Puberty and adolescence is an important period in human development characterized by rapid transformations in anatomy, physiology, and behaviour, and the establishment of social and economic resources to maintain health and wellbeing across the life course. Despite the importance of puberty, little is known on the patterns of various developmental changes during puberty. Early life environmental exposures and socioeconomic position are thought to influence later health but whether they influence pubertal development is unclear. This study will describe the timing of different markers of pubertal development in 3 cohorts from the UK, USA, and Denmark, and examine early life environmental and socioeconomic influence on the timing of puberty.

The Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium invites ALSPAC and Bristol researchers to take part in a large GWAS of blood pressure traits, which include systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP, i.e. SBP-DBP). The main aims of CHARGE's GWAS are to (1) identify novel loci for BP traits separately by sex; (2) identify gene-sleep interaction effects on BP traits by sex. These analyses will follow the most recent analysis plan (currently 'Phase II analysis plan for sleep and blood pressure' version 4.3) provided by CHARGE. Only summary statistics will be shared with CHARGE. Based on the final GWAS results, subsequent analyses (e.g. Mendelian randomization) would be conducted by CHARGE based on the summary statistics.

Adolescent mental health issues can have a significant impact on both the individual and their family. Understanding what factors relate to offspring mental health can help identify adolescents at greater risk of mental health issues. Previous research has investigated the role of parental religious belief, with inconsistent results. The aim of the present study was to re-examine whether a parent’s religious belief is related to their offspring’s mental health during adolescence. This is intended to build upon our previous study that looked at childhood mental health and parental religious belief.

The prevalence of food allergies has steadily increased in recent decades. This highlights the contribution of environmental and lifestyle factors, which act on the background of individual genetic susceptibility to shape the responsiveness of the immune system to allergenic triggers. A few genetic regions associated with food allergy have been identified but the number of genome-wide association studies (GWAS) on food allergy to date is limited and often restricted to one specific food allergen. Therefore, we aim to conduct a large-scale meta-analysis of GWAS on food allergies.

Many people feel their emotional wellbeing is affected by their social media use, in positive and/or negative ways. However, scientific research has made little progress in uncovering the mechanisms by which social media could affect mental health. We now know that social media use can be modelled as a reward-learning process, whereby people engage with social media partly in order to gain ‘rewards’ such as ‘Likes’ and followers. However, we do not know which individual differences cause people to pursue and react to these rewards differently, nor whether different responses to these ‘rewards’ might determine the effects of social media on wellbeing.

We propose to investigate, for the first time, reward-learning behaviours as a potential mechanism linking social media and mental health. We intend to use the unique Twitter-data linkage ALPSAC has established for its participants in recent years. We will link the multidimensional questionnaire data regarding interindividual differences and developmental trajectories in the ALSPAC cohort, to data from these individuals’ Twitter profiles. We will then use computational models of reward-learning to model the Twitter data. This will allow us to associate behavioural and emotional trajectories with reward-learning behaviours on Twitter.

We will attempt to answer the following questions:
- Are behavioural and emotional characteristics, and other individual differences, associated with reward-learning behaviours on Twitter?
- Do reward-learning behaviours, such as the extent to which people alter their posting in response to the numbers of ‘Likes’ they receive, predict mental health trajectories over subsequent years?

A recent EU-wide report by the European Union Agency for Fundamental Rights found that 22 percent of women had experienced Intimate Partner Violence (IPV) in their lifetime, and wide-cited estimates by the WHO suggest that the global incidence is significantly higher. The scale and impact of IPV, have attracted the attention from multiple academic disciplines that -- from different angles -- are trying to provide accurate evidence on this important and devastating phenomenon. Besides the indubitable and widely documented adverse impact of IPV on women’s physical and mental health, children exposed to IPV are also increasingly recognized as victims in their own right. The harm to children exposed to IPV may be both direct through the witnessing of abuse or indirect by affecting the mother-child interactions. Growing up in a family where the mother is abused by her partner might represent a grave shock for the child, potentially hindering the development of their human capital.

This project will provide evidence on the impact of children’s exposure to IPV on their cognitive and socio-emotional development between birth and age seven, and on the role of with mother’s responses to abuse. To this purpose, this project will implement and further develop a methodology recently introduced in economics to study the technology of human capital formation. The focus will be on the dynamics of the accumulation of skills, studying how skills co-evolve, and the role of mother-child interactions in this process. Most importantly, in relation to this highly successful recent literature, we will incorporate, for the first, time IPV as a negative input.

