The relatively high prevalence and duration of depression in the prenatal and postpartum periods reinforce the need for better understanding of maternal depression. The purpose of this article is to explore the main effects of depression to pregnancies' outcome and to early attachment reviewing research from the last decade and to find the best way to prevent the negative effects of maternal depression to infants. Recent studies have reported significant associations between maternal depression and several adverse obstetric, fetal, and neonatal outcomes. Antenatal depression has been associated with shorter gestation and lower birth weight, with consequences for infant development. A number of studies have demonstrated an association between prenatal depression and attachment difficulties, which seems to play an important mediating role in the development of further adverse outcomes for children. This review reveals some potential risks of untreated depression during the antenatal and postnatal periods, with possibly significant implications for practice and further research. Considering the high prevalence of depression, antenatal detection of depressive symptoms and intervention before childbirth has huge importance in prevention. Early interventions also may need to focus on mother-infant interactions as a key factor of later child development.

Cardiac autonomic balance (CAB) indexes the ratio of parasympathetic to sympathetic activation (Berntson, Norman, Hawkley, & Cacioppo, 2008), and is believed to reflect overall autonomic flexibility in the face of environmental challenges. However, CAB has not been examined in depression. We examined changes in CAB and other physiological variables in 179 youth with a history of juvenile onset depression (JOD) and 161 healthy controls, in response to two psychological (unsolvable puzzle, sad film) and two physical (handgrip, and forehead cold pressor) challenges. In repeated measures analyses, controls showed expected reductions in CAB for both the handgrip and unsolvable puzzle, reflecting a shift to sympathetic relative to parasympathetic activation. By contrast, JOD youth showed increased CAB from baseline for both tasks (ps<.05). No effects were found for the forehead cold pressor or sad film tasks, suggesting that CAB differences may arise under conditions requiring greater attentional control or sustained effort.

Affect regulation skills develop in the context of the family environment, wherein youths are influenced by their parents', and possibly their siblings’, regulatory responses and styles. Regulatory responses to sadness (mood repair) that exacerbate or prolong dysphoria (maladaptive mood repair) may represent one way in which depression is transmitted within families. We examined self-reported adaptive and maladaptive mood repair responses across cognitive, social, and behavioral domains in Hungarian 11–19 year old youth and their parents. Offspring included 214 probands with a history of childhood-onset depressive disorder, 200 never depressed siblings, and 161 control peers. Probands reported the most problematic mood repair responses, with siblings reporting more modest differences from controls. Mood repair responses of parents and their offspring, as well as within sib-pairs, were related, although results differed as a function of the regulatory response domain. Results demonstrate familiality of maladaptive and adaptive mood repair responses in multiple samples. These familial associations suggest that relationships with parents and siblings within families may impact the development of affect regulation in youth.

The findings have potential implications for our understanding of the impact of maternal depressive and anxiety symptoms on the developing mother-infant relationship.

There is increasing evidence that anxiety occurs frequently during pregnancy and can be one of the most important risk factors and predictors of postpartum depression (PPD). The aim of our study was to investigate whether antenatal anxiety is an independent predictor of PPD. We used the data of 476 women enrolled in a prospective study in a single maternity unit. The first assessment was conducted between 22 and 40 weeks gestation and a second time 8-12 months postpartum. Symptoms were measured using the Edinburgh Postnatal Depression Scale (EPDS) and the State Trait Anxiety Inventory (STAI). Based on our results, antenatal anxiety measured by a subscale of EPDS has predicted better PPD than the antenatal depressive subscale. However, the most relevant predictor of PPD might be the trait anxiety level of a women measured by STAI Trait Scale, whereas a cutoff value of 38 was identified to indicate higher risk of PPD.