Biological and pathological mechanisms leading to the birth of a small vulnerable newborn
- PMID: 37167990
- DOI: 10.1016/S0140-6736(23)00573-1
Biological and pathological mechanisms leading to the birth of a small vulnerable newborn
Abstract
The pathway to a thriving newborn begins before conception and continues in utero with a healthy placenta and the right balance of nutrients and growth factors that are timed and sequenced alongside hormonal suppression of labour until a mature infant is ready for birth. Optimal nutrition that includes adequate quantities of quality protein, energy, essential fats, and an extensive range of vitamins and minerals not only supports fetal growth but could also prevent preterm birth by supporting the immune system and alleviating oxidative stress. Infection, illness, undernourishment, and harmful environmental exposures can alter this trajectory leading to an infant who is too small due to either poor growth during pregnancy or preterm birth. Systemic inflammation suppresses fetal growth by interfering with growth hormone and its regulation of insulin-like growth factors. Evidence supports the prevention and treatment of several maternal infections during pregnancy to improve newborn health. However, microbes, such as Ureaplasma species, which are able to ascend the cervix and cause membrane rupture and chorioamnionitis, require new strategies for detection and treatment. The surge in fetal cortisol late in pregnancy is essential to parturition at the right time, but acute or chronically high maternal cortisol levels caused by psychological or physical stress could also trigger labour onset prematurely. In every pathway to the small vulnerable newborn, there is a possibility to modify the course of pregnancy by supporting improved nutrition, protection against infection, holistic maternal wellness, and healthy environments.
Copyright © 2023 Elsevier Ltd. All rights reserved.
Conflict of interest statement
Declaration of interests PA reports a grant from the Children's Investment Fund Foundation in support of the preparation of this manuscript (grant number 2004-04635). ALD is an unpaid Scientific Trustee of Tommy's Charity. CPD reports grant support from WHO, the US Agency for International Development, and National Institutes of Health (NIH; P30 DK040561); royalties from UpToDate; and grant support on behalf of his institution from Takeda and the American Society for Nutrition in work unrelated to this paper. UR receives honoraria from NIH for educational activities and her institution receives funding from NIH. All other authors declare no competing interests.
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