Diurnal cortisol patterns and psychiatric symptoms in pregnancy: Short-term longitudinal study

O’Connor, Thomas G.; Tang, Wan; Gilchrist, Michelle; Moynihan, Jan A.; Pressman, Eva; Blackmore, Emma Robertson

doi:10.1016/j.biopsycho.2013.11.002

Cited by 80 publications

(76 citation statements)

References 53 publications

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“…1,4,34,48 However, it is important to note that investigations of maternal depression and cortisol in pregnancy have reported mixed results. 12,13,[49][50][51][52][53][54] Nonetheless, it has been suggested that biological markers of prenatal stress may be better indicators of offspring outcomes than selfreport measures. 34 Thus, we expected that maternal cortisol would significantly predict infant NR3C1 IF and BDNF IV methylation.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies of prenatal depression have suggested that clinical diagnoses correlate more reliably with biological markers of depression, such as awakening cortisol, than do self-report measures. 12 Therefore, using clinical diagnoses to define the depressive symptom group may have revealed a potential relationship between depressed mood, maternal glucocorticoids, and epigenetic outcomes.…”

Section: Discussionmentioning

confidence: 99%

“…1,4 Indeed, symptoms of prenatal depression have been associated with increased diurnal salivary cortisol, 12 and exaggerated cortisol responses to an acute stressor. 13 Moreover, enduring changes in fetal DNA methylation have been proposed to be involved in entraining the fetal HPA axis in response to maternal distress.…”

Section: Introductionmentioning

confidence: 99%

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Maternal prenatal depressive symptoms predict infantNR3C11F andBDNFIV DNA methylation

et al. 2015

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Abbreviations: BDNF, gene encoding the brain-derived neurotrophic factor protein, BPA, bisphenol A, GR, glucocorticoid receptor, HPA, hypothalamic-pituitary adrenal, NR3C1, gene encoding the glucocorticoid receptor.Prenatal maternal psychological distress increases risk for adverse infant outcomes. However, the biological mechanisms underlying this association remain unclear. Prenatal stress can impact fetal epigenetic regulation that could underlie changes in infant stress responses. It has been suggested that maternal glucocorticoids may mediate this epigenetic effect. We examined this hypothesis by determining the impact of maternal cortisol and depressive symptoms during pregnancy on infant NR3C1 and BDNF DNA methylation. Fifty-seven pregnant women were recruited during the second or third trimester. Participants self-reported depressive symptoms and salivary cortisol samples were collected diurnally and in response to a stressor. Buccal swabs for DNA extraction and DNA methylation analysis were collected from each infant at 2 months of age, and mothers were assessed for postnatal depressive symptoms. Prenatal depressive symptoms significantly predicted increased NR3C1 1F DNA methylation in male infants (b D 2.147, P D 0.044). Prenatal depressive symptoms also significantly predicted decreased BDNF IV DNA methylation in both male and female infants (b D ¡3.244, P D 0.013). No measure of maternal cortisol during pregnancy predicted infant NR3C1 1F or BDNF promoter IV DNA methylation. Our findings highlight the susceptibility of males to changes in NR3C1 DNA methylation and present novel evidence for altered BDNF IV DNA methylation in response to maternal depression during pregnancy. The lack of association between maternal cortisol and infant DNA methylation suggests that effects of maternal depression may not be mediated directly by glucocorticoids. Future studies should consider other potential mediating mechanisms in the link between maternal mood and infant outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Maternal prenatal depressive symptoms predict infantNR3C11F andBDNFIV DNA methylation

et al. 2015

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“…This is largely because in non-pregnant populations symptoms of depression are associated with cortisol hyper-secretion (Bhagwagar et al, 2005;Cowen, 2002;Herbert, 2013). However, data linking symptoms of mood disturbance in pregnancy with changes in maternal HPA function have been mixed, with evidence both for (Giesbrecht et al, 2012;Murphy et al, 2014;O'Connor et al, 2013;Obel et al, 2005) and against (Hellgren et al, 2013;Pluess et al, 2012) cortisol hyper-secretion. One possible explanation for the disparate findings is that cortisol levels rise throughout pregnancy, regardless of mood state, due to the release of corticotrophin-releasing hormone (CRH) from the placenta.…”

Section: Introductionmentioning

confidence: 94%

Symptoms of prenatal depression are associated with raised salivary alpha-amylase levels

Braithwaite

Ramchandani

Lane

et al. 2015

Psychoneuroendocrinology

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“…Maternal depression during pregnancy has been associated with elevated mid-pregnancy corticotrophin releasing hormone (Rich-Edwards et al 2008;O'Keane et al 2011) and cortisol levels (Field et al 2006(Field et al , 2008, with altered diurnal pattern of cortisol secretion in the second trimester (O'Keane et al 2011;O'Connor et al 2013b), and with increased urinary cortisol at the middle to end of the third trimester (27-35 weeks) (Lundy et al 1999). Evidence is less clear when examining the relationship between maternal anxiety and/or symptoms of stress and changes in the maternal HPA axis.…”

Section: Changes In Circulating Levels Of Maternal Hormones During Prmentioning

confidence: 96%

Mechanisms Linking In Utero Stress to Altered Offspring Behaviour

Mina

Reynolds

2014

Behavioral Neurobiology of Stress-Related Disorders

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Development in utero is recognised as a determinant of health in later life, a concept known as early life 'programming'. Several studies in humans have now shown a link between in utero stressors of maternal stress, anxiety and depression and adverse behavioural outcomes for the offspring including poorer cognitive function and behavioural and emotional problems. These behaviours are observed from the very early neonatal period and appear to persist through to adulthood. Underlying mechanisms are not known but overexposure of the developing foetus to glucocorticoids has been proposed. Dysregulation of the maternal and offspring hypothalamic-pituitary-adrenal (HPA) axis has been proposed as a mechanism linking in utero stress with offspring behavioural outcomes. Studies suggest that altered circulating levels of maternal cortisol during pregnancy and/or changes in placental gene expression or methylation, which result in increased glucocorticoid transfer to the developing foetus, are linked to changes in offspring behaviour and in activity of the offspring HPA axis. Further understanding of the underlying pathways and identification of any gestation of vulnerability are needed to help design interventions to reduce in utero stress and improve behavioural outcomes in the offspring.

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Diurnal cortisol patterns and psychiatric symptoms in pregnancy: Short-term longitudinal study

Cited by 80 publications

References 53 publications

Maternal prenatal depressive symptoms predict infantNR3C11F andBDNFIV DNA methylation

Maternal prenatal depressive symptoms predict infantNR3C11F andBDNFIV DNA methylation

Symptoms of prenatal depression are associated with raised salivary alpha-amylase levels

Mechanisms Linking In Utero Stress to Altered Offspring Behaviour

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