Fetal ultrasound: Shedding light or casting shadows on the fetal origins of airway disease

Stephen W. Turner*, Graham Devereux

*Corresponding author for this work

Research output: Contribution to journalEditorial

3 Citations (Scopus)

Abstract

The fetal origins of chronic disease hypothesis proposes thatfetal undernutrition in middle to late gestation leads to dispro-portionate fetal growth and induces permanent changes in bodystructure, physiology, and metabolism that program the later de-velopment of coronary heart disease and related diseases (1).Although the fetal origins hypothesis did not encompass respi-ratory outcomes, there is evidence to support the principle of fetalorigins of obstructive airway disease. First, reduced birth weight hasbeen linked to reduced FEV1and increased asthma in children andadults (2). Second, accelerated postnatal growth is associated withincreased asthma, wheeze and reduced FEV1in children (3, 4).Third, the prevalence of obstructive airway disease was increasedin adults exposed to the Dutch famine midgestation, although suchovert maternal/fetal malnutrition is now rarely observed in affluentcountries (5). From these observations, it might be inferred that forwhatever reason, attenuation of fetal somatic and respiratorygrowth midgestation resulting in reduced birth weight and acceler-ated postnatal “catch-up” growth is associated with an increasedlikelihood of asthma and reduced ventilatory function
Original languageEnglish
Pages (from-to)694-695
Number of pages2
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume185
Issue number7
DOIs
Publication statusPublished - 1 Apr 2012

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