Three decades of research point to both biological and psychological risk

Three decades of research point to both biological and psychological risk factors for postpartum depression but very little research integrates the two. suggest that social and biological risk factors for postpartum depressive symptoms are intertwined and move us closer to an Palifosfamide integrated biopsychosocial understanding of postpartum depression. (Harris et al. 1994 O’Hara Schlechte Lewis & Wright 1991 O’Hara Zekoski Philipps & Palifosfamide Wright 1990 Okano & Nomura 1992 Pitt 1973 Approximately one in five women will experience a depressive show within the 1st year after birth (Gaynes et al. 2005 with the majority of cases happening within the initial 12 weeks after delivery (O’Hara & Swain 1996 Major depression and postpartum major depression are not regarded as distinct disorders from the fourth edition of the = ?0.30; O’Hara & Swain 1996 Controlled longitudinal studies possess documented for example that women who have smaller social networks or Corin who statement poor support from family or the baby’s father during pregnancy are more likely to develop postpartum major depression (Collins Dunkel-Schetter Lobel & Scrimshaw 1993 Logsdon & McBride 1994 Although interpersonal support comes in many forms perceived support-defined as the subjective feeling that the first is cherished and cared for and can count on others when in need-may become especially protecting against maternal major depression (Ramona & Ferketich 1988 One pathway through which perceived support protects against major depression is its part in mitigating the effects of stress (Cohen & Wills 1985 For example a multiethnic study of 192 mothers found that low-income ladies who reported relatively more perceived support from your baby’s father also reported less panic about their pregnancies and less overall stress and were less likely to have depressive symptoms postpartum (Norbeck & Anderson 1989 Sociable support has also been shown to dampen biological stress reactions in the nonpregnant state (observe Uchino Cacioppo & Kiecolt-Glaser 1996 for a review). A search of the literature produced no investigations screening whether interpersonal support is linked to lower stress hormone levels during pregnancy. Extension of this study to pregnancy could provide a important link between psychosocial theories of postpartum major depression involving the central part of interpersonal support and biological research implicating stress hormone exposure in pregnancy. Depressive disorders have been conceptualized as including dysregulation of the body’s stress response systems such that affective and biological stress responses happen in disproportion to events or persist for prolonged periods resulting Palifosfamide in negative feeling cognitive troubles heightened panic and physiological dysregulation (Ehlert et al. 2001 Pariante & Lightman 2008 This profile implicates involvement of the hypothalamic-pituitary-adrenal (HPA) axis a complex biological system that activates under stress exposure and enables the organism to meet the demands of the Palifosfamide stressor by increasing energy and vigilance toward potential threats. The release of corticotropin-releasing hormone (CRH) from the hypothalamus starts the HPA axis cascade and triggers the release of adrenocorticotropic hormone (ACTH) from the pituitary into the peripheral bloodstream. In turn the release of ACTH triggers cortisol to be released from the adrenal glands into the bloodstream. Cortisol adjusts its own further activity through a negative feedback system downregulating the HPA axis response by inhibiting the production of CRH in the hypothalamus and ACTH in the pituitary (S. M. Smith & Vale 2006 If the HPA axis is usually activated too often or too acutely this system can become dysregulated in the sense that it resists returning to homeostasis (for reviews see McEwen 1998 Nestler et al. 2002 Many people with depressive disorder show evidence of dysregulated HPA axis activity that remits with treatment (Arborelius Owens Plotsky & Nemeroff 1999 Gold Licinio Wong & Chrousos 1995; Holsboer 2001 Depressive says have also been linked to elevated levels of CRH in the brain (Arborelius et al. 1999 Holsboer 2001 Kasckow Baker & Geracioti 2001 Studies with rodents and primates highlight the striking parallels between symptoms of severe depressive Palifosfamide disorder and the effects of centrally administered CRH. These include increased stress and fearfulness decreased appetite decreased sexual behavior and increased heart rate and blood pressure Palifosfamide (Arborelius et al. 1999 Chrousos Torpy & Gold.