The Epigenetics of Stress Reactivity Related to the Risk for Cardiovascular Disease: The Impact of Maternal Stress Levels on Offspring
Open Access
Author:
Smith, Hannah
Area of Honors:
Biology (Altoona)
Degree:
Bachelor of Science
Document Type:
Thesis
Thesis Supervisors:
Esther Siegfried, Thesis Supervisor Laura Rotunno, Thesis Honors Advisor Mary K Kananen, Faculty Reader
Keywords:
epigenetics cortisol fetal programming HPA axis stress reactivity cardiovascular diseases metabolic syndrome fetal development embryonic development glucocorticoids
Abstract:
Intrauterine development establishes the systemic foundations that dispose the offspring to certain functional uniquities or health outcomes. During embryonic/fetal maturation, adverse conditions during critical periods vulnerable to structural/functional defects can spur disease processes in later life, such as cardiovascular diseases or metabolic syndromes. Aside from established teratogens and toxins, budding research is revealing that sustained maternal levels of excessive prenatal cortisol catalyzes an epigenetic cascade in the offspring that ultimately increases stress reactivity and risk for cardiovascular diseases/metabolic syndromes. This paper reviews literature discussing the epigenetic repercussions of excessive prenatal maternal cortisol levels on offspring and how these may influence outcomes. The literature identifies a correlational trend, but causal identification is limited by a discrepancy and laxity in methods. Conclusively, more longitudinal research with uniform methodology is necessary to strengthen the relationship between maternal prenatal stress and fetal outcomes.
