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

Fingerprint

Asthma
Birth Weight
Fetal Nutrition Disorders
Birth Order
Growth
Fetal Development
Starvation
Malnutrition
Coronary Disease
Chronic Disease
Mothers
Pregnancy

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Cite this

@article{8ec0af91be8b4ef79fa8b283c234f874,
title = "Fetal ultrasound: Shedding light or casting shadows on the fetal origins of airway disease",
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",
author = "Turner, {Stephen W.} and Graham Devereux",
year = "2012",
month = "4",
day = "1",
doi = "10.1164/rccm.201202-0180ED",
language = "English",
volume = "185",
pages = "694--695",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society - AJRCCM",
number = "7",

}

TY - JOUR

T1 - Fetal ultrasound

T2 - Shedding light or casting shadows on the fetal origins of airway disease

AU - Turner, Stephen W.

AU - Devereux, Graham

PY - 2012/4/1

Y1 - 2012/4/1

N2 - 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

AB - 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

UR - http://www.scopus.com/inward/record.url?scp=84859487757&partnerID=8YFLogxK

U2 - 10.1164/rccm.201202-0180ED

DO - 10.1164/rccm.201202-0180ED

M3 - Editorial

C2 - 22467801

AN - SCOPUS:84859487757

VL - 185

SP - 694

EP - 695

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 7

ER -