density, the proportion of fibroglandular tissue as detected by mammography or magnetic resonance imaging (MRI), is strongly associated with breast cancer risk. However, the mechanisms through which increased breast density leads to increased cancer risk are not well understood. This project aims to map the contribution of common genetic variation to breast density as detected by MRI in a subset of nulliparous women.
B4685 - Developing models of resilience against early-life adversity in adolescent mental health and educational achievement - 04/09/2024
Given similar histories of adversity, why do some children do better than others? We propose a project investigating this question of resilience against early-life adversity. We will explore potential protective factors against adversity with respect to two outcomes: mental health and educational achievement. We will conduct the study across two contexts: the United Kingdom, using ALSPAC data, and the Netherlands, using Generation R data. This project may help us better understand factors that promote mental health and educational achievement.
B4682 - Role of MICL in autoimmunity - 31/10/2024
We have discovered that autoantibodies to a C-type lectin MICL promote uncontrolled formation of neutrophil extracellular traps (NETs) that exacerbate autoimmune disease (PMID: 19025564). We have also identified the presence of these autoantibodies in a proportion of our healthy control cohorts and we wish to study this longitudinal cohort to see if the presence of these antibodies early in life predispose to the development of autoimmunity.
B4680 - Understanding Sexual Dimorphism In Bone Health With Prenatal Alcohol Exposure - 03/09/2024
The UK has the 4th highest rate of alcohol use in pregnancy worldwide. Alcohol exposure in pregnancy (prenatal alcohol exposure - PAE) can lead to a set of lifelong disabilities known as foetal alcohol spectrum disorder (FASD) - a neurodevelopmental disorder associated with over 400 comorbidities. In the UK, FASD affects an estimated 2–4% of schoolchildren, and 27% of children in care. FASD therefore presents a significant healthcare burden, estimated to be up to £152million. Young adults with FASD refer to it as a ‘whole body diagnosis’. However, with the exception of facial dysmorphia and growth deficiency, there is a paucity of evidence on the physical impacts of FASD, particularly beyond childhood.
Emerging evidence from small cross-sectional studies and non-representative surveys indicate indicate elevated rates of bone abnormalities and musculoskeletal conditions among young adults with PAE and FASD.. However, tTherefore, there is a critical need for longitudinal data to delineate the causal relationship between PAE and musculoskeletal health, including potential sexually dimorphic effects. This will offer important insights into mechanisms and potential opportunities for intervention, with. It is particularly important to examine any sex differences as these are currently under-researched in adults with PAE, and this could have important implications on for lifelong musculoskeletal health.
Using a mouse model, we recently found that PAE indeed has a sex-dependent effect on the skeleton. In adult males, PAE had a detrimental effect on bone volume and strength compared to controls. However female mice were protected. Moreover, these differences were not present in young mice, indicating the potential influence of environmental factors.
One such factor may be mechanical loading, which is known to exert beneficial effects on the skeleton through a process termed mechanoadaptation. This process is intimately linked to the bone vasculature, which we have shown to develop in a sex-dependent manner. Further, with PAE we found a reduction in the expression of genes related to blood vessel formation (e.g. VEGF) predominantly in male mice.
Therefore, it is currently unknown whether there are sex-differences in bone health in individuals with PAE, what the underlying mechanisms are, and what impacts these might have on physical functioning and health-service use.
Approach
Our proposal is at the interface of life and clinical sciences and, using ALSPAC data, will address the objective:
- Determine whether humans with PAE exhibit overall and sex-specific adverse impacts on musculoskeletal health and motor functioning and, if so, the extent to which this is mediated by bone composition
Benefits
This research will investigate the overall and sex-specific impacts of PAE on musculoskeletal health, aiming to inform targeted therapies and public health policies. By elucidating underlying mechanisms, it can improve FASD diagnosis and treatment, benefiting stakeholders including clinicians, researchers, policymakers, charities, and individuals with FASD.
B4679 - Estimation of body fat from impedance compared with ojective DXA measures - 29/08/2024
ALSPAC did not collect DXA measures of body composition at 7 or 8 years of age but did collect impedance. An equation has previously been derived to estimate body fat from impednace in adults and it has been shown that this also correlates well in chidlren but this has never been written up. We plan to examine associations between body fat estimated from impedance and boda fat estimated using DXA at all timepoints where both are available.
