Summary
LIVER-X addresses an important question: how does the environment impact the developmental origins of liver health and disease?
Poor liver health in childhood represents a major public health problem with long-term consequences. Elevated alanine aminotransferase, a marker of liver injury and screening tool for pediatric non-alcoholic fatty liver disease (NAFLD) risk, is increasingly reported at young ages, currently being detected in almost one out of ten children living in Europe and the western world. Although it is well known that an obesogenic diet and genetic predisposition play a role in the development of liver injury and disease, the contribution of the complex environment in which we grow up and live remains unclear. LIVER-X addresses this knowledge gap. The project will leverage the resources of the population-based HELIX and Generation R cohorts and follow an exposome-wide approach to the study of environmental impact by using rich biomonitoring and geospatial exposure data collected at the vulnerable early stages of the lifecourse (pregnancy and childhood). Advanced analysis techniques will be used to provide novel evidence on the individual and combined effects of a wide array of early-life ubiquitous environmental factors, including industrial chemical pollutants, toxic metals, air pollution, and characteristics of the urban natural and built environment, on liver injury markers in childhood and adolescence. The project will also assess whether children’s diet quality and polygenic risk for NAFLD modify vulnerability to environmental impact, and thus aid in identifying susceptible subpopulations and environmental priorities.
LIVER-X fosters research cooperation across disciplines and knowledge transfer. The project aligns with urgent challenges related to environmental pollution, the urban environment and the health of future generations, and thus its results are expected to be of high relevance for researchers, policy makers, and European citizens.
Poor liver health in childhood represents a major public health problem with long-term consequences. Elevated alanine aminotransferase, a marker of liver injury and screening tool for pediatric non-alcoholic fatty liver disease (NAFLD) risk, is increasingly reported at young ages, currently being detected in almost one out of ten children living in Europe and the western world. Although it is well known that an obesogenic diet and genetic predisposition play a role in the development of liver injury and disease, the contribution of the complex environment in which we grow up and live remains unclear. LIVER-X addresses this knowledge gap. The project will leverage the resources of the population-based HELIX and Generation R cohorts and follow an exposome-wide approach to the study of environmental impact by using rich biomonitoring and geospatial exposure data collected at the vulnerable early stages of the lifecourse (pregnancy and childhood). Advanced analysis techniques will be used to provide novel evidence on the individual and combined effects of a wide array of early-life ubiquitous environmental factors, including industrial chemical pollutants, toxic metals, air pollution, and characteristics of the urban natural and built environment, on liver injury markers in childhood and adolescence. The project will also assess whether children’s diet quality and polygenic risk for NAFLD modify vulnerability to environmental impact, and thus aid in identifying susceptible subpopulations and environmental priorities.
LIVER-X fosters research cooperation across disciplines and knowledge transfer. The project aligns with urgent challenges related to environmental pollution, the urban environment and the health of future generations, and thus its results are expected to be of high relevance for researchers, policy makers, and European citizens.
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More information & hyperlinks
Web resources: | https://cordis.europa.eu/project/id/101059245 |
Start date: | 01-09-2023 |
End date: | 31-08-2025 |
Total budget - Public funding: | - 181 152,00 Euro |
Cordis data
Original description
LIVER-X addresses an important question: how does the environment impact the developmental origins of liver health and disease?Poor liver health in childhood represents a major public health problem with long-term consequences. Elevated alanine aminotransferase, a marker of liver injury and screening tool for pediatric non-alcoholic fatty liver disease (NAFLD) risk, is increasingly reported at young ages, currently being detected in almost one out of ten children living in Europe and the western world. Although it is well known that an obesogenic diet and genetic predisposition play a role in the development of liver injury and disease, the contribution of the complex environment in which we grow up and live remains unclear. LIVER-X addresses this knowledge gap. The project will leverage the resources of the population-based HELIX and Generation R cohorts and follow an exposome-wide approach to the study of environmental impact by using rich biomonitoring and geospatial exposure data collected at the vulnerable early stages of the lifecourse (pregnancy and childhood). Advanced analysis techniques will be used to provide novel evidence on the individual and combined effects of a wide array of early-life ubiquitous environmental factors, including industrial chemical pollutants, toxic metals, air pollution, and characteristics of the urban natural and built environment, on liver injury markers in childhood and adolescence. The project will also assess whether children’s diet quality and polygenic risk for NAFLD modify vulnerability to environmental impact, and thus aid in identifying susceptible subpopulations and environmental priorities.
LIVER-X fosters research cooperation across disciplines and knowledge transfer. The project aligns with urgent challenges related to environmental pollution, the urban environment and the health of future generations, and thus its results are expected to be of high relevance for researchers, policy makers, and European citizens.
Status
SIGNEDCall topic
HORIZON-MSCA-2021-PF-01-01Update Date
09-02-2023
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