Abnormal Umbilical Artery Doppler Waveforms and Cord Blood Corticotropin-Releasing Hormone

Giles, Warwick B.; McLean, Mark; Davies, Joanne; Smith, Roger

doi:10.1016/0029-7844(95)00338-x

Cited by 66 publications

(28 citation statements)

References 20 publications

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“…Most studies have found that maternal stress affects birth weight by shortening gestational age (Copper et al 1996;Nordentoft et al 1996). However, some support exists for an effect on intrauterine growth restriction (IUGR; Wadhwa et al 2004), probably driven by higher levels of placental CRH resulting in decreased uteroplacental flow and hypoxemia, which are known risk factors for IUGR (Giles et al 1996;Goland et al 1993).…”

Section: Maternal Stress and Birth Weight: Accounting For Mechanismsmentioning

confidence: 97%

The Effect of Maternal Stress on Birth Outcomes: Exploiting a Natural Experiment

2011

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A growing body of research highlights that in utero conditions are consequential for individual outcomes throughout the life cycle, but research assessing causal processes is scarce. This article examines the effect of one such condition-prenatal maternal stress-on birth weight, an early outcome shown to affect cognitive, educational, and socioeconomic attainment later in life. Exploiting a major earthquake as a source of acute stress and using a difference-in-difference methodology, I find that maternal exposure to stress results in a significant decline in birth weight and an increase in the proportion of low birth weight. This effect is focused on the first trimester of gestation, and it is mediated by reduced gestational age rather than by factors affecting the intrauterine growth of term infants. The findings highlight the relevance of understanding the early emergence of unequal outcomes and of investing in maternal well-being since the onset of pregnancy.

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Section: Maternal Stress and Birth Weight: Accounting For Mechanismsmentioning

confidence: 97%

The Effect of Maternal Stress on Birth Outcomes: Exploiting a Natural Experiment

2011

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“…CRH is produced in large quantities by the healthy placenta in late pregnancy and contributes to the initiation of parturition (Frim et al, 1988; Giles et al, 1996). Placental 11-beta-hydroxysteroid dehydrogenase (11-beta-HSD, type 2 isoform) is produced to protect the fetus from overexposure to glucocorticoids.…”

Section: Towards Determination Of Mechanismsmentioning

confidence: 99%

Disruption of fetal hormonal programming (prenatal stress) implicates shared risk for sex differences in depression and cardiovascular disease

Goldstein

Handa

Tobet

2014

Frontiers in Neuroendocrinology

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Comorbidity of major depressive disorder (MDD) and cardiovascular disease (CVD) represents the fourth leading cause of morbidity and mortality worldwide, and women have a two times greater risk than men. Thus understanding the pathophysiology has widespread implications for attenuation and prevention of disease burden. We suggest that sex-dependent MDD-CVD comorbidity may result from alterations in fetal programming consequent to the prenatal maternal environments that produce excess glucocorticoids, which then drive sex-dependent developmental alterations of the fetal hypothalamic-pituitary-adrenal (HPA) axis circuitry impacting mood, stress regulation, autonomic nervous system (ANS), and the vasculature in adulthood. Evidence is consistent with the hypothesis that disruptions of pathways associated with gamma aminobutyric acid (GABA) in neuronal and vascular development and growth factors have critical roles in key developmental periods and adult responses to injury in heart and brain. Understanding the potential fetal origins of these sex differences will contribute to development of novel sex-dependent therapeutics.

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“…23 It appears plausible that the pathologies that lead to obstetric intervention and induction of labour or caesarean section also lead to a maternal or fetal stress response, increased cortisol and thence to elevated placental CRH synthesis. Further evidence for this conjecture comes from the analysis of cord blood samples from fetuses with abnormal Doppler flow characteristics, 24 from fetuses exhibiting intrauterine growth retardation 25 and from fetuses with abnormal fetal scalp pH values; fetal CRH levels are elevated in these pregnancies compared with matched controls. In vivo evidence for the role of cortisol in driving increased CRH has been provided by Challis' group who demonstrated that maternal plasma CRH increases in women given glucocorticoids to mature fetal lungs.…”

Section: Figurementioning

confidence: 92%

Pathological interactions with the timing of birth and uterine activation

Smith

Helden

Hirst

et al. 2007

Aust NZ J Obst Gynaeco

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The physiological processes that regulate the onset of parturition and birth are slowly being elucidated, and the points at which pathology can intervene are becoming more apparent. The data support the view that multiple pathways lead to myometrial activation. The clinical corollary is that combinations of tocolytics that operate via different mechanisms may be more effective than single agents. It may also be necessary to divide preterm labour into groups based on underlying mechanisms and to tailor therapy accordingly.

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Abnormal Umbilical Artery Doppler Waveforms and Cord Blood Corticotropin-Releasing Hormone

Abstract: The concentration of corticotropin-releasing hormone in the fetal circulation is significantly increased in pregnancies complicated by abnormal umbilical artery flow velocity waveforms. This may represent a stress-responsive compensatory mechanism in the human placenta.

Cited by 66 publications

References 20 publications

The Effect of Maternal Stress on Birth Outcomes: Exploiting a Natural Experiment

The Effect of Maternal Stress on Birth Outcomes: Exploiting a Natural Experiment

Disruption of fetal hormonal programming (prenatal stress) implicates shared risk for sex differences in depression and cardiovascular disease

Pathological interactions with the timing of birth and uterine activation

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