Method: Data were derived from the Avon Longitudinal Study of Parents and Children cohort, a longitudinal cohort study in the west of England that has followed mothers from pregnancy into the postnatal period. A total of 13,133 mothers reported on the number and conditions of previous perinatal losses and provided self-report measures of depression and anxiety at 18 and 32 weeks' gestation and at 8 weeks and 8, 21 and 33 months postnatally. Controls for pregnancy outcome and obstetric and psychosocial factors were included.
prenatal depression 2011
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Conclusions: Depression and anxiety associated with a previous prenatal loss shows a persisting pattern that continues after the birth of a subsequent (healthy) child. Interventions targeting women with previous prenatal loss may improve the health outcomes of women and their children.
This review of recent research on prenatal depression suggests that it is a strong predictor of postpartum depression and is more common than postpartum depression. Prenatal depression has been associated with excessive activity and growth delays in the fetus as well as prematurity, low birthweight, disorganized sleep and less responsiveness to stimulation in the neonate. Infants of depressed mothers have difficult temperament, and later in development attentional, emotional and behavioral problems have been noted during childhood and adolescence, as well as chronic illnesses in adulthood. Several variables have confounded the effects of prenatal depression including comorbid anxiety and anger as well as stressful life events. Potential mediating variables are low prenatal maternal dopamine and serotonin levels and elevated cortisol and norepinephrine. The associated intrauterine artery resistance may limit blood flow, oxygen and nutrients to the fetus. Some studies also suggest the heritability of developmental problems for the children of prenatally depressed mothers, including ADHD and antisocial behavior. Multivariate, longitudinal research is needed to disentangle these confounding and mediating variables.
Background: The adverse effect of both pre- and post-natal maternal anxiety and depression on the development of offspring is shown by a large body of research. No published studies, however, have simultaneously: (i) controlled for co-occurring prenatal risks that may influence maternal prenatal anxiety and depression; (ii) compared the relative contributions of prenatal and postnatal maternal anxiety and depression on child functioning; and (iii) assessed a full range of child psychopathology and functioning to determine the relative effects of prenatal and postnatal anxiety and depression in the mother.
Method: Using 3,298 mother-offspring pairs, the authors examined these factors in a single-path analytic model. Measurements of maternal anxiety and depression were collected at two time points: 32 weeks prenatal and 1.5 years postnatal. Other prenatal risks were assessed between 8 and 32 weeks of gestation. Child outcomes included (a) ordered-categorical measures of DSM-IV externalizing and internalizing disorders, and (b) an assessment of verbal IQ.
Results: In both the prenatal and postnatal periods, maternal depression had a wider impact on different types of child maladjustment than maternal anxiety, which appeared more specific to internalizing difficulties in the child. Of note, prenatal risks were prospectively associated with child externalizing difficulties and verbal IQ, beyond the effects of prenatal and postnatal maternal anxiety and depression.
Conclusion: The present results suggest that addressing both maternal anxiety and depression, in the prenatal and postnatal periods-as well as associated risk factors-may be the most effective approach to prevent adverse outcomes in the offspring.
