Is peripartum depression just another depression?

Depressive symptoms in pregnancy are common, reported by approximately 20% of pregnant women worldwide. Of these, around 4-7% fulfill the criteria for major depressive episode (MDE). The prevalence rates of MDE seem no different from those in non-pregnant women of childbearing ages, or may even be lower. Further, the clinical presentation of depressive symptoms in women of childbearing age does not differ depending on whether women are pregnant, postpartum or outside the peripartum period. For this reason, some researchers argue that peripartum depression is just another depression, merely occurring at a stressful point in life. Antenatal depression and antidepressant treatment have been associated with an increased risk of poor pregnancy outcomes, such as preterm birth, impaired placental function, decreased fetal body and head growth. Nevertheless, little is known about the biological mechanisms behind these complications and more research is needed to elucidate the underlying pathways. In this thesis we have studied 1) attentional bias in antenatal and postpartum depression, with or without antidepressant treatment and 2) peripheral inflammatory markers in pregnancy (depressed, SSRI-treated, healthy controls). The title for this thesis is: Is peripartum depression just another depression? Based on the findings we have obtained thus far, the answer would be no. One argument would be that, as presented in study I, women who suffer from antenatal and postpartum depression do not display the typical attentional bias to negative words that is characteristic of depressive states in the non-pregnant population. Whether this is due to protective mechanisms of pregnancy or due to features that distinguish antenatal and postpartum depression from non-peripartum depression remains to be demonstrated. Secondly, study II describes that women with antenatal depression had significantly lower levels of peripheral inflammatory markers than healthy pregnant controls. Hypothetically, this could be due to dysregulated switch to the antiinflammatory pro-M2 milieu that characterizes normal third trimester pregnancy. These findings are clearly at odds with the literature in non-pregnant samples, where depression has been associated with increased levels of proinflammatory cytokines, but should be interpreted in the context of pregnancy-induced changes in inflammatory response. Moreover, treatment for antenatal depression is not as straightforward as it is in non-pregnant patients. When considering treatment, the expecting mother has to be aware of the risk-benefit profile for herself and the child. While antidepressant therapy clearly improves the mood of treated women, our findings do not indicate that antidepressant treatment has any positive impact on their inflammatory profile