Prenatal Stress and Neurodevelopment of the Child: Focus on the HPA Axis and Role of the Placenta

O’Donnell, Kieran J.; O’Connor, Thomas G.; Glover, Vivette

doi:10.1159/000216539

Cited by 409 publications

(160 citation statements)

References 125 publications

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“…Our lack of support for mediation by cortisol has implications for the glucocorticoid mediation hypothesis, a leading hypothesis to explain how depression during pregnancy might impact fetal development (Goodman & Gotlib, 1999; O’Donnell, O’Connor, & Glover, 2009). Accumulating evidence suggests that mechanisms other than cortisol are more likely to be involved (DiPietro, 2012).…”

Section: Discussionmentioning

confidence: 88%

“…Accumulating evidence suggests that mechanisms other than cortisol are more likely to be involved (DiPietro, 2012). For example, there are polymorphisms in genes regulating the expression of glucocorticoid transporter proteins in the placenta, thereby altering its permeability to maternal stress hormones (Audus, Soares, & Hunt, 2002; O’Donnell et al, 2009). Thus, although antenatal cortisol may not be directly related to antenatal depression symptoms or infant NA, as we found in our sample of 3-month old infants, it continues to be an important focus of research, as it has been found to be directly related to a number of infant outcomes and also may predict postpartum depression (DiPietro, 2012).…”

Section: Discussionmentioning

confidence: 99%

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Perinatal depression influences on infant negative affectivity: Timing, severity, and co-morbid anxiety

Rouse

Goodman

2014

Infant Behavior and Development

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Accumulating evidence suggests that antenatal depression predicts infants’ negative affectivity, albeit with variable effect sizes. With a prospective longitudinal design, we sought to explain that variability by addressing questions about timing of the depression across pregnancy and the early postpartum, the role of high symptom levels relative to diagnosed depression, comorbidity with anxiety, and the potential mediating role of neuroendocrine functioning. Primiparous women (n = 77) with histories of depression prior to pregnancy were assessed for cortisol levels monthly beginning by mid-pregnancy. Depression symptom levels and diagnostic status were similarly assessed monthly in pregnancy and also until infants reached three months of age, when mothers completed the Infant Behavior Questionnaire – Revised to measure infant negative affectivity. Antenatal depression symptoms and infant negative affectivity were positively associated (r = .39). Controlling for depression symptom levels in other trimesters, only second trimester depression symptoms predicted higher infant negative affectivity (β = .44). With postpartum depression symptom levels in the model, only antenatal depression symptoms predicted infant negative affectivity (β = .45). In the context of depression, neither antenatal anxiety symptoms nor anxiety disorder diagnosis were associated with infant NA scores. The hypothesized role of elevated maternal cortisol as a mechanism for the association between antenatal depression and infant NA was not supported. Our findings contribute to efforts to more precisely identify infants of perinatally depressed mothers who are at greater risk for elevated negative affectivity, suggesting a window of vulnerability in mid pregnancy and the need for further study of potential mechanisms.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Perinatal depression influences on infant negative affectivity: Timing, severity, and co-morbid anxiety

Rouse

Goodman

2014

Infant Behavior and Development

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“…Indeed, there is now a growing body of knowledge highlighting the impact of prenatal stress exposure on the outcomes of offspring. However, the particular stressor used and behavioural parameters assessed in offspring are varied between studies and thus the outcomes within the current literature are diverse [40]. Key differences in the species used as well as the type and timing of stressor used are all major variables in determining the outcome of offspring and these factors must be considered when interpreting findings.…”