B4678 - Soci-Omics - 23/08/2024
Individuals of lower socio-economic position (SEP) develop diseases earlier and die earlier on average compared with their more advantaged counterparts. So ubiquitous is the association between SEP and health that it has been referred to as a ‘fundamental’ cause of disease. The damaging effects of low life course SEP can be seen in every major organ system of the human body which suggests that there are common biological pathways and mechanism(s) conveying increased risk for premature ageing. Recently, DNA methylation (DNAm) has emerged as a leading biomarker of ageing and evidence is growing to support its central role as a fundamental cause of ageing. Nevertheless, the recognition that ageing is affected more by environmental as opposed to genetic factors broadens our view of ageing beyond a narrow biological focus to encompass a wider range of social (e.g. socio-economic position) and ecological influences on the pace of ageing. I propose an ambitious programme of transdisciplinary research that will integrate the social and biological hallmarks of ageing using DNAm data. The primary aim is to elucidate the causal mechanisms through which SEP gets transduced at a more fundamental cellular or molecular level to precipitate earlier ageing of the socially disadvantaged. This proposal draws upon my existing expertise with longitudinal cohort studies of development and ageing and will employ cutting-edge statistical techniques, alongside ‘omics-based’ technologies, to provide new insights into the social epidemiology of the ageing process. The methodological approach will incorporate epidemiological (i.e. prospective cohort studies), naturalistic (i.e. twin studies) and experimental designs (i.e. challenging cells) to help elucidate whether DNAm serves as a biological intermediary between SEP and premature mortality.A large number of individual studies (8, 35-37) and meta-analyses (3, 4, 31) have documented socio-economic differentials in the pace of epigenetic ageing, but the paucity of longitudinal studies means the dynamics and persistence of embedding remains shrouded (7, 29). Presently, we have no resolution concerning when these differences first emerge, nor whether they widen, narrow, or remain stable over time. The epigenetic clock does not tick at a constant rate, but runs fastest in early life, settling into a more constant rate post-puberty, mirroring processes of physical growth and development. A recent study study suggests that mean DNAm changes are largest in infancy, changing by 3% per year compared with 0.1% per year in adulthood. I therefore hypothesise that early childhood represents a sensitive period for the biological embedding of SEP.
B4673 - The relationship between pathways environmental risk factors immune markers and mental health outcomes in early adulthood - 16/08/2024
The goal of this project application is to enable a PhD student to use data requested in previous applications.
We and others have identified numerous risk factors that influence mental health in young adults and early adulthood. These include adversity, cannabis use, population density, immigrant status (PMID: 29352556, 31563981), exposure to infections such as COVID (PMID: 35987197), obstetric and delivery complications (PMID: 12091183), and maternal characteristics and behaviours during pregnancy. Evidence for example suggests that offspring of mothers who smoked during pregnancy have an increased risk (38%) of developing schizophrenia (PMID: 27216261). Furthermore, infection during pregnancy is associated with an increased the risk of psychosis in offspring (PMID: 26303935). Additionally, in the ALSPAC cohort, we recently identified that suicidal ideation at age 17 is associated with 7-fold increased odds of psychotic disorder, and with depressive disorder and generalised anxiety disorder at age 24. Indeed, over 40% of those with psychotic disorder in early adulthood had experienced this symptom in late adolescence (Mongan et al, 2022).
We and others have also identified evidence for inflammatory marker dysregulation both preceding and in association with psychiatric disorders including psychosis, depression and recently, long COVID (PMID: 36085284, 35472304). Dysregulation of acute inflammatory markers [such as Interleukin (IL)-6 and C-Reactive Protein] and complement proteins has been reported prior to and in association with these outcomes (PMID: 25133871, PMID: 32857162).
Using ALSPAC data we identified for the first time the cross-sectional association of suPAR (soluble urokinase plasminogen activator receptor- an established marker of chronic inflammation) and IL-6 (an established marker of primarily acute inflammation) with psychotic disorder in young adults (PMID: 37004760). We previously found an inverse association between the anti-inflammatory marker n-3 fatty acid docosahexaenoic acid (DHA) at age 17 and psychotic disorder at age 24 in the ALSPAC cohort (PMID 34059620). Using ALSPAC data, we have also shown for the first time that elevated suPAR is associated cross-sectionally with cannabis exposure, itself a marker for mental ill health (Power et al., 2022 (under review)).
