Prenatal Stress, Telomere Biology, and Fetal Programming of Health and Disease Risk

Sci. Signal.  23 Oct 2012:

DOI: 10.1126/scisignal.2003580
A Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.


A substantial body of epidemiological, clinical, cellular, and molecular evidence converges to suggest that conditions during the intrauterine period of life play a critical role in developmental programming to influence subsequent health and susceptibility for common, complex disorders. Elucidation of the biological mechanisms underlying these effects is an area of considerable interest and investigation, and it is important to determine whether these mechanisms are distinct for different health outcomes or whether there are some common underlying pathways that may account for the effects of disparate prenatal and early postnatal conditions on various health and disease risk phenotypes. We propose that telomere biology may represent a common underlying mechanism connecting fetal programming and subsequent health outcomes. It appears that the initial establishment of telomere length and regulation of telomere homeostasis may be plastic and receptive to the influence of intrauterine and other early life conditions. Moreover, telomere homeostasis in various cell types may serve as a fundamental integrator and regulator of processes underlying cell genomic integrity and function, aging, and senescence over the life span. We advance the hypothesis that context- and time-inappropriate exposures to various forms of physiological stress (maternal-placental-fetal endocrine aberrations and immune, inflammatory, and oxidative stresses) during the intrauterine period of development may alter or program the telomere biology system in a manner that accelerates cellular dysfunction, aging, and disease susceptibility over the life span.

Full article available 30 October 2012, Vol. 5, Issue 248, pt12

Related Content