Elevated levels of umbilical cord plasma corticotropin-releasing hormone in growth-retarded fetuses.

Goland, Robin; Jozak, Sheila; Warren, Wendy B.; Conwell, Irene M.; Stark, Raymond I.; Tropper, Pamela

doi:10.1210/jcem.77.5.8077309

Cited by 127 publications

(71 citation statements)

References 2 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: 99%

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: 99%

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

2011

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“…In the human fetus, significant alterations occur in HPA function in pregnancies complicated by maternal undernutrition (Warnes et al 1998), maternal alcohol consumption (Wilcoxon et al 2003), maternal infection (Gravett et al 2000), fetal asphyixia (Procianoy et al 1988), intra-uterine growth restriction (Goland et al 1993) and pre-eclampsia (Procianoy and Cecin 1986). These changes in HPA function are predominantly defined by an increase in cord blood cortisol and a decrease in cord blood dihydroepiandrosterone sulphate (DHEAS).…”

Section: Hpa Functionmentioning

confidence: 99%

Sexually dimorphic effects of maternal asthma during pregnancy on placental glucocorticoid metabolism and fetal growth

Clifton

2005

Cell Tissue Res

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Human pregnancy is associated with sexually dimorphic differences in mortality and morbidity of the fetus with the male fetus experiencing the poorest outcome following complications such as pre-eclampsia, pre-term delivery and infection. The physiological mechanisms that confer these differences have not been well characterised in the human. Work conducted on the effect of maternal asthma during pregnancy, combining data collected from the mother, placenta and fetus has found some significant sex-related mechanistic differences associated with fetal growth in both normal pregnancies and pregnancies complicated by asthma. Specifically, sexually dimorphic differences have been found in placental glucocorticoid metabolism in male and female fetuses of normal pregnancies. In response to the presence of maternal asthma, only the female fetus alters placental glucocorticoid metabolism resulting in decreased growth. The male fetus does not alter placental function or growth in response to maternal asthma. As a result of the alterations in glucocorticoid metabolism in the female, downstream changes occur in pathways regulated by glucocorticoids. These data suggest that the female fetus adjusts placental function and reduces growth to compensate for maternal disease. However, the male fetus continues to grow in response to maternal asthma with no changes in placental function. This response by the male fetus may partially contribute to the increased risk of morbidity and mortality in this sex.

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“…However, the maternal cortisol that still crosses the placenta represents 25-50% of the plasma cortisol in the fetus, and therefore high levels of maternal glucocorticoids, exceeding the limit of placental 11 ␤-hydroxysteroid dehydrogenase, or pathological conditions impairing placental functions might lead to fetal exposure to excess glucocorticoids (5). In humans fetal cortisol levels are increased during fetal growth retardation (6,7), a situation that often is associated to impaired placental function (8). Prenatal excess of glucocorticoids modifies the development of several organs, including the lung, heart, gut, and kidney (9,10).…”

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confidence: 99%

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Ahlbom

Gogvadze

Chen

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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There is growing concern that prenatal exposure to excessive glucocorticoids may have deleterious effects on the development of various organs, including the nervous system. This study aimed at evaluating whether prenatal exposure to high levels of glucocorticoids might produce long-term effects on neuronal cell survival. Pregnant rats were injected i.p. with 0.1 mg͞kg dexamethasone (DEX) from day 14 postconception, and cerebellar granule cells (CGC) were prepared from 1-week-old rats from DEX-treated and control dams. After 7 days in culture, cells were exposed to H 2O2, methylmercury, or colchicine at concentrations known to induce apoptotic cell death. After exposure to H 2O2 or methylmercury, both inducing oxidative stress, the number of apoptotic cells was significantly higher in DEX-than in control-CGC. Because mitochondria play a key role in apoptosis, mitochondrial function was investigated, and a decrease in the threshold level of Ca 2؉ necessary for induction of mitochondrial permeability transition, in Ca 2؉ accumulation rate, and in oxygen consumption was detected in DEX-CGC. Moreover, the activity of the antioxidant enzyme catalase was significantly decreased in DEX-CGC. A similar decrease in catalase activity was observed in cerebellar homogenate from newborn and 40-day-old DEX-rats. In conclusion, these results indicate that prenatal exposure to high levels of glucocorticoids induces long-lasting changes in CGC rendering them more sensitive to oxidative stress. With the increasing use of multiple doses of glucocorticoids in preterm infants, the possibility that prenatal exposure to excess glucocorticoids may lead to long-term neurological consequences becomes a relevant issue.

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Elevated levels of umbilical cord plasma corticotropin-releasing hormone in growth-retarded fetuses.

Cited by 127 publications

References 2 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

Sexually dimorphic effects of maternal asthma during pregnancy on placental glucocorticoid metabolism and fetal growth

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

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