We now seek to expand our knowledge to mental health outcomes in early adulthood (using data collected at age 24 and age 30). We wish to examine cross-sectional and longitudinal associations between early life, childhood and later life risk factors with inflammation in relation to clinical thresholds of psychiatric disorders, as well as in relation to specific symptoms and symptom severity. In light of recent findings, (PMID: 34390805; PMID: 26033244), we are particularly interested in the relationship between adverse childhood events including physical, sexual and emotional abuse, bullying or victimisation, and inflammatory dysregulation in the development of psychiatric disorders. Elevated inflammatory levels (supar) for example have been reported in adolescents that have experienced persistent parent-child separation in childhood (PMID: 34454061).
Additionally, sexual minority groups can experience increased exposure to victimization and discrimination, as well as higher rates of anxiety, depression, suicidal thoughts and antisocial behaviour (PMID: 35572280). Recent evidence suggests the presence of increased inflammatory marker levels in such groups (PMID: 32930919).
Additionally, emerging evidence also suggests that exposure to adversity such as high stress across lifetime (PMID: 26673150) or exposure to sexual abuse (PMID: 29365106) influences epigenetic aging in adulthood. One recent meta-analysis quantified this age acceleration, showing that any exposure to childhood trauma was associated with an epigenetic “outpace” of as much as 6 months (PMID: 29452766).
We hypothesise that exposure to environmental risk factors and early-life adversity is associated with chronic inflammatory dysregulation, in line with recent evidence (PMID: 31682707, 26033244, 34990745). We also hypothesise that inflammatory dysregulation will be more common in those who go on to report mental disorders in adulthood (PMID: 25133871, PMID: 32857162). Crucially, we hypothesise that inflammatory dysregulation mediates the relationship between environmental exposures and adult mental disorders, which could provide evidence for a biological mechanism by which environmental exposures influences the risk of adult mental disorder. Alternatively, environmental exposures and biological risk factors may operate independently, but have a cumulative effect on the risk of mental disorders. We propose to investigate this using a combination of existing ALSPAC data, and new data derived from assays undertaken by us which assessed levels of the robust marker of chronic inflammation, suPAR, in age 24 plasma samples donated by ALSPAC participants.
Additionally, we would like to request data relating to general medical conditions and previous infections as accounting for these factors will be important to avoid potential confounding of our findings. For example, there are reports of associations between childhood infection, in particular viral CNS infections and increased risk for psychosis in adulthood (PMID: 29450471; PMID: 22704639). Regarding suPAR itself, there is also evidence of associations between elevated suPAR levels with the development of cancer, CVD, T2D and mortality in the general and psychiatric populations (PMID: 20561148).
We are interested in investigating the longitudinal associations between biological and environmental risk factors with subsequent mental ill-health at age 24 and age 30 (when available). In order to explain any potential relationships appropriately, we will need to include particular demographic variables (such as ethnicity) as co-varying factors.
Previous research has shown that the incidence of psychotic disorders is elevated in various ethnic groups (PMID: 28642258). Evidence has also indicated an association between ethnicity and inflammation, with Caucasian populations often having lower CRP or IL-6 levels compared to other ethnic groups (PMID: 15205215; PMID: 16123316). Based on such findings, we feel that it is important to determine the extent of the relationship between ethnicity, inflammation and later psychiatric outcomes.
Evidence has also shown that lifestyle factors including low physical activity can contribute to a higher suPAR levels (PMID: 30679937), as well as altered levels of acute inflammatory biomarkers (CRP) in healthy populations (PMID: 12038947). Physical activity was also shown to act as a potential protective mechanism against oxidative stress in first-episode psychosis patients (PMID: 32709912). Based on such findings, we would like to investigate how physical activity might influence the relationship between inflammation (as measured by suPAR, and/or CRP & IL-6) and later psychiatric outcome.
An earlier project, B4168 aims to investigate longitudinal associations between environmental risk factors and subsequent mental ill-health, and then if possible, to investigate whether inflammation mediates the relationship between these environmental risk factors and mental health outcomes. One such risk factor is childhood trauma.
There is some evidence that trauma exposure is associated with elevated inflammatory levels (PMID: 29741788) and with poor mental health outcomes (PMID: 23592532).
We aim to explore if these relationships exist in relation to age 24 chronic inflammatory marker - suPAR - and if inflammation (as measured by suPAR) mediates the relationship between trauma and poor mental health.
Recently, emerging evidence suggests that while trauma might be related to elevated inflammation levels, certain positive experiences in childhood are associated with lower levels of inflammation (PMID: 36420372). Therefore, we feel that in order to fully understand the relationship between trauma exposure, inflammation and later mental health outcomes, we must investigate and account for positive childhood experiences as an important confounder/contributor in the relationship.
