Ignite Creation Date:
2024-05-05 @ 4:34 PM
Last Modification Date:
2024-10-26 @ 9:21 AM
Study NCT ID:
NCT00269256
Status:
COMPLETED
Last Update Posted:
2016-02-03
First Post:
2005-12-21
Brief Title:
Stress Environment and Genetics in Urban Children With Asthma
Sponsor:
Brigham and Womens Hospital
Organization:
Brigham and Womens Hospital
Study Overview
Official Title:
Stress Environment and Genetics in Urban Asthma
Status:
COMPLETED
Status Verified Date:
2016-02
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The purpose of this study is to evaluate the multiple mechanisms through which stress physical environment and genetic predisposition contribute to asthma in urban children
Detailed Description:
BACKGROUND
The study design builds on the ACCESS Study a prospective pregnancy cohort study begun in 2003 of a cohort from birth to age four The present study includes two new aims regarding the interaction of stress and genetic or environmental variables reflecting a more comprehensive conceptualization of the multiple mechanisms by which stress can contribute to asthma In addition the current study proposes to follow the cohort until the age of three
DESIGN NARRATIVE
The study examines the role of psychosocial stressors in a systems biology framework considering multiple biologic pathways by which stress can contribute to asthma The investigators will not only study the independent effect of stress on asthmawheeze phenotypes in early childhood but also will consider stress as a modifier of physical environmental factors allergens cigarette smoking and diesel-related air pollutants and genetic predisposition on asthma risk They will determine the independent effect of maternal stress both prenatal and postnatal on early childhood asthma phenotypes They further hypothesize that multi-life stressors prevalent in disadvantaged populations can cumulatively influence immune system development and airway inflammation in early life thus making the populations more susceptible to other environmental factors and genetic risk factors explaining in part observed asthma disparities associated with SES and raceethnicity They will take a multi-level approach measuring both individual-level stress negative life events perceived stress pregnancy anxiety and community-level stress neighborhood disadvantage eg percent of subjects living in poverty percent unemployed diminished social capital and high crimeviolence rates They will also assess the influence of stress on the infant hormonal stress response and on T-helper cell differentiation as reflected in cytokine profiles and IgE expression a topic or pro inflammatory phenotype Additional physical environmental indoor allergens diesel-related air pollutants tobacco smoke and genetic factors will be assessed given their influence on the immune response and expression of early childhood asthmawheeze This interdisciplinary approach is unique because researchers are considering the context in which physical exposures and host susceptibility occur analyzing their multiplicative joint effects and considering multiple biologic pathways as such it is consistent with the NIH roadmap objectives
The study design builds on the ACCESS Study a prospective pregnancy cohort study begun in 2003 of a cohort from birth to age four The present study includes two new aims regarding the interaction of stress and genetic or environmental variables reflecting a more comprehensive conceptualization of the multiple mechanisms by which stress can contribute to asthma In addition the current study proposes to follow the cohort until the age of three
DESIGN NARRATIVE
The study examines the role of psychosocial stressors in a systems biology framework considering multiple biologic pathways by which stress can contribute to asthma The investigators will not only study the independent effect of stress on asthmawheeze phenotypes in early childhood but also will consider stress as a modifier of physical environmental factors allergens cigarette smoking and diesel-related air pollutants and genetic predisposition on asthma risk They will determine the independent effect of maternal stress both prenatal and postnatal on early childhood asthma phenotypes They further hypothesize that multi-life stressors prevalent in disadvantaged populations can cumulatively influence immune system development and airway inflammation in early life thus making the populations more susceptible to other environmental factors and genetic risk factors explaining in part observed asthma disparities associated with SES and raceethnicity They will take a multi-level approach measuring both individual-level stress negative life events perceived stress pregnancy anxiety and community-level stress neighborhood disadvantage eg percent of subjects living in poverty percent unemployed diminished social capital and high crimeviolence rates They will also assess the influence of stress on the infant hormonal stress response and on T-helper cell differentiation as reflected in cytokine profiles and IgE expression a topic or pro inflammatory phenotype Additional physical environmental indoor allergens diesel-related air pollutants tobacco smoke and genetic factors will be assessed given their influence on the immune response and expression of early childhood asthmawheeze This interdisciplinary approach is unique because researchers are considering the context in which physical exposures and host susceptibility occur analyzing their multiplicative joint effects and considering multiple biologic pathways as such it is consistent with the NIH roadmap objectives
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL080674 | NIH | None | httpsreporternihgovquickSearchR01HL080674 |