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Abstract
Purpose
The purpose of this review was to describe a psychoneuroimmunology (PNI) framework for postpartum depression (PPD) and discuss its implications for nursing research and practice for postpartum women.
Methods
This study explored the role of hypothalamic-pituitary-adrenal (HPA) axis and inflammation as possible mediators of risk factors for PPD through literature review.
Results
From this PNI view, human bodies are designed to respond with the reciprocal interactions among the neuro-endocrine and immune system when they are faced with physical or psychological stressors. Chronic stress induces alterations in the function of HPA axis, and a chronic low-grade inflammatory response is associated with depression. The dysfunctions of cytokines and HPA axis have been observed during the postpartum period. Stress promotes glucocorticoid receptor resistance, which can promote inflammatory responses. This, in turn, can contribute to the pathophysiology of depression. This can especially affect populations at vulnerable time-points, such as women in the postpartum.
Figures and Tables
Table 1
Summary of Review Articles regarding Impact of Hypothalamus-Pituitary-adrenal Axis Disturbance on Postpartum Depression
| Author | Subjects | Study variables | Measurement time | Main results | Significance |
|---|---|---|---|---|---|
| Glynn and Sandman (2014) [19] | 170 postpartum women | Maternal cortisol, ACTH, placental CRH concentration | 15, 19, 25, 31, 36 weeks' gestation; 3 and 6 month postpartum | Depressive symptoms at 3 month postpartum was related to elevated mid-gestational pCRH; pCRH was not predictive of PPD symptoms at 6 month. | Elevated pCRH is a marker of the risk for the development of PPD symptoms. |
| Depression measured by EPDS | |||||
| Jolley et al. (2007) [21] | 22 normal, healthy, non-depressed postpartum women | Maternal ACTH and cortisol; | 6 and 12 weeks postpartum before, during, and after 20 min. exercise | For non-depressed women: ↑ACTH, ↑cortisol; | HPA axis is dysregulated in the depressed group at 6 and 12 weeks postpartum. |
| Depression measured by postpartum depression screening scale | For depressed women: ↑ACTH, ↓cortisol | ||||
| Groer and Morgan (2007) [22] | 175 depressed and non-depressed women | Salivary cortisol; | Between 4~6 weeks postpartum | Depressed mothers had lower level of salivary cortisol concentration than non-depressed women. | PPD may be associated with a dysregulated HPA axis. |
| Depression measured by POMS -depression scale | |||||
| Taylor et al. (2009) [23] | 21 depressed and 30 non-depressed women, 21 non-perinatal controls | Salivary cortisol at waking, 30 min, and 3 and 12 hours postwaking | 7.5 weeks postpartum | Women with postpartum depressive symptoms: higher cortisol levels at waking and no increase at +30 min no cortisol awakening response. | In vulnerable women, it may reflect a response to the marked cortisol withdrawal that occurs after delivery. |
| Depression measured by EPDS | 4 weeks postpartum |
Table 2
Summary of Review Articles regarding Impact of Inflammation on Postpartum Depression
| Author | Subjects | Study variables | Measurement time | Main results | Significance |
|---|---|---|---|---|---|
| Groer and Morgan (2007) [22] | 175 depressed and non-depressed women | Salivary cortisol | Between 4~6 weeks postpartum | Depressed women had lower levels of IFN-γ, IFN-γ/IL-10 than non-depressed women | PPD may be associated with possible depressed cellular immunity. |
| Depression measured by POMS-depression scale | |||||
| Groer et al. (2015) [24] | 72 healthy postpartum women | A panel of cytokines from whole blood; plasma levels of hs-CRP, IL-2 | During 6 months postpartum | In early postpartum, IFN-γ, IL-2, and TNFα were low; plasma hsCRP and IL-2 were higher levels with changes by 3 months. | Return to normal cellular immune function may take 3~4 months in the postpartum. |
| Dysphoric mood by POMS total score | Dysphoric moods are higher in the early postpartum. | Dysphoric mood was not related to immune factors or hormones. | |||
| Corwin et al. (2008) [25] | 26 postpartum women | Interleukin-1 beta and Interleukin-6 in urine | Day 7, 14, and 28 postpartum | An increase in IL-1beta was seen on Day 14 in women with symptoms of depression on Day 28. | Elevated IL-1beta early in the postpartum period may increase the risk of PPD. |
| Depression measured by CES-D | Day 28 postpartum | ||||
| Boufidou et al. (2009) [26] | 56 postpartum women | TNFα and IL-6 from a blood sample (n=23) and a CSF sample (n=33) | At delivery | Cytokine levels were associated with depressive mood during the first four days postpartum (CSF IL-6, CSF TNFα, and serum TNFα) and at sixth week postpartum (CSF IL-6, CSF TNFα). | Immune mechanisms may play a role in the etiopathology of postpartum depressive mood shifts. |
| Depressive mood by Postpartum Blues Questionnaire | On admission and day 1~4 postpartum | ||||
| Postpartum Depressive symptoms by EPDS | first and sixth week postpartum | ||||
| Kondo et al. (2011) [27] | 139 lactating women | total TGF-β2 from breast milk | 3 months postpartum | Women with depression had higher TGF-β2 concentrations than mothers without depression. | Depression, as the consequence of psychosocial stress, may be a strong determinant of TGF-β levels in breast milk. |
| Fransson et al. (2012) [28] | 27 women delivering preterm and 37 mothers delivering at term | Blood samples from women in labor and cord samples (23 preterm and 33 term delivery) | At delivery | In the preterm group only, associations were found between negative emotions and maternal IL-6 and cord IL-6, IL-8, IL-10, and IL-13. | There are associations in preterm delivery between negative emotions and both maternal and neonate immune activity. |
| Positive/negative affect | Day 5 postpartum |
ACTH=adrenocorticotropic hormone; CRH=corticotrophin-releasing hormone; CSF=Cerebrospinal fluid; EPDS=Edinburgh Postnatal Depression Scale; HPA=hypothalamus-pituitary-adrenal; hs-CRP=high sensitivity C-reactive protein; IFN-γ=interferon-gamma; IL=Interleukin; POMS=Profile of Mood States; PPD=postpartum depression; TGF-β=Transforming growth factor-beta; TNFa=Tumor necrosis factor α
Summary Statement
▪ What is already known about this topic?
Research in the field of PNI has revealed that depression is associated with inflammation manifested by increased levels of pro-inflammatory cytokines because of chronic stress.
▪ What this paper adds?
This study reviewed articles about postpartum depression within the PNI perspective. We found that physical and psychological stressors increase inflammation.As inflammation process increases during postpartum period, the result of this review suggests that psychosocial, behavioral and physical stressors increase the risk for the development of postpartum depression.
▪ Implications for practice, education and/or policy
Nurses need to understand PNI perspective to identify the risk factors forpostpartum depression. According to the PNI perspective postpartum depression can be preventable by reducing maternal stress and inflammation. Careful nursing assessment is essential to evaluate the risk of postpartum depression during the postpartum period.
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