No new data is requested - Only data from B4168 will be used.
B4635 - Considering a multiverse of pubertal timing effects Do different operationalizations produce different results - 16/08/2024
A growing body of evidence suggests that pubertal timing (i.e., onset compared to same-aged, same-sexed peers) is one important predictor of subsequent adjustment behaviors. There is substantial disagreement, however, regarding the optimal way to measure pubertal timing, namely: how many times it should be assessed, when it should be measured, what instrument should be considered, and which analytic strategy should be used. These differences (also known as ‘researcher degrees of freedom’) could lead to drastically different operationalizations of pubertal timing, which in turn, can lead to notably different conclusions about pubertal timing’s short- and long-term effects on behavior. The goal of this registered report is to leverage and combine multiple large, publicly available secondary datasets to determine the degree to which different operationalizations affect the robustness of associations between pubertal timing and depressive symptoms. Results from this multiverse analysis will suggest the impact that differences in operationalizations of pubertal timing have on its associations with outcomes, as well as provide a roadmap for future researchers using puberty data.
B4677 - A life course approach to examining the association between passive tobacco smoke exposure and pubertal timing - 16/08/2024
Pubertal timing refers to the pace at which individuals reach certain stages of puberty relative to their same-age and same-sex peers. The global trend towards earlier pubertal timing is of concern due to its associated adverse health implications including cardiovascular diseases, type Ⅱ diabetes and sex steroid-sensitive cancers(2). In addition, earlier pubertal timing may also lead to increased risky behaviours during adolescence including depression, early sexual activity and substance abuse(2). Therefore, identifying modifiable factors that influence pubertal timing is important to mitigate these adverse outcomes. Studies suggest that passive tobacco smoke exposure is associated with puberty timing, e.g., several birth cohorts have shown that maternal smoking during their third trimester associates with an earlier age of menarche. Life course epidemiology theory may help us understand how passive tobacco smoke exposure relate to pubertal timing. Under this theory, we proposed three life course models to explain the association between passive tobacco smoke exposure and pubertal timing: the critical period model, the risk accumulation model and a compound model of risk accumulation with a sensitive period. The critical period model assumes that exposure during a limited time window has an adverse impact on development, contributing to disease onset in later life, and this impact cannot be modified by subsequent exposures. In contrast, the risk accumulation model posits that as the number and/or duration of exposure increases, there is cumulative damage to biological systems. Additionally, a compound model of risk accumulation with a sensitive period suggests that within the risk accumulation model, there is stronger association between exposure and outcome during a specific developmental period relative to other periods. To our knowledge, no previous study has examined the contribution of passive tobacco smoke exposure during different early life periods (prenatal, infancy and childhood) to pubertal timing.
B4674 - Double precarity among young adults interrogating the impact on mental health - 16/08/2024
B4676 - Extension of G0 clinic to collect additonal vision hearing and cognition data - 13/09/2024
The @30 clinic which has collected data on the original parents of ALSPAC has some gaps in the vision and hearing data as these measures were not ready to be collected from the start. We would also like to collect cognition data which was not collected in the original clinic (although was funded and originally proposed). These data will be used in a wide variety of studies, focussed on aging in the parent cohort and used as baseline for future funding proposals
B4675 - Genetic-environment interaction in the association between early-life exposure and long-term mental health outcomes - 16/08/2024
The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that early life, beginning from pregnancy, is a critical exposure window influencing an individual's health and disease risk. This period is especially vital for neurodevelopment, given the significant plasticity of the neural system. Extensive research has demonstrated that gestational complications, parental lifestyle, and environmental exposures during early life can impact the neurodevelopment of offspring, leading to diminished cognitive abilities, increased behavioral and emotional issues, and a higher risk of mental health problems. These exposures might influence early neurodevelopment through complicated genetic-environment interactions. Despite these findings, there remain significant gaps in our understanding of the effects, their underlying mechanisms, and modifiable factors.
This project aims to explore the genetic-environment interactions in the association between early-life exposures and long-term mental health outcomes utilizing data from the ALSPAC cohort. Additionally, we will investigate the potential mechanisms and modifiable factors underlying these associations through a multi-omics approach. This study aims to generate novel insights for early prevention and intervention strategies to enhance childhood and adolescent mental health.
