Post-Partum Depression

Around one in seven women each year will develop post-partum depression (PPD), which is defined as a major depressive episode just following childbirth.[1] The DSM-IV requires the episode to occur within four weeks, but it has been shown to occur within the first three months.[2] As described in Baker et al, symptoms include sadness, frequent crying, lack of motivation, low interest in food of self-care, difficulty concentrating and low interest in the new baby.[3] While we do not know what exactly causes a woman to develop PPD, there have been several correlates found in those who go on to develop it, ranging from the food she eats, to her genes, to how she feels during pregnancy. Mothers are prepared for the journey of motherhood after being rewired during pregnancy: what is it about the post-partum mother that makes her so different? Studies have shown differences in brain activation patterns and levels of certain factors that distinguish post-partum mothers from their counterparts. It is crucial to understand PPD, and how to treat it, because of its effects on maternal behaviour, which has great influence on infant development. Mothers with PPD show suboptimal bonding behaviour, which leads to dysregulated infant behaviour and delays in social and cognitive development in the infant.[4] Understanding PPD highlights the importance of plasticity within the brains of mothers and babies alike.

Symptoms of PPD

1.0 Correlates

It is not clear what causes PPD. However, several significant risk factors have been found for those who go on to develop PPD, including depression before or during pregnancy, anxiety and stressful events during pregnancy, and low partner support.[5] In this section we will focus on two minor, but particularly interesting correlates – omega-fats and oxytocin.

1.1 Omega-fats

Omega-3 Fats and Depression
Image Unavailable
Figure 1.[9] Correlation between depressive symptoms and intake of
omega-3 fatty acids from seafood in diet. It was found that lower intake
of omega-3 fatty acids from fish during pregnancy was correlated with
higher prevalence of depressive symtpoms at 32 weeks of gestation.

Omega-3 fats are important for the developing fetal brain. During pregnancy, maternal omega-3 fats are depleted as they are incorporated into the fetus’ growing brain.[6] Such depletion is not limited to pregnancy, either; omega-3s are also released to the infant through breast milk.[7] Lower levels of omega-3 fats in the maternal brain results in greater production of omega-6 fats, which are subsequently substituted into the myelin sheath instead.[7] Unfortunately, these fats are less efficient than their omega-3 counterparts; mothers with especially low omega-3 fat levels, and thus more of this substitution, may be more likely to develop PPD. Acting through eicosanoids, omega-3 fats have anti-inflammatory effects, whereas omega-6 fats have pro-inflammatory ones; low omega-3 fat consumption has thus been associated with inflammatory disorders and depression.[8]

There have been correlations found between low intake of omega-3 fats from seafood and depression during pregnancy (see Figure 1).[9] Moreover, it has been found that consuming omega-fats in a ratio of greater than 9:1 (omega-6 : omega-3) during pregnancy is associated with developing depressive symptomology postpartum, as these women are not able to compensate for the depletion through their diet.[7] Countries with the highest incidence of PPD are also those with lowest consumption of fish [10], one of the richest sources of omega-3 fats. Only about 15% of women meet the recommended intake amount of DHA and EPA, two major omega-3 fats.[9]

Some have taken these results to suggest a possible treatment for PPD: supplemental omega-3 fats. However, results have been inconclusive; a small sample size has often precluded authors from definitively stating whether the effect was truly significant. One study found no significant differences between a group receiving pills with DHA (an omega-3 fat), and the control group.[11] Another trial found that administering omega-3 fats for eight weeks post-partum at various doses did alleviate depressive symptoms, and found no differences between doses, such that 0.5g/day is sufficient to see an effect; however, they too suffered from a small sample size and lacked a control.[12]

1.2 Oxytocin

Oxytocin has been implicated in several maternal functions (ex. uterine contractions during labour and inducing milk letdown during breastfeeding), and is released during social behaviours like interacting with offspring.[13] Single nucleotide polymorphisms (SNPs), or mutations, in a particular oxytocin peptide gene (rs2740210) have been found to interact with early life experience to predict PPD and maternal behaviour.[14] Mothers who are homozygous for the C allele of the gene and experienced high early life adversity were more likely to develop depression postpartum. Those with the C allele also experienced shorter breastfeeding duration, which suggests that perhaps the resulting change in oxytocin resulted in less efficient milk letdown, which discouraged further breastfeeding. With breastfeeding being such an important bonding point for mother and child, mothers with this mutation may thus struggle with bonding to their infant, which has been shown for mothers with PPD (discussed below). On the other hand, women with high early care quality by their own mothers reported lower depression, especially if they were homozygous for the C allele, suggesting that this gene mediates the effects in both directions.[15]

Past the genes, plasma levels of oxytocin itself during pregnancy have also been found to correlate with the development of postpartum depression. Having lower levels of oxytocin during pregnancy at 30th-34th weeks of gestation significantly predicted PPD symptoms.[16] Oxytocin has been found to reduce the stress response and inhibit amygdala hyperactivity;[17] having lower levels of oxytocin leaves mothers more vulnerable to the stresses of the postpartum period, and thus more likely to develop PPD.

