Maternal Perinatal Depression – Impact on Infant and Child Development
and who were exposed to early stress, had greater likelihood to develop depression as adults.98
The serotonin transporter gene codes
for the serotonin transporter protein (SERT), which regulates the amount of serotonin in the neuronal synapses. The neurotransmitter serotonin aids neuronal communication found to contribute to mood regulation. Recent work has consistently linked a functional length polymorphism in the promoter region of the serotonin transporter gene (SLC6A4, variant 5-HTTLPR) to increased susceptibility to poor functioning and psychopathology.99–101
This polymorphism has
functional importance in that the short (s) allele variant is less transcriptionally efficient than the long (l) variant,102
resulting in lower
serotonin transporter levels and reduced serotonin uptake, which has functional effects on neural circuits regulated by serotonin.103 Serotonergic output is lowest in homozygote s/s 5-HTTLPR carriers compared with those who are homozygote l/l or heterozygote s/l. The presence of the short allele has been associated with predisposition to anxiety and negative emotionality in human adults,104 and to heightened shyness in children.105
The s/s 5-HTTLPR variant has been shown to interact with environmental adversity to create increased susceptibility to psychopathology, such as depression.98,106
children interacts with maternal reports of social support to predict the child’s later inhibited behaviour – pre-school children with one or two copies of the short allele of the 5-HTT gene who also had mothers who perceived themselves as low in social support were more likely to be very shy and inhibited at the age of seven, compared with those with homozygotes for the long allele who had mothers with high social support.100
However, there are also studies
that have failed to demonstrate any association between the 5-HTTLPR gene polymorphism and anxiety107,108
It has been suggested that gene-by-environment interactions may not create direct risk for psychiatric illness, but may be better understood as creating vulnerability to more proximal psychological experiences (e.g., negative affectivity or fearfulness) that then contribute to later vulnerability.99,111
Infants, for example, who were
s/s 5-HTTLPR homozygotes showed greater irritability in the context of exposure to suboptimal parenting compared with those with at least one copy of the long allele.17
Similarly, Barry and colleagues112
found that seven-month-old infants with genetic risk (homozygote s/s 5-HTTLPR), who were exposed to unresponsive maternal parenting showed greater likelihood of insecure attachment to their mothers at 15 months of age. In contrast, for infants without genetic risk, there was no association between maternal responsivity and attachment style.
In summary, while these results indicate that infant genetics may potentiate the risks of early environmental exposures, they also clearly support the need for early detection of parenting risk among
1. Kessler RC, Zhao S, Blazer DG, et al., Prevalence, correlates, and course of minor depression and major depression in the National Comorbidity Survey, J Affect Disord, 1997;45(1–2):19–30.
2. Weissman MM, Olfson M, Depression in women: implications for health care research, Science, 1995;269(5225):799–801.
3. Brown MA, Solchany JE, Two overlooked mood disorders in women: subsyndromal depression and prenatal depression, Nurs Clin North Am, 2004;39(1):83–95.
4. Gotlib IH, Whiffen VE, Mount JH, et al., Prevalence rates and demographic characteristics associated with depression in pregnancy and the postpartum, J Consult Clin Psychol, 1989;57(2):269–74.
5. Beck CT, A meta-analysis of predictors of postpartum depression, Nursing Research, 1996;45(5):297–303.
depressed mothers, and suggest the potential power of early parenting interventions in ameliorating genetic risk and preventing manifestation of later child psychopathology.
Can we Interrupt Intergeneration Transmission of Risk of Depression? Various research groups using both pharmaco- and psychotherapeutic methods have addressed this challenge. Infants of depressed mothers who accepted antidepressant treatment while pregnant showed lower, more normal baseline cortisol levels and reactivity compared with infants of untreated depressed women.113 Children of mothers who remit in depression in early post-partum due to pharmacotherapy have lower rates of psychiatric problems in subsequent years compared with untreated and unremitted depressed mothers.114
Furthermore, post-partum interventions that
enhance parenting and support the development of secure attachment between mother and child are also efficacious in improving outcomes for infants of depressed mothers.115
The 5-HTT status of
For example, a recent study highlighted the protective power of secure attachment during late infancy in ameliorating prenatal risk exposure on the child’s cognitive development.116
in utero to maternal depression and elevated stress cortisol levels had impairments in their cognitive performance as toddlers. However, this was only the case if the toddlers also had insecure attachments with their mothers in late infancy, whereas children with secure attachments to their mothers were protected from the adverse in utero exposure to maternal depression. Thus, interventions that improve maternal perinatal depression and positively impact mother–child attachment in infancy are powerful to protect against long-term negative child outcomes.
Maternal perinatal depression adversely impacts a range of foetal and infant outcomes, including negative influences on infant temperament and emotion regulation, functionality of biological stress response and establishment of secure attachments to care-givers. Transmission of risk from depressed mother to child may be mediated through inheritance of genetic risk, in utero exposure to stress hormones, or dysfunctional post-partum care-giving practice. Risk for the child is also impacted by his or her own genetic risk status (e.g., s/s 5-HTTLPR homozygotes), which interacts with exposure to environmental risk (e.g., life stress, poor parenting). Treating maternal depression and/or improving maternal care-giving may avert and/or ameliorate problematic child outcomes. Future research should continue to attempt identifying potential pathways of epigenetic risk transmission, with the ultimate goal of creating highly personalised interventions and reducing intergenerational conveyance of risk. n
6. Hölzel L, Härter M, Reese C, et al., Risk factors for chronic depression – a systematic review, Journal of Affective Disorders, 2011;129(1–3):1–13.
7. Buist A, Janson H, Childhood sexual abuse, parenting and postpartum depression – a 3-year follow-up study, Child Abuse Negl, 2001;25(7):909–21.
8. Muzik M, Thelen K, Rosenblum K, Perinatal depression: detection and treatment, Neuropsychiatry, 2011;1(2):179–95.
9. Altshuler LL, Cohen LS, Moline ML, et al., Treatment of depression in women: a summary of the expert consensus guidelines, J Psychiatr Pract, 2001;7(3):185–208.
10. Diego MA, Field T, Hernandez-Reif M, et al., Prenatal depression restricts fetal growth, Early Hum Dev, 2009;85(1):65–70.
11. England MJ, Sim LJ (eds); Committee on Depression, Parenting Practices, and the Healthy Development of Children; National
Research Council; Institute of Medicine, Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention, Washington: The National Academies Press, 2009:448.
12. Hoffman S, Hatch MC, Depressive symptomatology during pregnancy: evidence for an association with decreased fetal growth in pregnancies of lower social class women, Health Psychol, 2000;19(6):535–43.
13. Lundy B, Aaron Jones N, Field T, et al., Prenatal depression effects on neonates, Infant Behavior and Development, 1999;22(1):119–29.
14. Glover V, Do biochemical factors play a part in postnatal depression?, Prog in Neuropsychopharmacol Biol Psychiatry, 1992;16(5):605–15.
15. Teixeira JM, Fisk NM, Glover V, Association between maternal
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