B4672 - Infant2Adult Neurobiological mechanisms of adverse mental health outcomes following early regulatory problems - 16/08/2024
The first years of life have a profound impact on later behavioural, emotional and social development. An intriguing and modifiable risk factor for later psychopathology is the early regulation of bodily functions, such as the sleep-wake cycle, self-soothing and food ingestion, which goes awry in about 20% of infants leading to regulatory problems (RPs) with crying, sleeping and/or feeding. About 2-8% of infants and toddlers experience multiple or prolonged RPs. Mounting evidence shows that RPs can have adverse long-term effects on behavioural, emotional and/or social outcomes. The proposed project will investigate the impact of early RPs on mental health outcomes from childhood to adulthood, examining multimodal neurobiological markers as possible underlying mechanisms. We will go beyond the state of-the-art in three ways. Firstly, we will analyse rich phenotypic and neuroimaging data of three population-based studies from three countries (Generation R, ALSPAC and BLS). To enable cross-timepoint and cross-dataset brain surface analysis, we will develop novel robust vertex-wise mixed modelling, meta-analysis and federated mega-analysis tools as part of an existing open-source R package. Secondly, we will examine neurobiological pathways of the RP-mental health association, via brain structure (i.e., cortex morphology) and function (i.e., intrinsic functional connectivity). Thirdly, we will employ the hierarchical dimensional HiTOP framework to characterize adverse outcomes of early RPs with better precision and generalizability. This may result in new findings on neurobiology and effects of RPs on dimensional mental health phenotypes, and crosswalk models for the research community.
B4671 - Eczema phenotypes - ethnic differences early life risk factors and genetics A comparative study of four birth cohorts in dive - 05/08/2024
Eczema (atopic dermatitis) is a skin condition that causes dry, itchy and sore skin. It affects up to 20% of children in the UK, the US and Europe. For some children with eczema, symptoms improve and resolve as they get older, but in others the symptoms can persist throughout childhood and severely impact quality of life.
There is an urgent need to better understand different patterns of childhood eczema and to identify factors linked to resolution or persistence of symptoms. Children at risk of having persistent or severe eczema can then be identified at an earlier age, when interventions, such as systemic treatment with new biologics, may be more effective.
There have been several studies to define subtypes of eczema, and to try to identify which early life factors are associated with each subtype. However, most research to date has focussed on children of European ancestry in high-income countries (HICs) such as the US, UK and other European countries. This means that the existing research findings in this area cannot necessarily be generalised to non-European children in HICs, or to children in low-and-middle income countries (LMICs). This has important implications in terms of the prevention, diagnosis and treatment of eczema in these populations.
The focus of the current proposal is therefore on identifying eczema subtypes (phenotypes) and assessing possible risk factors for the various subtypes in four birth cohorts in diverse settings; the Born in Bradford (BiB) study and the Avon Longitudinal Study of Parents and Children (ALSPAC) in the UK, the Ecuador Life study (ECUAVIDA) in Ecuador, and the Entebbe Mother and Baby Study (EMaBS) in Uganda.
B4670 - An Investigation of the Associations between Obsessive Compulsive Disorder and Psychosis - 02/08/2024
Obsessive Compulsive disorder (OCD) is a chronic and debilitating condition characterised by the presence of obsessions (i.e., recurrent, or intrusive thoughts or images) and/or compulsions (repetitive and ritualised behaviours carried out in an attempt to alleviate anxiety) (American Psychiatric Association, 2022). OCD is thought to affect 1-4% of adults in the general population (NICE, 2018). In contrast, psychotic disorders are classified as eight distinct diagnoses in the DSM-5-TR, each featuring a combination of hallucinations, delusions, disorganised speech, abnormal psychomotor behaviour and negative symptoms (American Psychiatric Association, 2022). It is estimated that psychotic disorders have a lifetime prevalence of 3% (Perälä et al, 2007).
