Oxytocin and postpartum depression: A systematic review

Postpartum depression (PPD) is a significant mental health concern, especially for women in vulnerable populations. Oxytocin (OT), a hormone essential for a variety of maternal tasks, including labor, lactation, and infant bonding, has also been hypothesized to have a role in postpartum depression. Women are routinely given synthetic oxytocin to induce or augment labor and to prevent postpartum hemorrhage. The aim of this study was to review the quality and reliability of literature that examines potential relationships between OT and PPD to determine if there is sufficient data to reliably assess the strength of these relationships. We conducted a literature search in December of 2018 using five databases (PubMed, Web of Science, Embase, PsycInfo, and CINAHL). Eligible studies were identified, selected, and appraised using the Newcastle-Ottawa quality assessment scale and Cochrane Collaboration's tool for assessing risk of bias, as appropriate. Sixteen studies were included in the analysis and broken into two categories: correlations of endogenous OT with PPD and administration of synthetic OT with PPD. Depressive symptoms were largely measured using the Edinburgh Postnatal Depression Scale. OT levels were predominately measured in plasma, though there were differences in laboratory methodology and control of confounders (primarily breast feeding). Of the twelve studies focused on endogenous oxytocin, eight studies suggested an inverse relationship between plasma OT levels and depressive symptoms. We are not able to draw any conclusions regarding the relationship between intravenous synthetic oxytocin and postpartum depression based on current evidence due to the heterogeneity and small number of studies (n = 4). Considering limitations of the current literature and the current clinical prevalence of synthetic OT administration, we strongly recommend that rigorous studies examining the effects of synthetic OT exposure on PPD should be performed as well as continued work in defining the relationship between endogenous OT and PPD.