![Sample our Behavioral Sciences journals, sign in here to start your access, latest two full volumes FREE to you for 14 days]({"type":"image" , "src" : "/sda/110801/TOC-Subject-Sample-2021-Behavioral-Sciences.jpg"})
Abstract
The developmental origins of disease or fetal programming model predicts that early exposures to threat or adverse conditions have lifelong consequences that result in harmful outcomes for health. The vast majority of the studies in support of the programming model in human beings are retrospective and most rely on surrogate measures of early experience such as birth weight or preterm birth. Recently, a small number of prospective studies have been reported that have documented the developmental consequences of exposures to stressful intrauterine conditions. These studies of gestational stress have clearly shown that fetal exposures to psychosocial and/or biological markers of adversity have significant and largely negative consequences for fetal, infant and child neurological development. Fetal exposure to stress, especially early in gestation, results in delayed fetal maturation and impaired cognitive performance during infancy and results in decreased brain volume in areas associated with learning and memory in children. The accumulating evidence supports the conclusion that fetal exposure to stress profoundly influences the nervous system, with consequences that persist into childhood and perhaps beyond.
Financial & competing interests disclosure
Curt A Sandman is supported by the NIH grants NS-41298, HD-51852 and HD-28413 and Elysia P Davis is supported by the NIH grant HD-50662. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Acknowledgements
Cheryl Crippen is gratefully acknowledged for her assistance.