Early life predictors of child growth trajectories and early adolescent cardiovascular health
- Autores: Parisa Montazeri
- Directores de la Tesis: Martine Vrijheid (dir. tes.)
- Lectura: En la Universitat Pompeu Fabra ( España ) en 2021
- Idioma: español
- Tribunal Calificador de la Tesis: Susana Moreira da Silva Santos (presid.), Xavier Basagaña (secret.), María José López Espinosa (voc.)
- Programa de doctorado: Programa de Doctorado en Biomedicina por la Universidad Pompeu Fabra
- Materias:
- Enlaces
- Tesis en acceso abierto en: TDX
- Resumen
Research over the previous decades has shown us that early life influences have long-term effects on health and disease. Under the Developmental Origins of Health and Disease (DOHaD) hypothesis several factors have been shown to increase risk for chronic diseases in later life. Rates of obesity and cardiovascular diseases (CVD) have increased at an astounding rate over recent decades. Lifestyle factors alone fail to fully account for the magnitude of this epidemic. Emerging science supports a role in the pathogenesis of obesity and CVD for novel risk factors like maternal metabolic health, socioeconomic position (SEP), and endocrine disrupting chemicals (EDCs). The main aim of this thesis was to examine the role of early life predictors, focusing on maternal, chemical and social factors, on child growth and early adolescent cardiovascular health using traditional and novel measures of preclinical phenotypes.
We used data from two longitudinal birth cohort studies. A variety of non-persistent and persistent EDCs were included to characterize chemical exposure. SEP was included as maternal education and employment status, family affluence score, and social class. Child growth was analyzed using child body mass index (BMI) growth trajectories from birth to 4 or 9 years, and cardiovascular health was measured at 11 years old using traditional and novel measures of macro- and microvascular health.
We found that maternal prepregnancy BMI and gestational weight gain were associated with offspring’s BMI trajectories characterized by accelerated growth during early childhood, and these same trajectories were related to macrovascular health function during early adolescence. Regarding EDCs, we found that chemical exposure differs by SEP, and those of higher SEP are potentially at greater risk of exposure. Further, we found that prenatal exposure to EDCs, particularly organochlorine compounds (DDE, HCB, PCBs) are related to BMI trajectories characterized by accelerated growth in childhood. However, prenatal exposure to non-persistent EDCs (phthalates, phenols) does not appear to be associated with early adolescent cardiovascular health.
In conclusion, the findings of this thesis suggest that early life exposure to maternal metabolic parameters and EDCs appear to have a potentially adverse effect on child growth and early adolescent cardiovascular health, which may be modified by SEP. Given how widespread exposure to EDCs is, the importance of maternal health status prior to pregnancy, and the increasing rates of obesity and CVD, these findings are of critical importance.
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