The association between pregnancy intention, fertility treatment use, and postpartum depression.

RATIONALE: Understanding whether postpartum depressive (PPD) symptoms vary by pregnancy intention and use of fertility treatments has implications for reproductive health policies and practices. OBJECTIVE: The first aim of this study was to determine whether PPD symptoms differ between women who had unintended pregnancies, women who conceived spontaneously and were unsure about their pregnancy intention, women who used fertility treatments to conceive, and women who conceived spontaneously and intentionally. The second aim was to determine whether PPD symptoms differed based on the fertility treatment used to conceive (fertility drugs only, medicated insemination, or assisted reproductive technology [ART]). METHODS: Data from the Pregnancy Risk Assessment Monitoring System (2012-2019), a cross-sectional survey administered to women throughout the U.S. who have recently given birth, was used to carry out our aims. RESULTS: For the first aim (unweighted N = 243,677), compared to women who had spontaneous, intended pregnancies, women who had unintended pregnancies (OR: 1.32, 95% CI: 1.26-1.39, p < 0.01) and those with spontaneous pregnancies who were unsure about their intention (OR: 1.30, 95% CI: 1.23-1.38, p < 0.01) had higher odds of elevated PPD symptoms, adjusting for a range of covariates. Women who conceived with fertility treatments did not have higher odds of elevated PPD symptoms (OR: 0.97, 95% CI: 0.84-1.10, p = 0.61). For the second aim (unweighted N = 2,210), compared to those in the ART group, those who conceived using only fertility enhancing drugs had greater odds of developing elevated PPD symptoms (OR: 2.00, 95% CI: 1.24-3.24, p < 0.01). CONCLUSIONS: These findings suggest that giving birth to an unintended pregnancy in the U.S. increases risk of elevated PPD symptoms. While overall women who conceive with the use of fertility treatments are not at increased risk of experiencing elevated PPD symptoms, there may be variability in risk based on the specific fertility treatments used.

Smoking status: A tacit screen for postpartum depression in primary care settings.

BACKGROUND: Universal screening for postpartum depression (PPD) remains an unachieved national priority. A tacit screen that requires no additional resources for administration can help to achieve this priority. We examine the predictive utility of using smoking as a tacit screen for PDD. We first establish smoking is a valid proxy for more prominent psychosocial determinants of PPD and is a predictor for PPD. METHODS: We analyzed PRAMS data (2012-2015; N=134,435). Time of smoking was categorized as nonsmoker, during the prenatal period, the postpartum, or continuously; PPD was assessed using two PHQ-2 style questions. RESULTS: Compared to nonsmokers, women who smoked only during the prenatal period (OR: 1.41; 95% CI: 1.06 - 1.86), only during the postpartum (OR: 1.33; 95% CI: 1.18 - 1.49), and continuously throughout both periods (OR: 1.54; 95% CI: 1.41 - 1.69) were more likely to experience PPD. Smoking assessed at a prenatal visit (SN: 0.90, SP: 0.21), postpartum visit (SN: 0.86, SP: 0.25), or assessed at both visits (SN: 0.90, SP: 0.19) performed relatively well as a tacit screen for PPD, performing better among unmarried women (SN: 0.75 - 0.81; SP: 0.29 - 0.36). LIMITATIONS: In this study, the criterion of positivity used was PRAMS' adapted version of the PHQ-2. This tacit screen may perform differently relative to a clinical diagnosis. CONCLUSIONS: Time of smoking predicts risk of PPD and can be used to tacitly screen for PPD with reasonable accuracy without requiring any additional time in settings with limited resources for routine screening of PPD.

Evidence supporting a role for astrocytes in the regulation of cognitive flexibility and neuronal oscillations through the Ca2+ binding protein S100ß.

The medial prefrontal cortex (mPFC) is important for cognitive flexibility, the ability to switch between two task-relevant dimensions. Changes in neuronal oscillations and alterations in the coupling across frequency ranges have been correlated with attention and cognitive flexibility. Here we show that astrocytes in the mPFC of adult male Sprague Dawley rats, participate in cognitive flexibility through the astrocyte-specific Ca2+ binding protein S100ß, which improves cognitive flexibility and increases phase amplitude coupling between theta and gamma oscillations. We further show that reduction of astrocyte number in the mPFC impairs cognitive flexibility and diminishes delta, alpha and gamma power. Conversely, chemogenetic activation of astrocytic intracellular Ca2+ signaling in the mPFC enhances cognitive flexibility, while inactivation of endogenous S100ß among chemogenetically activated astrocytes in the mPFC prevents this improvement. Collectively, our work suggests that astrocytes make important contributions to cognitive flexibility and that they do so by releasing a Ca2+ binding protein which in turn enhances coordinated neuronal oscillations.