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Purpose: To describe trends, patterns, and determinants of prescription drug use during pregnancy and postpartum., Methods: This is a retrospective, population-based study of all women who gave birth between January 2002 and 31 December 2011 in British Columbia, Canada. Study population consisted of 225,973 women who had 322,219 pregnancies. We examined administrative datasets containing person-specific information on filled prescriptions, hospitalizations, and medical services. Main outcome measures were filled prescriptions during pregnancy and postpartum. We used logistic regressions to examine associations between prescription drug use and maternal characteristics., Results: Approximately two thirds of women filled a prescription during pregnancy, increasing from 60% in 2002 to 66% in 2011. The proportion of pregnant women using medicines in all three trimesters of pregnancy increased from 20% in 2002 to 27% in 2011. Use of four or more different types of prescription drug during at least one trimester increased from 8.4% in 2002 to 11.7% in 2011. Higher BMI, smoking during pregnancy, age under 25, carrying multiples, and being diagnosed with a chronic condition all significantly increased the odds of prescription drug use during pregnancy., Conclusions: The observed increase in the number of prescriptions and number of different drugs being dispensed suggests a trend in prescribing practices with potentially important implications for mothers, their neonates, and caregivers. Monitoring of prescribing practices and further research into the safety of most commonly prescribed medications is crucial in better understanding risks and benefits to the fetus and the mother.

Prenatal exposure to maternal depression and serotonin reuptake inhibitor (SRI) antidepressants both affect the development of the hypothalamic–pituitary–adrenal (HPA) system, possibly via the neurotransmitter serotonin (5HT). In a community cohort, we investigated the impact of two factors that shape prenatal 5HT signaling (prenatal SRI [pSRI] exposure and child SLC6A4 genotype) on HPA activity at age 6 years. Generalized estimating equation (GEE) models were used to study associations between cortisol reactivity, pSRI exposure, and child SLC6A4 genotype, controlling for maternal depression, child age, and sex (48 pSRI exposed, 74 nonexposed). Salivary cortisol levels were obtained at five time points during a laboratory stress challenge: arrival at the laboratory, following two sequential developmental assessments, and then 20 and 40 min following the onset of a stress‐inducing cognitive/social task. Cortisol decreased from arrival across both developmental assessments, and then increased across both time points following the stress challenge in both groups. pSRI‐exposed children had lower cortisol levels across all time points. In a separate GEE model, we observed a lower cortisol stress response among children with LG/S alleles compared with children with La/La alleles, and this was particularly evident among children of mothers reporting greater third trimester depressed mood. Our findings suggest that pSRI exposure and a genetic factor associated with modulating 5HT signaling shaped HPA reactivity to a laboratory stress challenge at school age. [ABSTRACT FROM AUTHOR]

Background: Prenatal antibiotic exposure induces changes in the maternal microbiome, which could influence the development of the infant's microbiome–gut–brain axis. Objectives: We assessed whether prenatal antibiotic exposure is associated with an increased risk of autism spectrum disorder (ASD) in offspring born at term. Methods: This population‐based retrospective cohort study included everyone who delivered a live singleton‐term infant in British Columbia, Canada between April 2000 and December 2014. Exposure was defined as filling antibiotic prescriptions during pregnancy. The outcome was an ASD diagnosis from the British Columbia Autism Assessment Network, with a follow‐up to December 2016. To examine the association among pregnant individuals treated for the same indication, we studied a sub‐cohort diagnosed with urinary tract infections. Cox proportional hazards models were used to estimate unadjusted and adjusted hazard ratios (HR). The analysis was stratified by sex, trimester, cumulative duration of exposure, class of antibiotic, and mode of delivery. We ran a conditional logistic regression of discordant sibling pairs to control for unmeasured environmental and genetic confounding. Results: Of the 569,953 children included in the cohort, 8729 were diagnosed with ASD (1.5%) and 169,922 were exposed to prenatal antibiotics (29.8%). Prenatal antibiotic exposure was associated with an increased risk of ASD (HR 1.10, 95% confidence interval [CI] 1.05, 1.15), particularly for exposure during the first and second trimesters (HR 1.11, 95% CI 1.04, 1.18 and HR 1.09, 95% CI 1.03, 1.16, respectively), and exposure lasting ≥15 days (HR 1.13, 95% CI 1.04, 1.23). No sex differences were observed. The association was attenuated in the sibling analysis (adjusted odds ratio 1.04, 95% CI 0.92, 1.17). Conclusions: Prenatal antibiotic exposure was associated with a small increase in the risk of ASD in offspring. Given the possibility of residual confounding, these results should not influence clinical decisions regarding antibiotic use during pregnancy. [ABSTRACT FROM AUTHOR]

