Prenatal maternal stress and the severity of autism spectrum disorder: A cross-sectional study.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder linked to several genetic and environmental factors including antenatal stress. Hence, we aimed to examine whether a mother's stress during pregnancy is associated with the severity of autism spectrum disorder in children. The study was conducted with 459 mothers of children with autism (aged 2-14 years) who were attending rehabilitation and educational centers in the two major cities of Makkah and Jeddah in Saudi Arabia. Environmental factors, consanguinity, and ASD family history were assessed using a validated questionnaire. The Prenatal Life Events Scale questionnaire was used to assess whether the mothers were exposed to stress during pregnancy. Two models of ordinal regression analysis were conducted including gender, child age maternal age, parental age, maternal education, parental education, income nicotine exposure, mother taking medication during pregnancy, family history of ASD, gestation, consanguinity, exposure of prenatal life events (in model 1), and severity of prenatal life events (in model 2). Family history of ASD showed a statistically significant association with the severity of ASD in both regression models (p = .015, odds ratio [OR]: 4.261 in Model 1, and p = .014, OR: 4.901 in model 2). In model 2, the moderate severity prenatal life events showed higher statistically significant adjusted odds ratio for ASD severity compared to no stress (p = .031; OR: 3.82). Within the limitations of this study, prenatal stressors showed some potential contribution to ASD severity. Family history of ASD was the only factor that showed a persistent association with ASD severity. A study that assesses the effect of COVID-19 stress on ASD prevalence and severity is recommended.

Maternal environment and placental vascularization in small ruminants.

Uteroplacental development is a crucial step facilitating conceptus growth. Normal placental development comprises extensive placental angiogenesis to support fetoplacental transport, meeting the metabolic demands of the fetus. Compromised pregnancies due to maternal stressors such as over or undernutrition, maternal age or parity, altered body mass index, or genetic background result in altered vascular development of the placenta. This negatively affects placental growth and placental function and ultimately results in poor pregnancy outcomes. Nonetheless, the placenta acts as a sensor to the maternal stressors and undergoes modifications, which some have termed placental programming, to ensure healthy development of the conceptus. Sex steroid hormones such as estradiol-17ß and progesterone, chemokines such as chemokine ligand 12, and angiogenic/vasoactive factors such as vascular endothelial growth factors, placental growth factor, angiopoietins, and nitric oxide regulate uteroplacental development and hence are often used as therapeutic targets to rescue compromised pregnancies. Interestingly, the presence of sex steroid receptors has been identified in the fetal membranes (developing fetal placenta). Environmental steroid mimetics known as endocrine disrupting compounds disrupt conceptus development and lead to transgenerational impairments by epigenetic modification of placental gene expression, which is another area deserving intense research efforts. This review attempts to summarize current knowledge concerning intrinsic and extrinsic factors affecting selected reproductive functions with the emphasis on placental development.