OCD, when present in psychotic disorders, has been linked to complications in treatment of either condition (Cederlof et al, 2015). Additionally, this comorbidity is associated with increased symptom severity, decreased quality of life, more depressive symptoms and higher rates of suicidaility and overall poorer prognosis (Cunill et al., 2008; Lieuwe de Haan et al., 2012; Niendam et al, 2009; Sharma & Reddy, 2019). Some research has explored the cross-sectional relationship between OCD and psychosis. One study conducted in Sweden found that individuals diagnosed with OCD were 12 times likelier to have a diagnosis of psychosis (Cederlof et al, 2015). Similarly, within a population of individuals diagnosed with psychosis, 25% also presented with obsessive compulsive symptoms (OCS) and 15% met diagnostic criteria for OCD (Scotti-Muzzi & Saide, 2017). Whilst current literature documents cross-sectional links between the two disorders, there is a dearth of literature exploring whether OCD is prospectively associated with psychosis, or whether psychosis is prospectively associated with OCD. Additionally, whether this association is true for OCS and psychotic-like experiences. There is also very little known about the mechanisms which may explain this association. One research study found significant associations between the presence of delusions and obsessions as well as auditory hallucinations and compulsions, suggesting that they could share common mechanisms (Guillem et al, 2009). Through developing a better understanding of the association between OCD/OCS and psychosis/ psychotic experiences at a symptom level, psychological interventions may be adapted or developed for individuals who present with both.
This project proposes to re-use the dataset B2172 in order to explore the research question, whilst also requesting additional variables (please see exposures, outcomes and confounders for a list of the data to re-use request and new variables to request).
References:
American Psychiatric Association. (2022) Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, DSM-5-TR. American Psychiatric Association
Cederlöf, M., Lichtenstein, P., Larsson, H., Boman, M., Rück, C., Mikael Landén, & Mataix-Cols, D. (2014). Obsessive-Compulsive Disorder, Psychosis, and Bipolarity: A Longitudinal Cohort and Multigenerational Family Study. Schizophrenia Bulletin, 41(5), 1076–1083. https://doi.org/10.1093/schbul/sbu169
Cunill, R., Castells, X., & Simeon, D. (2008). Relationships Between Obsessive-Compulsive Symptomatology and Severity of Psychosis in Schizophrenia. The Journal of Clinical Psychiatry, 70(1), 70–82. https://doi.org/10.4088/jcp.07r03618
Guillem, F., Satterthwaite, J., Pampoulova, T., & Stip, E. (2009). Relationship between psychotic and obsessive compulsive symptoms in schizophrenia. Schizophrenia Research, 115(2-3), 358–362. https://doi.org/10.1016/j.schres.2009.06.004
Lieuwe de Haan, Sterk, B., & Renate. (2012). Presence of obsessive compulsive symptoms in first‐episode schizophrenia or related disorders is associated with subjective well‐being and quality of life. Early Intervention in Psychiatry, 7(3), 285–290. https://doi.org/10.1111/j.1751-7893.2012.00377.x
NICE. (2018) Obsessive-compulsive disorder: How common is it?
Niendam, T. A., Berzak, J., Cannon, T. D., & Bearden, C. E. (2009). Obsessive compulsive symptoms in the psychosis prodrome: Correlates of clinical and functional outcome. Schizophrenia Research, 108(1-3), 170–175. https://doi.org/10.1016/j.schres.2008.11.023
Perälä, J., Jaana Suvisaari, Saarni, S. I., Kimmo Kuoppasalmi, Erkki Isometsä, Pirkola, S., Timo Partonen, Annamari Tuulio-Henriksson, Jukka Hintikka, Tuula Kieseppä, Tommi Härkänen, Koskinen, S., & Jouko Lönnqvist. (2007). Lifetime Prevalence of Psychotic and Bipolar I Disorders in a General Population. Archives of General Psychiatry, 64(1), 19–19. https://doi.org/10.1001/archpsyc.64.1.19
Scotti-Muzzi, E., & Saide. O. L, (2016). Schizo-obsessive spectrum disorders: an update. CNS Spectrums, 22(3), 258–272. https://doi.org/10.1017/s1092852916000390
Sharma, L. P., & Reddy, J. (2019). Obsessive–compulsive disorder comorbid with schizophrenia and bipolar disorder. Indian Journal of Psychiatry, 61(7), 140–140. https://doi.org/10.4103/psychiatry.indianjpsychiatry_527_18
B4669 - Effects of Adverse childhood events on temporary lower appetite - 05/08/2024
Our research aims to uncover the lesser-known effects of childhood physical abuse on temporary changes in appetite and dietary habits. Previous studies in animal models have shown that exposure to physical trauma can lead to a temporary decrease in appetite, a finding that contrasts with the common belief and some human studies suggesting that abuse might lead to an increase in Body Mass Index (BMI) over time. Interestingly, our preliminary studies in older adult cohorts have also indicated a potential long-term increase in baseline BMI in individuals who experienced abuse during childhood. This project seeks to explore these dynamics in a child population using the rich data available from the ALSPAC cohort, focusing on immediate dietary responses and developmental outcomes following episodes of physical abuse.