These results have lead to research into using oxytocin to treat PPD. However, the results have been largely inconclusive.[18] The issue with administering oxytocin is that it will affect individuals very differently, depending on their oxytocin receptor function, endogenous oxytocin production and early caregiving experience, and it could be that oxytocin will only benefit a particular subgroup of women.[18] One study found that after administering intranasal oxytocin to mothers with PPD, they described their babies more negatively and reported a more negative mood, suggesting that oxytocin may bring their negative emotions to the forefront and make them more salient.[19]

1.3 Cortical and limbic connectivity

When affected by PPD and major depressive disorder (MDD) alike, the brain works differently: on fMRI scans, various parts of the brain can be shown to be more or less active. The connections between various cortical and limbic areas, including the nucleus accumbens, dorsolateral prefrontal cortex, amygdala and hippocampus are found to be weaker in mothers with PPD.[20] Curiously, only some regions affected in MDD were also affected in PPD, which suggests that there are differences between these two conditions.[20] In an attempt to find a cause for the disparity, Deligiannidis et al (2013) also considered levels of neuroactive steroids (progesterone, pregnenolone, pregnanolone and allopregnanolone) present in those with PPD.[20] However, they found no significant differences between these levels in mothers with PPD and in individuals with MDD, which does not support a significant role of neuroactive steroids in causing the unique differences in PPD.

1.4 Brain-Derived Neurotopic Factor

In general, maternal brain-derived neurotropic factor (BDNF) levels are lower than those for non-pregnant women.[21] BDNF has been implicated in MDD. Similarly, serum BDNF levels have been found to be inversely related to scores on depression indices for PPD[22], indicating higher levels of depressive symptomology. These lower levels of BDNF can persist even two months postpartum.[21]

2.0 Effects on infant-maternal attachment and child development

Post-partum depression is reflected in changes in typical maternal behaviour. However, such behaviour is crucial for the creation of a bond between mother and infant, which is important for the proper development of the child. Depressed mothers are often found to exhibit two of the more negative parenting styles: intrusive, controlling and over-stimulating, or withdrawn, passive and under-stimulating.[22] Moreover, even the way depressed mothers touch their infants is different, tending to do it less frequently and less affectionately.[23] Often their touches are more negative, a term used to characterize rougher forms of poking, tickling, shaking, or pulling on the infant’s limbs.[23] Evidently there is a connection between the depressed state of the mother and how she then interacts with her child.

PPD and Developmental Delay
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Figure 2.[25] Scatterplot of developmental delay as it relates to
maternal-fetal attachment and maternal attachment style. Infants
were significantly more likely to be delayed in development if their
mothers rated low maternal-fetal attachment during pregnancy and
if they exhibited an avoidant attachment style.

Infants of depressed mothers have been found to show greater negative affect in response to sad stimuli, and during mother-infant interaction in something like a game of peek-a-boo.[24] Moreover, they had a shorter delay before they would start crying when the mother left the room, and their cries were of higher intensity, often involving more screaming or hyperventilating. This suggests that they react more to stress, and are less able to regulate their arousal; perhaps it is a shortcoming of the mother’s help in developing this ability. EEGs of these infants also revealed greater power in the left frontal lobe, which was consistent with results found in previous studies of depressed adults and infants of depressed mothers, as well as studies of depressed individual’s brains using different imaging technology.[24] This asymmetry was found during baseline as well, suggesting that this negative affect may be more of a general trait. A longitudinal study looked at the relationship between maternal-fetal attachment, a measure of the emotional connection a mother has to her unborn child, post-partum depression, and infant outcomes.[25] It confirmed findings like the one above, where post-partum depression was associated with avoidant and anxious maternal styles. Further, lower maternal-fetal attachment scores were also associated with these maternal styles, which suggests that maternal-fetal attachment is part of the greater maternal attachment style, including postpartum, in such a way that the connection the mother develops with the unborn child later manifests in her behaviour, which we then use to measure attachment. A crucial finding was that lower maternal-infant attachment predicted delayed development of the child, and that attachment avoidance and anxiety, as well as PPD symptoms, all correlated with delayed development (see Figure 2). This demonstrates the crucial link between maternal style and infant development, and also makes an argument for why treating PPD is so important. Measures like the maternal-fetal attachment also provide a possible mechanism for assessing the mother’s psychological state during pregnancy, which allows doctors to identify the high-risk mothers for PPD and certain maternal styles, allowing them to start intervention early to avoid developmental delays for the child. Many psychological treatments for PPD focus on improving the mother-infant bond.

