Social inequalities in health are a phenomenon affecting societies both in emerging economies and developed countries. Evidence for a social gradient in disease incidence has been firstly identified by Michael Marmot in a British cohort of civil servants (Marmot, 1984) suggesting the crucial role played by socioeconomic determinants, such as position in the social hierarchy and occupational status, in the uneven distribution of morbidity and mortality rates across the population. The relevance of this issue in terms of public health is dramatic, especially because it has been widely underestimated by epidemiologists and health authorities until 2000s. Therefore, the social determinants theory aims to provide a reliable guidance for policy making to reduce the gap in terms of life expectancy and disease incidence between higher and lower layers of society. This Thesis investigates the social determinant theory by testing the hypothesis according to which epigenetics, and in particular DNA methylation of pro-inflammatory genes, may act as mediator in the association of socioeconomic variables with chronic disease onset. Results, consistently with findings of previous studies (Stringhini, 2015), underline that social status is associated with dysregulated methylation patterns of genes involved in immune-system and inflammation related pathways, such as NFATC1 and CXCL2, which are in turn correlated with uneven incidence of chronic disease between lower and higher layers of society. Though this suggests the existence of a mediation effect of epigenetics, further research with a larger and purpose-build sample is required to confirm this hypothesis.
Determinanti sociali della salute: un' ipotesi epigenetica per l'impatto di status socio-economico sulle condizioni di di salute
RAVIOLA, PIETRO
2015/2016
Abstract
Social inequalities in health are a phenomenon affecting societies both in emerging economies and developed countries. Evidence for a social gradient in disease incidence has been firstly identified by Michael Marmot in a British cohort of civil servants (Marmot, 1984) suggesting the crucial role played by socioeconomic determinants, such as position in the social hierarchy and occupational status, in the uneven distribution of morbidity and mortality rates across the population. The relevance of this issue in terms of public health is dramatic, especially because it has been widely underestimated by epidemiologists and health authorities until 2000s. Therefore, the social determinants theory aims to provide a reliable guidance for policy making to reduce the gap in terms of life expectancy and disease incidence between higher and lower layers of society. This Thesis investigates the social determinant theory by testing the hypothesis according to which epigenetics, and in particular DNA methylation of pro-inflammatory genes, may act as mediator in the association of socioeconomic variables with chronic disease onset. Results, consistently with findings of previous studies (Stringhini, 2015), underline that social status is associated with dysregulated methylation patterns of genes involved in immune-system and inflammation related pathways, such as NFATC1 and CXCL2, which are in turn correlated with uneven incidence of chronic disease between lower and higher layers of society. Though this suggests the existence of a mediation effect of epigenetics, further research with a larger and purpose-build sample is required to confirm this hypothesis.File | Dimensione | Formato | |
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https://hdl.handle.net/20.500.14240/115535