Prenatal Stress & Asthma Development
A recent study published in the BioMed Research International journal suggests that maternal stress during pregnancy is able to increase offspring risk and susceptibility to asthma.
What is prenatal maternal stress (PNMS)?
Prenatal maternal stress refers to the stress that a mother experiences during her pregnancy. An estimated 30% of pregnant women report psychosocial stress in their daily lives including job strain and depressive or anxiety symptoms.
Stress during pregnancy is a risk factor that may have significant consequences for the developing fetus. In fact, stress during pregnancy may result in lasting effects on the infant’s health status, the development and function of the infant’s immune system; and the cognitive development of the infant.
Prenatal programming research indicates that “the womb may be more important than the home” with respect to offspring health outcomes. Maternal prenatal stress influences offspring neurodevelopment and birth outcomes including the ratio of males to females born.
Prenatal stress can be chronic, linked to ongoing events in a woman’s life, or acute, linked to sudden changes in a women’s daily routine or environment. Timing is everything, especially for the effects of prenatal maternal stress (PNMS). New research findings show that the first two trimesters are the most sensitive to prenatal stress.
Prenatal stress affects children’s cognition and behaviour. Children exposed to this stress may show difficulties with paying attention, and have aggressive attitudes. Prenatal stress may also result in obstetrical complications, such as low birth weight, and delayed physical development. Maternal psychosocial stress may increase the risk of preterm birth.
Prenatal stress may also affect the mental health, such as an increased risk of autism, schizophrenia and depression of the children. For more information visit the following link: www.douglas.qc.ca/info/prenatal-stress.
Previous research also indicates that prenatal and early-life stress can modify infant immune function in the long-term, including conferring a higher risk for childhood asthma (MK Pincus-Knackstedt et al., 2006; AL Kozyrskyj et al., 2011) most likely driven via a stress-induced T cell helper (Th2) shift (IJ Elenkov & Chrousos GP, 1999; von Hertzen LC, 2002).
In January 1998, the Quebec Ice Storm, considered one of the worst natural disasters in Canada’s history, left millions of people without electricity for up to 40 days.This event, through the McGill University’s Project Ice Storm provided almost unique opportunity to study the long-term effects of in utero exposure to prenatal maternal stress on various aspects of the children’s development from birth through childhood.
Anne-Marie Turcotte-Tremblay and colleagues from the University of Montreal Hospital Research Centre and the McGill University, Montreal, QC, Canada were able to follow a cohort of women who were pregnant during the disaster and have conducted regular assessments of their children. Last year, in 2014 they published their observations in the BioMed Research International journal.
In their follow up of the children at the age of 11 to 12 years, the authors found that the offspring of the mothers who reported that they had suffered high levels of stress during pregnancy were more likely to be diagnosed with asthma, had higher incidences of wheezing, and used more inhaled corticosteroids. Interestingly, asthma symptoms were observed in girls; but not in boys.
The reason for these stress-related sex-specific asthma outcomes is not entirely clear, but the authors discuss previous experimental research suggesting that prenatal stress may affect the male and female offspring differently. Thus, increased anxiety, depression and higher stress response are much common in female offspring; whereas, male offspring suffer much more with learning and social disabilities (V Glover & Hill J., 2012).
The relatively small study supports previous evidence that maternal stress during pregnancy contributes to fetal programming of the immune system, and indicates that further studies along these lines are warranted.
An update and conclusion by Konstantinos Douros, Maria Moustaki, […], and Kostas N. Priftis
The underlying mechanism of maternal prenatal stress (MPS) is not fully understood. It is more than 15 years that evidence from cohort studies and animal models linked, increasingly stronger, MPS with the development of childhood asthma.
Mechanism of maternal prenatal stress in asthma predisposition in the offspring. GC, glucocorticoids; CRH, corticotrophin releasing hormone; 11 b-HSD2, 11-b hydroxysteroid dehydrogenase-type 2; HPA, hypothalamic–pituitary–adrenal. From Konstantinos Douros, Maria Moustaki, […], and Kostas N. Priftis, Front. Pediatr., 2017. Public domain.
However, its complexity is emphasized by the number of purportedly involved pathways namely, placental deregulated metabolism of maternal steroids, impaired maturation of fetal Hypothalamic-Pituitary-Adrenal (HPA) axis, imbalanced efflux of commensal bacteria across the placenta, and skewed immune development toward T cell helper (Th2) phenotypes and responses.
Maternal GC, along with the improper activation of placental–fetal HPA axis, are considered the main mediators of this predisposition. However, there are various other pathways through which maternal stress may increase the offspring’s propensity for asthma. Amongst them, MPS imposed imbalances in fetal and offspring’s microbiota, is the less explored and the more promising to unravel—at least partially—the complex association between MPS and asthma.
Source: Biomed Res Int, 2014, ID201717. DOI: 10.1155/2014/201717
Read more: hindawi.com
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