Early-life psychosocial adversity, HPA-axis function, and stress-related mental disorders: Exploring the interplay between environmental and genetic
Lead Research Organisation:
UNIVERSITY COLLEGE LONDON
Department Name: Epidemiology and Public Health
Abstract
Full project title: Early-life psychosocial adversity, HPA-axis function, and stress-related mental disorders: Exploring the interplay between environmental and genetic influences across the life course.
Summary: The aim of the PhD project is to provide a comprehensive examination of the biopsychosocial pathways through which exposure to early-life adversity may affect the development of the stress response system (i.e., HPA-axis) and vulnerability to stress-related psychopathology such as depression and anxiety disorders. Furthermore, it will consider the complex interplay between genetic and environmental influences on HPA-axis and mental health function across the life course. To this end, my project will integrate environmental, biological, and genetic data from a cohort of young adults (i.e., Avon Longitudinal Study of Parents and Children) and a cohort of older people (i.e., English Longitudinal Study of Ageing) focusing on four main objectives:
1) To examine the longitudinal associations between early-life adversity (i.e., cumulative risk, dimensions, timing), HPA-axis activity, and depression and anxiety.
2) To investigate the possible mediational role of HPA-axis function in the pathways linking early-life adversity with depression and anxiety.
3) To explore the genetic aetiology of cortisol, depression, and anxiety disorders using polygenic approaches.
4) To test the role of the aforementioned genetic liabilities in the associations between early-life adversity, cortisol, and stress-related psychopathology, examining both their main effects and potential polygenic gene-environment interactions.
Summary: The aim of the PhD project is to provide a comprehensive examination of the biopsychosocial pathways through which exposure to early-life adversity may affect the development of the stress response system (i.e., HPA-axis) and vulnerability to stress-related psychopathology such as depression and anxiety disorders. Furthermore, it will consider the complex interplay between genetic and environmental influences on HPA-axis and mental health function across the life course. To this end, my project will integrate environmental, biological, and genetic data from a cohort of young adults (i.e., Avon Longitudinal Study of Parents and Children) and a cohort of older people (i.e., English Longitudinal Study of Ageing) focusing on four main objectives:
1) To examine the longitudinal associations between early-life adversity (i.e., cumulative risk, dimensions, timing), HPA-axis activity, and depression and anxiety.
2) To investigate the possible mediational role of HPA-axis function in the pathways linking early-life adversity with depression and anxiety.
3) To explore the genetic aetiology of cortisol, depression, and anxiety disorders using polygenic approaches.
4) To test the role of the aforementioned genetic liabilities in the associations between early-life adversity, cortisol, and stress-related psychopathology, examining both their main effects and potential polygenic gene-environment interactions.
Organisations
People |
ORCID iD |
| Andrew Steptoe (Primary Supervisor) | |
| Eleonora Iob (Student) |
Publications
Iob E
(2020)
Adverse childhood experiences and depressive symptoms in later life: Longitudinal mediation effects of inflammation.
in Brain, behavior, and immunity
Iob E
(2020)
Levels of Severity of Depressive Symptoms Among At-Risk Groups in the UK During the COVID-19 Pandemic.
in JAMA network open
Iob E
(2020)
Abuse, self-harm and suicidal ideation in the UK during the COVID-19 pandemic.
in The British journal of psychiatry : the journal of mental science
Iob E
(2020)
Persistent depressive symptoms, HPA-axis hyperactivity, and inflammation: the role of cognitive-affective and somatic symptoms.
in Molecular psychiatry
Iob E
(2020)
The long-term association of adverse childhood experiences with C-reactive protein and hair cortisol: Cumulative risk versus dimensions of adversity.
in Brain, behavior, and immunity
Iob E
(2020)
Identifying risk factors involved in the common versus specific liabilities to substance use: A genetically informed approach
in Addiction Biology
Iob E
(2018)
Positive and negative social support and HPA-axis hyperactivity: Evidence from glucocorticoids in human hair.
in Psychoneuroendocrinology
Iob E
(2019)
Cardiovascular Disease and Hair Cortisol: a Novel Biomarker of Chronic Stress.
in Current cardiology reports
Studentship Projects
| Project Reference | Relationship | Related To | Start | End | Student Name |
|---|---|---|---|---|---|
| ES/R501050/1 | 30/09/2017 | 29/09/2021 | |||
| 1907703 | Studentship | ES/R501050/1 | 30/09/2017 | 07/07/2021 | Eleonora Iob |
| Description | - Older adults who experienced adverse childhood experiences (e.g. abuse, neglect, parental separation) have increased levels of plasma inflammatory markers and depressive symptoms. - Elevated levels of inflammatory markers in later life are associated with higher depressive symptoms. - Inflammation is one of the biological mechanisms through which exposure to adverse childhood experiences might influence the development of depression in adulthood. - The negative impact of adverse childhood experiences on the risk of high inflammation and depression is greater amongst individuals at high genetic risk for these disorders. - Young people reporting adverse childhood experiences are at increased risk of elevated cortisol levels and depression in young adulthood, independently of genetic confounding. - Elevated levels of cortisol might partly explain the association between adverse childhood experiences and depression in young adulthood. |
| Exploitation Route | This PhD project will benefit a wide range of stakeholders including researchers, clinicians, policy makers, the charitable sector, and the general public. In particular, it will provide a more comprehensive understanding of the mechanisms through which early life experiences may affect the risk of depression. Such understanding of the life course pathways linking early-life stress with mental health will have the potential to inform interventions for the prevention, detection, and treatment of ACEs and depression. These may include, for instance, psychosocial interventions to manage the negative effects of childhood adversity and reduce stress levels amongst children and their families; pharmacological therapies to ameliorate depressive symptoms; and genetic testing to identify individuals at higher risk early in development and tailor treatment plans. The research findings will also provide policymakers with reliable and extensive data with which a more streamlined process of policy development might be better manoeuvred. |
| Sectors | Communities and Social Services/Policy Healthcare |
| URL | https://scholar.google.com/citations?user=UKneVekAAAAJ&hl=en |
| Description | I am establishing new collaborations with mental health charities (e.g. MQ mental health) to share the findings of my latest studies through their online platforms. |
| First Year Of Impact | 2021 |
| Sector | Communities and Social Services/Policy |
| Impact Types | Societal Policy & public services |