We want to study how a baby’s first months of life, including factors like their birth, family and living conditions might affect how they cope with common illnesses like coughs, colds and stomach bugs, or more serious infections.

This study will look back at the lives of a group of babies to understand how their early experiences might affect how their immune system develops and their ability to handle infections as children. We will analyse information collected about these babies, including details about the pregnancy and birth, their family lifestyle and living conditions as well as how often and what kind of illnesses they have during childhood.

The study aims to find out if any of these early factors influence how well children cope with infections. For example, the study might find that that certain living conditions, like their housing, spending time outdoors or having siblings or pets can make children more or less likely to get sick.

The goal is to identify patterns and factors that could help improve health outcomes for children by understanding what makes some babies more resilient to infections. This information could be used to guide parents and healthcare providers in making decisions that support better health during a child's early years.

The aim of this project is to explore if having Autism Spectrum Disorder (ASD) increases the risk of Post-Partum Depression (PPD). PPD is the most common mental disorder experienced by women after pregnancy, affecting 10% to 20% of new mothers. Research suggests that individuals with ASD may face a higher risk of PPD due to challenges specific to autism, such as difficulties adjusting to change, lower self-esteem, and social stigma.

Also, there is evidence that mental health outcomes differ based on when individuals with ASD are diagnosed. Those diagnosed later in life often experience more loneliness, lower self-esteem, and use less effective coping strategies, which are known risk factors for PPD. This project will investigate whether the risk of PPD is amplified in late-diagnosed autistic individuals, who may face added emotional challenges during the postpartum period. To date, no existing longitudinal studies have explored these potential mechanisms.

Currently, significant gaps remain in understanding how autism impacts the transition to motherhood, as research in this area often reflects a neurotypical perspective. This study seeks to address this gap by examining the long-term outcomes for individuals with ASD as they become mothers, using a longitudinal approach to provide new insights into the link between ASD and PPD.

Around two thirds of adults do not respond to the first trial of antidepressants meaning depression often goes untreated leading to severe complications. This may be due to antidepressants targeting the wrong mechanisms underlying depression, meaning alternative anti-depressive pathways must be targeted. Alternative routes include inflammatory pathways which have been associated with the development and pathogenesis of depression, demonstrated in a prospective study linking cytokine Interleukin 6 (IL-6) in childhood to depression later in life. The ways in which IL-6 contribute to depression remain unclear, and this study aims to investigate this relationship.
This study will investigate the role of cognitive biases, specifically negative biases, in the association between inflammation and depression. Cognitive biases are systematic deviations from normality when processing information; negativity bias refers to a negative shift in emotional processing. The neurocognitive model of depression suggests that negative biases have an important role in the development and maintenance of depressed mood. While there is a significant amount of research mapping neurotransmitter pathways of these cognitive mechanisms, the role of inflammatory pathways is largely unknown. This study aims to bridge this knowledge gap investigating the causal relationship between IL-6 serum levels with emotional processing, specifically negativity bias. This may highlight a new neurocognitive pathway between inflammation and depression, suggesting that IL-6 levels may cause changes in emotional processing subsequently maintaining depressed mood.
There is a small amount of research already suggesting an association, however there are significant experimental issues meaning a causal relationship cannot be drawn. Most research uses small samples of specific populations e.g. breast cancer patients in cross sectional designs. The extant research is at risk of inflated effect sizes due to moderation of chronic inflammatory disease, meaning the relationship between inflammation and negativity bias may be larger than in healthy populations. Additionally, there is a risk of depression mediating this relationship. Current research lacks a large sample prospective study, adjusted for moderation of chronic inflammatory illness, mediating effect of depression and several confounding variables.
This study will use ALSPAC data to investigate the relationship between IL-6 serum levels in childhood through to early adulthood and negativity bias in early adulthood. Using a large longitudinal data set allows for a temporal, directional relationship to be determined. Adjusting for confounders, testing for moderation of disease and mediation of depression means a valid, causal association can be investigated between IL-6 and negativity bias.

Cardiovascular diseases (CVDs) and depression are globally prevalent health concerns with substantial impacts. CVDs, including ischemic heart disease and stroke, rank among the leading global health burdens (WTO, 2023). Research indicates a high rate of comorbidity between CVD and depression (Karami et al., 2023; Rafiei et al., 2023), with the onset of CVD significantly increasing the risk of depression (Whooley & Wong, 2013). Conversely, depression elevates CVD risk by 1.5 times and doubles to triples the incidence of cardiac events in individuals with coronary artery disease (Frasure-Smith & Lesperance, 2009; Goldston & Baillie, 2008; Rudisch & Nemeroff, 2003; Van der Kooy et al., 2007). However, it remains unclear how adolescent depression contributes to heightened cardiovascular risk in adulthood, as defined by indicators such as BMI, HDL (high-density lipoprotein cholesterol), total cholesterol and systolic blood pressure (SBP).
Emerging evidence suggests that inflammation may be a common biological mechanism underlying the comorbidity of depression and CVD (Chen et al., 2018; Shao et al., 2020). Recent research has identified 185 genes significantly associated with both depression and coronary artery disease (CAD), many of which are linked to inflammatory and cardiomyopathic phenotypes (Singh et al., 2024). Our current research (in progress, 2024) has identified several inflammatory biomarkers—such as CRP/hs-CRP, IL-6, and TNF-α—that are shared between depression and CVD.
This study aims to (1) test the hypothesis that adolescent depression predicts an elevated cardiovascular risk in adulthood, (2) map the trajectory of cardiovascular risk factors from adolescence to adulthood, and (3) investigate how changes in inflammation, as indicated by inflammatory biomarkers and DNA methylation, influence the progression of cardiovascular risk factors in both depressed and non-depressed groups.