The strength of this method will be fully exploited by using an exceptionally rich source of data –internationally unique in containing all the necessary information for this analysis within a large representative population. The Avon Longitudinal Study of Parents and Children (ALSPAC) is a UK cohort study that includes (i) annual indicators of the incidence of IPV; (ii) high-frequency and reliable measures of children’s cognitive and socio-emotional skills; (iii) extremely detailed set of information on mother-child interactions as well as mother’s mental health.

Specifically, the project will address three research questions that will further the understanding of how children’s development is hampered by exposure to IPV. First, how large are the direct effects of children’s exposure to IPV on their development of cognitive and socio-emotional skills? This in effects casts exposure to IPV as a form of harmful maltreatment. Second, what are the indirect effects generated by change in mother-child interactions as a response to IPV? Such interactions can potentially amplify or compensate for the negative impact of IPV on children witnessing IPV. Third, what interactions between skills, and between skills and mother-child interactions, shape the dynamic effects of IPV on children’s development of socioemotional and cognitive skills over their early life years? Such interactions are crucial for suggesting the optimal nature and timing of policy interventions.
The current project will hence contribute to a highly influential and rapidly growing economic literature studying the importance of early childhood conditions for development and will allow new important insights to be gained by fully exploiting the richness of an existing unique data resource. In developing this analysis, our project will draw on, and contribute, to a research that spans multiple disciplines including sociology, psychology, pediatrics and criminology. The findings of this project respond to the need of thoroughly documenting and further studying the damaging effect of IPV within the family with the purpose of suggesting effective policy recommendations to alleviate its effect.

Emotion recognition is an important part of social interaction, and difficulties in recognising others’ emotions can have a negative impact on this. In addition, these difficulties may subsequently impact social function and mental health. It is also possible that difficulties in this area e.g., social anxiety, could disrupt school attendance in children. Previous studies which have examined these relationships tend to be small and cross-sectional. We propose using a large existing cohort with data at multiple timepoints to overcome these limitations and allow the direction of association to be examined as well. It is important to further understand these relationships particularly given that poorer emotion recognition is observed in autistic individuals, or those with more autistic traits, and therefore these relationships will be particularly relevant for autistic individuals with emotion recognition difficulties.

We will examine the bidirectional association between emotion recognition and outcomes related to social traits, wellbeing/mental health and school attendance. Data from the Avon Longitudinal Study of Parents and Children (ALSPAC) will be used for this. Data will be used from different time points to attempt to understand the direction of any associations found. This work would be useful in informing what downstream effects there may be with interventions targeting emotion recognition, for example, in autistic individuals.

The current project is a student project that is linked to the already approved project: B3840 Developmental pathways to mental health problems. All needed data are available through B3840.

Psychotic disorders are often severe and have high heritability. Despite a small proportion of the population being affected by psychotic disorders, they have the highest disability weight. Beside impairing health in their own, these disorders further increase risks for other health outcomes such as suicide. To understand the mechanistic pathways leading to development of psychotic disorders, it is important to study individuals with at risk, either individuals at clinical risk or individuals with genetic risk. Clinical risk refers to the presence of symptoms, but that the full diagnostic criteria are not met. Genetic risk is in an ALSPAC MRI substudy operazationalied as high polygenic risk for schizophrenia. Further, studying individuals at risk reduces confounding for medication or chronic illness to some extent.

Substantial efforts have been dedicated to identify neural factors associated with risk for psychotic disorders. Despite these efforts, the picture of how psychotic disorders develop is not clear and our knowledge about which factors contribute to this development is limited. There is thus a demand for further research to identify the brain structural and microstructural correlates associated with psychosis risk. Moreover, directly comparing individuals with clinical (symptom-based) risk for psychosis and individuals with genetic risk for psychosis can possibly reveal both shared and distinct neural mechanisms.