Section: Discussionmentioning

confidence: 99%

Prenatal Stress Alters Hippocampal Neuroglia and Increases Anxiety in Childhood

et al. 2015

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Prenatal stress has been associated with detrimental outcomes of pregnancy, including altered brain development leading to behavioural pathologies. The neurosteroid allopregnanolone has been implicated in mediating some of these adverse outcomes following prenatal stress due to its potent inhibitory and anxiolytic effects on the brain. The aims of the current study were to characterise key markers for brain development as well as behavioural parameters, adrenocortical responses to handling and possible neurosteroid influences towards outcomes in guinea pig offspring in childhood. Pregnant guinea pig dams were exposed to strobe light for 2 h (9-11 a.m.) on gestational days 50, 55, 60, and 65 and were left to deliver spontaneously at term and care for their litter. Behavioural testing (open-field test, object exploration test) of the offspring was performed at postnatal day 18 (with salivary cortisol and DHEA measured), and brains were collected at post-mortem on day 21. Markers of brain development myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were assessed via immunohistochemistry, and the neurosteroid allopregnanolone and its rate-limiting enzymes 5α-reductase types 1 and 2 (5αR1/2) were measured in neonatal brains by radioimmunoassay, reverse transcriptase polymerase chain reaction (RT-PCR), and Western blot, respectively. Brain-derived neurotrophic factor protein was measured as a marker of synaptic plasticity, and GABA_A receptor subunit expression was also assessed using RT-PCR. Neonates born from mothers stressed during late pregnancy showed a reduction in both MBP (p < 0.01) and GFAP (p < 0.05) expression in the CA1 region of the hippocampus at 21 days of age. Pups of prenatally stressed pregnancies also showed higher levels of anxiety and neophobic behaviours at the equivalent of childhood (p < 0.05). There were no significant changes observed in allopregnanolone levels, 5αR1/2 expression, or GABA_A receptor subunit expression in prenatally stressed neonates compared to controls. This study shows alterations in markers of myelination and reactive astrocytes in the hippocampus of offspring exposed to prenatal stress. These changes are also observed in offspring that show increased anxiety behaviours at the equivalent of childhood, which indicates ongoing structural and functional postnatal changes after prenatal stress exposure.

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“…Prenatal stressors should increase the risk of autism and maternal stress during pregnancy is weakly associated with raised maternal cortisol 47 . Thus, more research is needed in this area.…”

Section: Discussionmentioning

confidence: 99%

Autism prevalence in the United States with respect to solar UV-B doses: An ecological study

Grant

Cannell²

2013

Dermato-Endocrinology

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Evidence is mounting that vitamin D deficiency is intimately involved in autism. We report on autism prevalence by US state for those aged 6–17 y in 2010 with respect to indices of solar UV-B (UVB) doses. We calculated autism prevalence rates for white, black and Asian Americans by using total prevalence and relative populations of minors for each ethnic group by state. Analyses omit AK and HI (considered extreme cases), WY (no data), along with AZ and ND for black Americans (low numbers) and DC, ME, MT, ND and SD for Asian Americans (low numbers). For white Americans, the regression coefficient for solar UVB doses and autism prevalence ranged from -0.52 in January to -0.57 in October. For black Americans, the regression coefficient for latitude was 0.61, whereas those for solar UVB ranged from -0.55 to -0.61. For Asian Americans, the values for solar UVB ranged from -0.28 to -0.38. The inverse correlation between solar UVB and autism prevalence is similar to that for many types of cancer in the US. The journal literature indicates that adverse effects on fetal brain development during pregnancy due to vitamin D deficiency can explain these findings. However, we cannot rule out a role of vitamin D deficiency in early life. These results add to the evidence that vitamin D deficiency may be an important risk factor for autism and suggest that pregnant women and autistic individuals raise their serum 25-hydroxyvitamin D concentrations above 30 ng/ml.

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Prenatal Stress and Neurodevelopment of the Child: Focus on the HPA Axis and Role of the Placenta

Cited by 409 publications

References 125 publications

Perinatal depression influences on infant negative affectivity: Timing, severity, and co-morbid anxiety

Perinatal depression influences on infant negative affectivity: Timing, severity, and co-morbid anxiety

Prenatal Stress Alters Hippocampal Neuroglia and Increases Anxiety in Childhood

Autism prevalence in the United States with respect to solar UV-B doses: An ecological study

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