Cleft palate is a congenital condition that occurs when the tissues of the roof of the mouth do not join together properly during foetal development. Although the exact cause is unknown, it's believed to result from a combination of genetic and environmental factors. Cleft palate repair involves a complex surgical procedure aimed at reconstructing the palate to improve speech, feeding, and overall quality of life. The healing process following cleft palate surgery is crucial and can be influenced by several factors, including those derived from the surgical process itself but also from the individual healing process (genetics, excessive tissue tension, infection, inflammation, etc).
Multiple genetic studies in individuals affected by cleft palate have identified several susceptibility genes, including IRF6, MSX1, SATB2, TBX22, COL2A1, FBN1, PCGF2, KMT2D, MYC, PTCH1, VAX1, SPRY2, NOG, MAFB and TAF1B, among others.
To facilitate the understanding of the genetic architecture and gain a better understanding of the genetic basis underlying cleft palate, we will look into the DNA of ALSPAC participants that codes the proteins, to identify variants in genes associated with cleft palate disorders. Then we will investigate if those variants have an impact on the manifestation of traits related with wound healing, such as levels of markers involved in the immune system and inflammatory processes.

This project is based on our earlier research theory, which integrates psychometric, cognitive, and developmental models of the human mind. The theory postulates that the profile of cognitive abilities changes with development, according to the processes that need to be mastered at successive age periods. Control of episodic interactions with persons and objects, control of representation-based executive processes, inferential control, and truth and cognitive cohesion control dominate in infancy, early childhood, middle and late childhood, and adolescence, respectively. So far, the theory is based on many cross-sectional studies and some longitudinal studies conducted in our laboratory. The main aim of this project is to test theory on an independent sample that has been longitudinally examined, to test if the patterns obtained so far replicate here.

Not having enough money to buy food—known as food insecurity—is a serious issue, affecting over one in ten households in the UK during 2022/23. This struggle impacts both physical and mental health. New findings suggest that food insecurity is also linked to eating disorders. Adults who experience food insecurity are more likely to show symptoms of disordered eating, including behaviors like binge eating, restrictive eating, and compensatory behaviours (e.g., meal skipin, dieting). These patterns have been observed across various groups, including adults, teenagers, students, and people in treatment for eating disorders. This evidence highlights the need to consider food insecurity as a critical risk and/or maintenance factor for eating disorders. Yet, most research has focused on the USA despite the similar prevalence of food insecurity households in the UK. However, findings from the USA may not directly translate to the UK due to cultural and welfare differences (e.g., the US offers monthly food benefits, while UK food bank access varies regionally and by policy). Our study will use data from the UK to explore how food insecurity and eating disorders are associated among adults in the general population.

Increasing evidence suggests that social processes including weight-related stigma are key to explaining many consequences of overweight and obesity. For instance, people carrying genetic variants linked to obesity are at higher risk of depression, even where those variants have no known metabolic consequences. This strongly implicates social, not just biological, processes by which body weight affects mental health. Among the different facets of stigma is internalized weight stigma (self-attribution of negative obesity-related stereotypes) which may have especially negative consequences.
Despite strong theoretical work in this area, our empirical understanding of weight stigma’s causes and consequences is limited. This includes how social, psychological, and familial factors across the lifecourse influence weight stigma internalization, and the consequences for mental health and social functioning. This is because research has been almost entirely based on small, non-representative samples. This PhD project will use the data on internalized weight stigma at age 31, completed by ALSPAC participants of all weight statuses, to investigate causes and consequences of weight stigma internalization in a large sample of young people.

We have found that rare changes in DNA are associated with a diagnosis of heart failure in a large study called UK biobank. In general, these mutations are exceptionally rare in UK Biobank, but we know that the design of UK Biobank can lead to inadvertent exclusion of groups of people which can lead to inaccurate estimates of how common mutations in some genes are. This study, ALSPAC, included the majority of people born during a certain time period in the Avon region. As such, it is less susceptible to some of these problems. As such, we want to use it to refine our estimates of how common these mutations are.