Maternal–Foetal Medicine
cortisol levels, and the effects are mediated by the teen mothers’ above-average over-controlling parenting behaviours.81 Feldman and colleagues20
Similarly, report on depressed mothers’ decreased
social engagement and emotional attunement when interacting with their infants compared with healthy matched controls, and these infants display exaggerated cortisol reactivity to stress compared with infants of healthy mothers.
Dysregulation of HPA axis functionality early in development appears to have long-lasting consequences. Four-year-old children of concurrently depressed mothers show dysfunctional daytime patterns of cortisol production (i.e., elevated morning cortisol) if they were exposed to maternal depression in infancy.82
However, if the
pre-schoolers were exposed to maternal depression at only one time point, that is either in infancy or concurrently at the age of four, but not at both time points, they did not show any ‘unhealthy’ HPA axis alterations during daytime and had comparable patterns to children of healthy control mothers. Moreover, only the pre-schoolers exposed to maternal depression both concurrently and in early infancy showed increased behavioural problems in first grade.82
These findings suggest
that early infant experiences of suboptimal care-giving (secondary to maternal depression) may be associated with hyperactivity and ‘sensitisation’ of the infant HPA stress system, and may be an early risk marker for the functionality of the child’s bio-behavioural regulatory capacity later in development. Supportive of this hypothesis is the recent finding that alternations in infant cortisol reactivity are associated with later child attention, anxiety and depression problems.83
This is consistent with work in young adults,
where exaggerated cortisol awakening response (i.e., the rise of cortisol production from awakening to 45 minutes thereafter) predicted the onset of depressive episodes one year later,84
supporting
the notion that dysregulation in cortisol reactivity is a significant component of depression aetiology.
Attachment
Finally, one key determinant for a child’s socio-emotional development is his or her attachment to primary care-givers. Attachment is believed to stem from an innate drive to seek proximity to a care-giver in order to maximise safety and, ultimately, survival.85
Attachment is
universal and develops in all infants, regardless of their care-givers’ parenting behaviours, but individual differences in the quality of attachment patterns do reflect differences in the care-giving environment, and are reliably measured via behavioural procedures by 12 months of age.86
While all infants are believed to be attached to
their care-givers, the quality of the individual’s attachment to a specific care-giver is unique to that specific attachment relationship, and thus a reflection of the unique quality of a specific care-giver–child relationship across the first year of life. Infants develop distinct attachment patterns with their care-givers based on the care-giver’s sensitivity and emotional availability during times of distress, during which the infant’s attachment system is activated and he or she is likely to display a variety of hard-wired attachment behaviours (e.g., crying, reaching out to be picked up) that are meant to clearly signal to the care-giver the need for soothing.86
Based on the lived experience and
working memory of many distress-soothing cycles with a particular care-giver across the first year of life and thereafter, children over time form a more generalised cognitive-affective relationship template that guides their current and future appraisals of interpersonal relationships.86,87
reliably assessed via the Strange Situation Test (SST),86 28
Individual differences in attachment relationships are an experimental
However, transmission of depression risk from mother to child is elevated when the infant is ‘genetically sensitive’ to life stress. Caspi and colleagues98
published a groundbreaking paper highlighting effects of gene-by-environment influences, such that children who had a variation of the serotonin transporter gene that coded for less optimal transporter functionality (s/s 5-HTTLPR variant, see below),
EUROPEAN OBSTETRICS & GYNAECOLOGY
paradigm that elicits distress and activates the infant’s attachment system. Based on the infant’s strategy for behaving in relation to the care-giver during the SST, children are labelled either securely or insecurely attached to their care-giver. Secure infants, when stressed, signal their distress to the care-giver and are able to be comforted; in turn, care-givers of secure infants tend to be emotionally available, perceptive and responsive to their infants across the first year of life.86,88 By contrast, insecurely attached infants are either unable to openly show distress under known stressful circumstances (avoidant infants), or they display heightened mixed emotions towards their care-giver and cannot be soothed (ambivalent-resistant infants). Parents of insecure infants tend to be emotionally unavailable, aloof and rejecting (for avoidant infants) or emotionally unpredictable and insensitive (for ambivalent-resistant infants).86,88
Finally, infants with
disorganised attachment to their care-givers lack a coherent strategy for coping with stress and interacting with their care-givers, and typically their care-givers use frightening, neglectful or abusive parenting styles.89
Studies suggest that maternal perinatal depression is significantly associated with increased likelihood of both insecure and disorganised attachment.22,23,90
Maternal depression and anxiety has
also been linked to insensitive maternal behaviour during mother–infant interactions and hyper-reactive neuroendocrine HPA stress axis in the child.90
The severity and chronicity of maternal
perinatal depression is especially salient for the quality of infant attachment; infants of depressed mothers in clinical samples are particularly at risk for high-risk attachment status compared with infants of depressed women in community samples.91
Infant attachment classifications are relatively stable across the lifespan, with greatest stability for securely attached children (75 %).92 The quality of infant attachment serves as robust early predictor for subsequent child socio-emotional adjustment, such that infants with insecure or disorganised attachment classifications in early infancy show greater risk for internalising and externalising problem behaviours later in childhood and during adolescence.93–95
In summary, the presence of maternal perinatal depression adversely impacts the quality of the infant’s attachment with the affected care-giver, such that these infants are more likely to be insecurely attached to their depressed mothers. In turn, these less-optimal attachment patterns are carried forward in development and adversely impact children’s emotional and social developmental trajectories.
Interacting Influence of Infant Genetics and Maternal Depression on Child Outcomes Epidemiologic studies confirm that depression has a strong genetic basis, as rates of depression are higher among biologically related relatives compared with biologically unrelated family members.96 more recent years, Sullivan et al.97
In conducted a meta-analytic review
on the role of genetics in depression, and claim that only a little more than 30 % of the parent-to-child transmission is due to heritability.
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