The negative effects on the child’s development persist well into adolescence. First off, mothers with PPD were found to experience more depression, past the initial episode post-partum, well into the child’s adolescent years.[26] One study videotaped mothers, both who had suffered PPD and who had not, interacting with their children at ages five and eight in typical family environments like getting snack or helping with homework.[26] Researchers coded the mother’s utterances for how much they offered cognitive support; it was found that mothers who had PPD commonly had difficulties providing such cognitive support. This longitudinal study also had the children fill out a test for academic performance at age sixteen, to measure more long-term effects. They found that boys whose mothers offered low cognitive support at ages five and eight, which was significantly more common in mothers with PPD, performed poorer on these tests. The same effect was not found for girls. Thus the effects of PPD on the child last well beyond infancy, which emphasizes the importance of its treatment.

3.0 Treatment

3.1 Anti-Depressants

As it is a form of depression, it should come as no surprise that anti-depressants are the usual treatment for PPD. Selective serotonin reuptake inhibitors (SSRIs) have been found to be a valid and efficacious treatment for PPD in many studies, especially in the acute phase.[27],[28] Despite this, mothers and physicians alike are often hesitant to treat using SSRIs because they have been shown to cross the placenta as well as into breast milk.[29] Neonates and young infants are especially vulnerable to drugs they are exposed to through breast milk because of their underdeveloped blood-brain barrier. However, the only adverse effects on infant health that have been reported have been individual cases and have included changes in sleep patterns, gastrointestinal problems, respiratory problems and seizures.[2] These sorts of cases have not been confirmed to necessarily be caused by the antidepressants because there is no established association between adverse effects and increased level of drug in the infant’s blood. Not all SSRIs are created equal; to be on the safe side, mothers should generally be prescribed SSRIs with lower clearance into breast milk, like sertraline and paroxetine.[2] Perhaps mothers should aim to breastfeed just before taking their medication, such that the dose in their milk is the lowest.[28] It has been argued that the detrimental effects of PPD on both mother and infant outweigh the risks posed by SSRI passage into the newborn’s system, which still remain widely unknown.[2]

3.2 Psychological Treatment

Psychological treatment has also been found to greatly benefit mothers with PPD.[2],[28]-[30] These interventions can focus on a range of issues, from the mother’s mood, to attachment to the infant, to feelings towards and relationship with the infant. While focusing on the mother’s mood will alleviate her symptoms, this will not prevent the negative developmental consequences in the child that are associated with PPD.[30] Therapy should also help the mother establish a link between her own childhood experience and conflicts and her current concerns about her parenting; guiding her through this insightful activity can promote more competent mothering styles. It has even been found that medication along with psychological treatment was not significantly better at treating PPD than psychological treatment on its own, suggesting that stand-alone psychotherapeutic methods can also be effective.[30]

