Biological Stress Response in Women at Risk of Postpartum Psychosis

Biological stress response in women at risk of postpartum psychosis: The role of life events and inflammation

Postpartum psychosis (PP), the most severe postpartum psychiatric disorder, has various risk factors that could increase one’s susceptibility to developing the illness. This 2019 study examined whether abnormalities in biological stress responses were a risk factor for postpartum psychosis (PP), given that such abnormalities in stress responses are typically associated with psychosis unrelated with the puerperium. While assessing the risk factors for PP is difficult due to the rarity of the illness, it is imperative that further research is done on these risk factors so that clinicians can better understand different patients’ vulnerabilities to PP.

This study had 56 subjects: 30 postpartum women (14 currently experiencing an episode of PP and 16 at-risk of PP due to a history of bipolar/schizoaffective disorders) and 26 healthy women. Information regarding the subjects’ recent stressful life events was obtained through a List of Threatening Experiences questionnaire, which identified stressful experiences regarding illness and injury, deaths of close friends and family, unemployment, etc. Then, perceived stress was determined using the Perceived Stress Scale. Women with PP and women at-risk for PP had comparable reports on their stressful life events and perceived stress levels, though healthy women reported much fewer stressful life events as well as lower perceived stress levels.

In addition to perceived stress, researchers also estimated the biological stress responses in the subjects by measuring their salivary cortisol. Salivary cortisol is the hormone present in saliva that is released in response to stress, and levels of cortisol can be used to estimate the hypothalamic-pituitary adrenal (HPA) activity in each of the subjects. HPA activity is also a biological indicator of stress, and researchers hypothesized that women with, or at-risk for PP would demonstrate greater HPA activity than healthy women as a result of more stressful life experiences. Salivary cortisol was measured both at awakening (15, 30, and 60 min after awakening) and at specific times throughout the day. Furthermore, as immune system dysfunction is also implicated in psychotic disorders, different immune biomarkers were evaluated from subjects’ blood samples to assess their vulnerabilities to PP.

Ultimately, results show that in comparison to healthy controls, women with PP presented more recurrent stressful life events, higher perceived stress, and higher levels of cortisol throughout the day. These findings go hand-in-hand with the idea that women with PP display immune-HPA hyperactivity, suggesting that they physiologically experience more intense stress than healthy women and that stress may be an underlying causal factor involved in the onset of PP. Also, women with more severe psychosis symptoms demonstrated higher perceived stress and cortisol levels than women with less severe PP, further supporting the role of stress as a risk factor associated with PP. The stress and immune response values of the 16 women at-risk for PP fell in between those of women currently with PP and healthy women, potentially due to their histories with mental disorders. Overall, the heightened stress levels measured through the questionnaire and the biomarkers largely account for the variance in the risk of developing PP: 78% of the variance in group status between women with PP and healthy women and 46% of variance of in group status between women at-risk for PP and healthy women. Understanding these findings, it is highly likely that both current stress from threatening life events, as well as dysregulation of the HPA axis and immune system present a biological predisposition to psychosis in the puerperium.

Limitations: This study has several limitations. Given that the study’s results were based on only 56 women in total, it is extremely difficult to draw such broad conclusions and apply them to the entire population of women with PP. Further research on the association between stress levels and PP must be done on a larger scale for such implications to confidently be made. Another limitation faced is that the salivary cortisol of subjects was measured on a single day, making it difficult for researchers to assume causality between stress and PP. However, the authors note that two-day collection of cortisol yielded extremely similar results to their one-day method. Also, socio-economic factors were not accounted for in this study, and these factors could potentially influence the stress responses and perceived stress levels of these women. Lastly, a major limitation of the study is that the women with PP were 20 weeks into their postpartum period, while the women at-risk for PP and the healthy controls were 12 and 13 weeks in, respectively. The fact that women with PP were farther along in their postpartum period is significant because immune and cortisol responses as well as HPA activity are in a suppressed state following pregnancy for about 12 weeks. This suggests that the relatively longer period between child delivery and assessment of stress levels in women with PP could account for their higher cortisol levels compared to at-risk and control subjects. Yet, the authors point out that results remained significant even when this lengthier interval was included as a covariate, meaning that these interval differences cannot entirely explain the associations found between stress levels and PP.

Conclusion: Despite these limitations, this study effectively pioneered the research on stress as a potential biological risk factor predating the onset of PP. The results offered initial evidence supporting the idea that current levels of stress as well as biomarkers of both stress and immune responses play a role in the pathophysiology of PP in this underrepresented clinical population. Only by further investigating the relationships between abnormalities in biological responses and the presence of PP can we discover more about this illness’ risk factors, and better understand different patients’ vulnerabilities and predispositions to postpartum psychosis.

Written by Dhiya Sani

Aas M, Vecchioa C, Paulsa A, Mehtaa A, Williamsa S, Hazelgrovea K, Biaggia A, Pawlbya S, Conroya S, Seneviratnea G, Mondellia V, Pariantea CM, Dazzana P. Biological stress response in women at risk of postpartum psychosis: The role of life events and inflammation. Elsevier Psychoneuroendocrinology. 2019 Dec 19.

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©2018 by Massachusetts General Hospital Postpartum Psychosis Project (MGHP3).