Understanding Postpartum Depression — BrainPost | Easy-to-read summaries of the latest neuroscience publications

Post by Lani Cupo

In many communities worldwide, childbirth is celebrated as a joyous time. Despite new stressors and nights without sleep, many parents welcome their new child enthusiastically. For almost 20% of people who give birth, however, symptoms of anxiety and depression may occur during the postpartum period. This under-reported experience can bring feelings of confusion and shame to new parents.

What is PPD and what are the risk factors?

According to the Diagnostic and Statistical Manual used by psychiatrists to guide diagnoses, postpartum depression (PPD) refers to the onset of a depressive episode within four weeks of childbirth. Many researchers and clinicians extend this diagnostic window up to a year after giving birth. Physical, hormonal, social, psychological, and emotional factors can all play an important role in triggering PPD. This is referred to as the biopsychosocial model of depression.

So, what are the strongest risk factors for PPD? Evaluating findings from many studies via meta-analysis, researchers have identified potential risk factors: depression and anxiety during pregnancy, acute sadness during the days following birth (“postpartum blues”), previous history of depression, stressful life events, poor marital relationship, and poor social support. The context of PPD resembles the context of many other depressions, and there is still debate whether PPD is catalyzed by a factor unique to birth, or simply coincidence of childbirth and depression onset. As we move towards regular screening for PPD following childbirth, and identifying high-risk individuals, some have voiced criticism regarding the potential to over-pathologize mood symptoms and overestimate an individual’s risk of PPD.

What’s the underlying biology of PPD?

Since more severe postpartum blues correlates strongly with the emergence of PPD, many researchers have begun to consider symptoms on a spectrum from “blues” to more severe psychiatric outcomes, such as PPD or postpartum psychoses. The predominant hypothesis underlying postpartum blues posits that mood changes result from abrupt hormone withdrawal following birth. In more severe cases of PPD, however, it is likely that other factors play a role in the emotional disturbances experienced after pregnancy. Several hormones rise over the course of pregnancy, including estradiol, a major female sex hormone; progesterone, a steroid hormone involved in menstruation, pregnancy, and embryogenesis; estriol, a minor female sex hormone almost undetectable outside of pregnancy; and estrone, a minor female sex hormone. Research has shown that there is a heightened sensitivity to mood changes in response to these hormonal fluctuations.

A variety of neurochemical changes in the brain have been associated with PPD, in particular to the monoamine system, a key system involved in mood regulation. Levels of MAO-A, an enzyme that metabolizes monoamines like serotonin and norepinephrine, have been shown to be elevated in PPD, suggesting this could be a cause of lower monoamine levels and low mood. Further, research shows that the level of serotonin receptors in the brain is also lower in individuals with PPD, meaning there could be a lower activity of the serotonergic system in PPD. Very few magnetic resonance imaging (MRI) studies investigate the impact of PPD on brain volume, activity, and metabolism, largely due to the difficult nature of recruiting participants soon after delivery. Studies that do investigate PPD with MRI usually demonstrate similarities between PPD and major depressive disorder (MDD) in terms of brain structural changes.

What’s the impact on parent and child?

PPD outcomes can be measured in terms of the parent, the child, and their relationship. For parents, PPD can lower mood and self-esteem, increase anxiety, and impact physical health. Further, PPD has been shown to increase risk of suicide, highlighting the urgent need for treatment for PPD. For infants, there is some evidence that PPD is associated with reduced weight gain, though findings are mixed. Accumulating evidence also associates PPD with diverse infant health concerns, such as overall pain, disrupted sleep, delays in cognitive and language development, increased fear and anxiety, and increased behavioral problems. Finally, examining infant-parent relationships, PPD is correlated with poor parent-infant bonding in the first months of life, lower emotional involvement, insecure attachment, early cessation of breast-feeding, and alterations in maternal behavior. It is important to note, however, that many of the aforementioned studies are purely associative and do not represent causal relationships between PPD and negative outcomes. Future research should be mindful of the criticism many parents already experience, so as not to unintentionally contribute to the stigmatization of parents’ involuntary experience of PPD.

How do we treat PPD?

There are several treatments for PPD that may be effective. Short-term interpersonal psychotherapy can help reduce depressive symptoms. Antidepressant treatments like SSRIs (influencing the serotonin system) have shown promise in treating PPD, with some research reporting remission and no negative outcomes in children. Nevertheless, there is a growing database of observational data on the side effects of antidepressants in breast-fed infants. Dietary supplements consisting of monoamine precursors (to combat elevated MAO-A enzyme levels) have also demonstrated potential in reducing depressive symptoms in PPD. Risk from PPD must be weighed against risk of possible infant exposure to pharmaceuticals and the benefit conferred by breast-feeding, often an important bonding opportunity for the parent and infant. As clinicians, researchers, and parents become increasingly aware of PPD, the development of advanced screening tools and reduction of stigma around symptomatology may allow for earlier treatment. Together, parents and doctors can develop a plan that best suits their individual needs.

References +

Schiller CE et al. Estradiol modulates anhedonia and behavioral despair in rats and negative affect in a subgroup of women at high risk for postpartum depression. Physiol Behav. 2013. 119: 137–144.

Wang T et al. Injection of oxytocin into paraventricular nucleus reverses depressive-like behaviors in the postpartum depression rat model. Behav Brain Res. 2018. 336: 236–243.

Slomian J et al.. Consequences of maternal postpartum depression: A systematic review of maternal and infant outcomes. Womens Health. 2019.15: 1745506519844044.

Sacher et al. Relationship of Monoamine Oxidase-A Distribution Volume to Postpartum Depression and Postpartum Crying. Neuropsychopharmachology. 2015: 40, 429–435.

Fiorelli M et al. Magnetic Resonance Imaging Studies of Postpartum Depression: An Overview. Behav Neurol. 2015. 2015: 913843.

Zonana J, Gorman JM. The Neurobiology of Postpartum Depression. CNS Spectr. 2005.10: 792–9, 805.

Duan C et al.. Understanding Peripartum Depression Through Neuroimaging: a Review of Structural and Functional Connectivity and Molecular Imaging Research. Curr Psychiatry Rep. 2017.19: 70.

Dowlati et al. Selective dietary supplementation in early postpartum is associated with high resilience against depressed mood. PNAS. 2017. 114(13)3509-3514.

Moses-Kolko et al. Serotonin 1A receptor reductions in postpartum depression: a PET study. Fertility and Sterility. 2008. 89(3): 685-692.