1. Gaynes BN, United States. Agency for Healthcare Research and Quality, Research Triangle Institute-University of North Carolina Evidence-based Practice Center. Perinatal Depression: Prevalence, Screening Accuracy, and Screening Outcomes. Evidence Report/Technology Assessment No. 119 (2005).
2. Fitelson E, Kim S, Baker AS, Leight K. Treatment of postpartum depression: clinical, psychological and pharmacological options. International Journal of Women’s Health (2011) 3:1-14.
3. Baker, L, et al. Prevalence of Postpartum Depression in a Native American Population. Matern Child Healt J (2005). 9(1):21-25.
4. Conroy, S., et al. Maternal Psychopathology and Infant Development at 18 Months: The Impact of Maternal Personality Disorder and Depression. J Am Acad Child Psy. (2012) 51(1):51-61.
5. Milgrom J, Gemmill AW, Bilszta JL, et al. Antenatal risk factors for postnatal depression: a large prospective study. J Affect Disord. (2008) 108(1–2):147–157.
6. Min Y, Ghebremeskel K, Crawford MA, et al. Pregnancy reduces arachidonic and decosahexaenoic in plasma triacylglycerols of Korean women. Int J Vitam Nutr Res. (2000) 70:70–75.
7. da Rocha CMM, Kac G. High dietary ratio of omega-6 to omega-3 polyunsaturated acids during pregnancy and prevalence of post-partum depression. Matern Child Nutr. (2010) 8:36-48.
8. Sontrop J, Avison WR, Evers SE, et al. Depressive symptoms during pregnancy in relation to fish consumption and intake of n-3 polyunsaturated fatty acids. Paediatr Perinat Ep. (2008) 22:389-399.
9. Golding J, Steer C, Emmett P, et al. High Levels of Depressive Symptoms in Pregnancy With Low Omega-3 Fatty Acid Intake From Fish. Epidemiology. (2009) 20(4):598-603.
10. Hibbeln JR. Seafood consumption, the DHA content of mothers' milk and prevalence rates of postpartum depression: a cross-national, ecological analysis. J Affect Disord. (2002) 69:15–29.
11. Doornbos B, van Goor SA, Dijck-Brouwer DAJ, et al. Supplementation of a low dose of DHA or DHA+AA does not prevent peripartum depressive symptoms in a small population based sample. Prog Neuro-Psychoph. (2009) 33:49-52.
12. Freeman MP, Hibbelin JR, Wisner KL et al. Randomized dose-ranging pilot trial of omega-3 fatty acids for postnatal depression. Acta Psychiatr Scand. (2006) 113:31-35.
13. Kendrick, K.M. Oxytocin, motherhood and bonding. Exp Physiol. (2000) 85:111S–124S.
14. Jonas W, Mileva-Seitz V, Girard AW, et al. Genetic variation in oxytocin rs2740210 and early adversity associated with postpartum depression and breastfeeding duration. Genes Brain Behav. (2013) 12:681-694.
15. Mileva-Seitz V, Steiner M, Atkinson L, et al. Interaction between Oxytocin Genotypes and Early Experience Predicts Quality of Mothering and Postpartum Mood. PLoS ONE (2013) 8(4):e61443.
16. Skrundz M, Bolten M, Nast I, et al. Plasma Oxytocin Concentration during Pregnancy is associated with Development of Postpartum Depression. Neuropsychopharmacol. (2011) 36:1886-1893.
17. Labuschagne I, Phan KL, Wood A, et al. Oxytocin attenuates amygdala reactivity to fear in generalized social anxiety disorder. Neuropsychopharmacol. (2010) 35:2403–2413.
18. Kim S, Soeken TA, Cromer SJ, et al. Oxytocin and postpartum depression: Delivering on what's known and what's not. Brain Res. (2013): 1-14.
19. Mah BL, Van IJzendoorn MH, Smith R, Bakermans-Kranenburg MJ. Oxytocin in postnatally depressed mothers: Its influence on mood and expressed emotion. Prog Neuro-Psychoph. (2013) 40:267-272.
20. Deligiannidis KM, Sikoglu EM, Shaffer SA, et al. GABAergic neuroactive steroids and resting-state functional connectivity in postpartum depression: A preliminary study. J Psychiat Res. (2013) 47:816-828.
21. Lommatzsch M, Hornych K, Zingler C, et al. Maternal serum concentrations of BDNF and depression in the perinatal period. Psychoneuroendocrino. (2006) 31:388-394.
22. Gazal M, Motta LS, Wiener CD, et al. Brain-Derived Neurotrophic Factor in Post-Partum Depressive Mothers. Neurochem Res. (2012) 37:583-587.
23. Malphurs JE, Raag T, Field T, et al. Touch by intrusive and withdrawn mothers with depressive symptoms. Early Dev Parenting. (1996) 5:111–115.
24. Jones NA. EEG during different emotions in 10-month-old infants of depressed mothers. J Reprod Infant Psyc. (2001). 19(4):295-312.
25. Alhusen JL, Hayat MJ, Gross D. A longitudinal study of maternal attachment and infant developmental outcomes. Arch Womens Ment Health. (2013) 16:521-529.
26. Murray L, Arteche A, Fearon P, et al. The effects of maternal postnatal depression and child sex on academic performance at age 16 years: a developmental approach. J Child Psychol Psyc. (2010) 51(10):1150-1159.
27. De Crescenzo F, Perelli F, Armando M, Vicari S. Selective serotonin reuptake inhibitors (SSRIs) for post-partum depression (PPD): A systematic review of randomized clinical trials. J Affect Disorders. (2014) 152-154:39-44.
28. Eberhard-Gran M, Eskild A, Opjordsmoen S. Use of psychotropic medications in treating mood disorders during lactation: practical recommendations. CNS Drugs. (2006) 20(3):187-198.
29. Canadian Paediatric Society. Maternal depression and child development. Paediatric Child Health. (2004) 9:575–83.
30. Thompson KS, Fox JE. Post-partum depression a comprehensive approach to evaluation and treatment. Mental Health in Family Medicine. (2010) 7:249-257.

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