Perinatal depression can have devastating consequences for the affected woman, her children, and family,15-18 and has been linked to poor childbirth outcomes such as preterm delivery and low birth weight19,20 and to detrimental effects on maternal sensitivity in the postpartum period.21,22 Mothers who are more sensitive and responsive to their children are more likely to have children with secure attachment, and therefore the symptoms of maternal depression can lead to unresponsive, inconsistent, unavailable, or rejecting care by the mother toward the child (ie, decreased sensitivity).21,22 Consequently, depressed mothers are more likely to have infants with colic,23 to be intrusive and harsh with their infants,21,22 and to exhibit other impaired parenting behaviors such as lower rates of infant safety practices17,18 such as car seats and childproof latches on cabinets,24,25 and decreased healthy child development behaviors such as reading, singing, and playing games with their child.26
Moreover, children exposed to perinatal (either during pregnancy or postpartum) maternal depression have higher cortisol levels than infants of mothers who were not depressed27-30 and this finding continues through adolescence.30 Importantly, maternal treatment of depression during pregnancy appears to help normalize infant cortisol levels.31 These findings may partially explain the mechanism for an increased vulnerability to psychopathology in children of mothers with perinatal depression.32
In a normal HPA axis, the delivery of CRH from the paraventricular nucleus of the hypothalamus triggers the stimulation of adrenocorticotropic hormone (ACTH) from the anterior pituitary and, consequently, cortisol from the adrenal cortex. This hormonal system is regulated by negative feedback mediated by cortisol receptors in the anterior pituitary, hypothalamus, and hippocampus, as well as ACTH receptors in the anterior pituitary and CRH autoreceptors in the hypothalamus.50 In depressed patients, it has been shown that there is a change in the regulation of the HPA axis.51 A hallmark feature that characterizes the HPA axis in depression is the altered response to stress and inability to maintain regulation: indeed, hyperactivity of the HPA axis is one of the most robust biological findings in major depression.51
Both women with PPD and women with nonpuerperal MDD show abnormalities in HPA axis activity. In general women (and men) suffering from MDD exhibit high baseline cortisol and an exaggerated response to the dexamethasone/corticotrophin-releasing hormone (DEX/CRH) test. However, in the first few weeks postpartum, euthymic women demonstrate an HPA axis that remains refractory to external CRH challenge. In contrast, women with PPD have been shown to experience an ongoing blunting of ACTH response to corticotrophin-releasing hormone (CRH) at 6 to 12 weeks postpartum compared with nondepressed women, interpreted as reflecting an ongoing hyporeactive HPA axis.43 Additionally, Bloch et al observed that currently euthymic women with a past history of PPD experienced an increased cortisol response and onset of significant depressive symptoms when exposed to a protocol consisting of high-dose gonadal steroid administration followed by abrupt withdrawal. This observed effect in those women with a history of PPD was in marked contrast to the group of women without a history of PPD who experienced no observed mood disturbance when exposed to the same protocol. Thus, this work suggests either a trait vulnerability related to the onset of PPD or a consequence of an earlier depression.45
Interestingly, the HPA axis has also been a focus of recent efforts to identify a biomarker for those at risk for perinatal or postpartum depression. In particular, elevated placental CRH has been a potential candidate with earlier literature demonstrating conflicting results.52,53 The increasing production of placental CRH (pCRH) throughout pregnancy can be measured in maternal peripheral blood54 and within hours after childbirth, levels of pCRH quickly drop and become undetectable.55 Nonetheless, the role of midpregnancy pCRH as a biomarker of maternal prenatal and PPD does not appear to be clinically useful, and the most recent report did not demonstrate an association between increased midpregnancy pCRH and increased risk for either depression during pregnancy nor PPD.56
Other recent animal literature demonstrates that maternal psychological status, in particular anxiety and depression during and immediately after pregnancy, confers increased vulnerability for mental illness in offspring. Furthermore, perinatal maternal depression and anxiety cause detrimental effects on maternal sensitivity, which may result in impaired mothering behaviors associated with insecure maternal/infant bonding and attachment.48 Moreover, the consequences of impaired maternalinfant attachment occurring at a critical time for infant early brain development are serious and may lead to detrimental effects on both infant brain morphology and physiology, altered stress reactivity and socioemotional and neurocogitive development, as well as long-term behavioral and emotional problems persisting into adulthood.48,58,60
Regarding treatment of depression during pregnancy, antidepressant use in pregnant women is often necessary in order to prevent maternal psychiatric illness. Recent collaborative consensus statements by the American Psychiatric Association and the American College of Obstetricians and Gynecologists provide a useful framework for the interpretation of data about the safety of psychotropic medications during pregnancy and lactation. Therefore, individualized recommendations based on the patient's past history should ideally be implemented prior to pregnancy with a goal of minimizing exposures.
The first analysis examined whether stillbirths predicted subsequentdepressive and anxiety symptoms more strongly than miscarriage. Thenon-parametric Wilcoxon rank sum test was applied to each visit to checkwhether there was any difference in depression and anxiety symptom scoresbetween mothers who experienced a previous miscarriage and mothers whoexperienced a previous stillbirth. Results indicated that the differencebetween stillbirth and miscarriage was not significant (P = 0.27).Thus, stillbirth and miscarriage were combined in the analyses below. 2ff7e9595c
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