Hypertension is one of the strongest risk factors for cardiovascular disease, which is the leading cause of death worldwide (1). Early-life exposures have been associated with blood pressure and the development of hypertension (2), with differential DNA methylation suggested as a potential underlying mechanism (3). Two large epigenome-wide association studies (EWAS) on systolic and diastolic blood pressure in adults have identified associations with DNA methylation (DNAm) levels of multiple Cytosine-phosphate-Guanine (CpG) sites (4,5). In the CHARGE consortium, one large-scale multi-ethnic EWAS on blood pressure in n=9,828 adults identified 13 CpGs annotated to 8 genes that were associated with blood pressure (4). A DNAm risk score based on these CpGs explained 1.4% and 2.0% of the inter-individual variation in systolic and diastolic BP, respectively. Another, more recent, EWAS on 4,820 multi-ethnic adults (6), identified 33 CpGs that explained an additional 3.3% and 4.0% of the inter-individual variation in systolic and diastolic blood pressure, respectively, beyond the traditional blood pressure risk factors age, sex, and body mass index (BMI), with 3 CpGs overlapping with the CHARGE study. The majority of the discovered CpG sites have been linked with other metabolic phenotypes including obesity, lipids, CRP, insulin resistance, and type 2 diabetes mellitus by previous epigenome-wide association studies (6), indicating that DNAm may be one of the common factors related to the concurrence of multiple cardiometabolic abnormalities.

Much less is known about the associations between DNAm and blood pressure in children. It is also not known if blood pressure associations with DNAm found in adults are already apparent in early childhood, late childhood and adolescence. Therefore, in this project, we aim to test the ability of a methylation risk score, developed using CpGs previously identified to be associated with SBP and DBP in adult EWAS meta-analysis by Richard (4) and Huang (6), to predict blood pressure at multiple timepoints in childhood and adolescence, and its added value compared to a risk score constructed only from the basic covariates age, sex and BMI.
This weighted methylation risk score was developed using the CpGs from the adult studies that survived a penalized elastic net regression in the ALSPAC adult data.

1. Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, et al. A comparative risk assessmentof burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet (London, England).2012;380(9859):2224-60.
2. Lackland DT. Fetal and Early Life Determinants of Hypertension in Adults. Hypertension. 2004;44(6):811-2.
3. Wang X, Falkner B, Zhu H, Shi H, Su S, Xu X, Sharma AK, Dong Y, Treiber F, Gutin B, et al.. A genome-wide methylation study on essential hypertension in young African American males. 2013; 8:e53938.
4. Richard MA, Huan T, Ligthart S, Gondalia R, Jhun MA, Brody JA, Irvin MR, Marioni R, Shen J, Tsai PC,Montasser ME, Jia Y, Syme C, Salfati EL, Boerwinkle E, Guan W, Mosley TH Jr, Bressler J, Morrison AC,Liu C, Mendelson MM, Uitterlinden AG, van Meurs JB; BIOS Consortium, Franco OH, Zhang G, Li Y, Stew-art JD, Bis JC, Psaty BM, Chen YI, Kardia SLR, Zhao W, Turner ST, Absher D, Aslibekyan S, Starr JM,McRae AF, Hou L, Just AC, Schwartz JD, Vokonas PS, Menni C, Spector TD, Shuldiner A, Damcott CM,Rotter JI, Palmas W, Liu Y, Paus T, Horvath S, O'Connell JR, Guo X, Pausova Z, Assimes TL, SotoodehniaN, Smith JA, Arnett DK, Deary IJ, Baccarelli AA, Bell JT, Whitsel E, Dehghan A, Levy D, Fornage M. DNAMethylation Analysis Identifies Loci for Blood Pressure Regulation. Am J Hum Genet. 2017 Dec7;101(1):888-902.
5. Kazmi N, Elliott HR, Burrows K, Tillin T, Hughes AD, Chaturvedi N, et al. (2020) Associations between highblood pressure and DNA methylation. PLoS ONE 15(1): e0227728.
6. Huang Y, Ollikainen M, Muniandy M, Zhang T, Dongen Jv, Hao G, et al. Identification, Heritability, and Re-lation With Gene Expression of Novel DNA Methylation Loci for Blood Pressure. Hypertension.2020;76(1):195-205.
7. Gervin, K., Salas, L.A., Bakulski, K.M. et al. Systematic evaluation and validation of reference and library selection methods for deconvolution of cord blood DNA methylation data. Clin Epigenet 11, 125 (2019).