Postpartum Depression
New Insights Into Postnatal Depression and Breastfeeding
How oxytocin may be disrupted in postnatal depression.
Posted May 18, 2025 Reviewed by Tyler Woods
Key points
- Oxytocin inhaled via a nasal spray increases breast milk oxytocin, but has less effect in depressed mothers.
- This suggests that in mothers experiencing postnatal depression the oxytocin system is affected.
- The findings have implications for new mothers experiencing postnatal depression and their child.
This article describes the recent findings from our lab at University College London, published in the journal Psychoneuroendocrinology. The study explored the relationship between postnatal depression and breastfeeding in new mothers, and the possible role of oxytocin in the breastfeeding challenges reported by mothers experiencing depression after childbirth.
What is the hormone oxytocin?
Oxytocin is popularly referred to as the "love hormone" as it increases intimate and romantic relationships. But its activity extends further than this. It is produced in the hypothalamus in the brain and connects with oxytocin receptors located in areas across the brain to regulate social communication, perspective-taking, emotional connection with others, and trust. It is therefore important in building relationships, and it is particularly active in mother-infant bonding.
Oxytocin also plays a role in social relationships by reducing anxiety and interacting with the dopaminergic reward system in the brain to increase a sense of pleasure and positive associations with cues, including specific individuals. It is therefore central in the attachment process between new mothers and their infants and is an important mechanism in promoting children’s early social development.
How oxytocin is involved in breastfeeding
In breastfeeding, oxytocin is further released from the brain into the body, where it plays an essential role, being responsible for the ‘let-down’ reflex that releases a mother’s milk. Oxytocin receptors located around the body are also stimulated in mothers and infants during breastfeeding by skin-to-skin touch and the infant suckling. These, in turn, activate sensory nerves that send messages back to the brain to release more oxytocin, in a feedback loop.
This involvement of oxytocin typically helps mothers and infants feel relaxed and connected with each other during breastfeeding, which encourages more breastfeeding, that promotes mother–-nfant bonding and the infant’s early development.
The impact of postnatal depression
In our study, we investigated the links between oxytocin, breastfeeding, and postnatal depression in new mothers. Postnatal depression occurs in approximately 20% of women in the year following childbirth. It can prompt feelings of disconnection from their baby, sadness, and anxiety, with a sense of loss.
Mothers experiencing postnatal depression often report increased stress during breastfeeding and difficulties with their milk let-down, which often leads to early weaning. However, it has been unclear why there is a link between postnatal depression and reduced breastfeeding, particularly considering that there are many mothers who may feel depressed and want to breastfeed but still encounter significant difficulties.
Previous research has indicated that postnatal depression may interfere with the oxytocin system, which we reasoned could make it more difficult for mothers who are experiencing depression to breastfeed. However, so far, the investigations in this area have been scarce.
The Study
To explore this relationship more deeply, we examined the brain-to-breastmilk oxytocin pathway in mothers with and without symptoms of postnatal depression, to test for any differences.
62 new mothers, aged between 23 and 44 years old and who had an infant aged between 3 and 9 months old, took part. All mothers were invited to use a nasal spray prior to breastfeeding which contained either the oxytocin hormone or a placebo. Breast milk samples were collected during breastfeeding.
Key Findings
Our study showed that the oxytocin nasal spray, which sends oxytocin directly into the brain, led to an increase in oxytocin levels detected in breast milk, confirming that oxytocin travels from the brain to the breast and plays a role in feeding.
However, the findings also revealed, for the first time, that there was a reduced effect of this in mothers experiencing postnatal depression, compared to mothers who were not depressed. This suggests that although oxytocin has a role in releasing breast milk and strengthening the mother–infant bond during breastfeeding, postnatal depression can interfere with this. A disruption in the oxytocin system may therefore make it more difficult for mothers experiencing postnatal depression to benefit from oxytocin during breastfeeding.
For example, mothers who have a reduced oxytocin response may find it difficult to bond with their baby. It may also exacerbate feelings of sadness or isolation in a mother’s mental health, and have an impact on the developing oxytocin system of her new baby as well. This could be one way in which mental health vulnerability may transfer from mothers to their children in cases of postnatal depression.
Steps to improving support
Our study offers a new insight as to why some mothers with postnatal depression may experience challenges with breastfeeding. By understanding the mechanisms underlying these challenges, new treatments can be developed to improve the effectiveness of the support that can be offered to new mothers.
For example, developing interventions that facilitate oxytocin release in new mothers experiencing postnatal depression might boost its positive effects in breastfeeding, and in mother-infant bonding more generally, during the perinatal period when it is crucial. These questions, stemming from the new results of our study, will be important to investigate further, to improve the care pathways for both new mothers and their children.
References
More information on this study can be found at:
https://www.sciencedirect.com/science/article/pii/S0306453025000976?via%3Dihub#sec0065