Background and Hypothesis Maternal schizophrenia heightens the risk for certain perinatal complications, yet it is not known to what degree future childhood chronic health conditions (Childhood-CC) might arise. Study Design This population-based cohort study using health administrative data from Ontario, Canada (1995–2018) compared 5066 children of mothers with schizophrenia to 25 324 children of mothers without schizophrenia, propensity-matched on birth-year, maternal age, parity, immigrant status, income, region of residence, and maternal medical and psychiatric conditions other than schizophrenia. Cox proportional hazard models generated hazard ratios (HR) and 95% confidence intervals (CI) for incident Childhood-CCs, and all-cause mortality, up to age 19 years. Study Results Six hundred and fifty-six children exposed to maternal schizophrenia developed a Childhood-CC (20.5/1000 person-years) vs. 2872 unexposed children (17.1/1000 person-years)—an HR of 1.18, 95% CI 1.08–1.28. Corresponding rates were 3.3 vs. 1.9/1000 person-years (1.77, 1.44–2.18) for mental health Childhood-CC, and 18.0 vs. 15.7/1000 person-years (1.13, 1.04–1.24) for non-mental health Childhood-CC. All-cause mortality rates were 1.2 vs. 0.8/1000 person-years (1.34, 0.96–1.89). Risk for children exposed to maternal schizophrenia was similar whether or not children were discharged to social service care. From age 1 year, risk was greater for children whose mothers were diagnosed with schizophrenia prior to pregnancy than for children whose mothers were diagnosed with schizophrenia postnatally. Conclusions A child exposed to maternal schizophrenia is at elevated risk of chronic health conditions including mental and physical subtypes. Future research should examine what explains the increased risk particularly for physical health conditions, and what preventive and treatment efforts are needed for these children. [ABSTRACT FROM AUTHOR]

Background: Up to 20% of mothers experience antenatal depression and approximately 30% of these women are treated with serotonergic psychotropic pharmacological therapy during pregnancy. Serotonergic antidepressants readily cross the placenta and the fetal blood-brain barrier, altering central synaptic serotonin signaling and potentially altering serotonin levels in the developing fetal brain. Objective: The aim of this study is to assess the impact of prenatal exposure to serotonergic antidepressants, accounting for maternal mood disturbances, on markers of stress regulation during childhood. Methods: We will follow PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines and will search MEDLINE, Embase, CINAHL, PsycINFO, and ClinicalTrials.gov for full-length studies that assessed physiological (eg, cortisol level, heart rate variability, salivary amylase, pupillary size, C-reactive protein) indices of stress regulation in children of pregnant people who were treated with a serotonergic antidepressant at any point during pregnancy. We will assess the quality of observational studies using the Newcastle-Ottawa Scale and the quality of experimental studies using the Cochrane risk-of-bias tool. When possible, we will conduct a random-effects meta-analysis. If meta-analysis is not possible, we will conduct a narrative review. If a sufficient number of studies are found, we will perform subgroup analysis and assess outcomes measured by drug class, dose, trimester of exposure, and child’s age and gender. Results: We registered our review protocol with PROSPERO (International Prospective Register of Systematic Reviews; CRD42021275750), completed the literature search, and initiated title and abstract review in August 2021. We expect to finalize this review by April 2022. Conclusions: Findings should identify the impact of prenatal antidepressant effects on stress regulation and distinguish it from the impact of prenatal exposure to maternal mood disturbances. This review should inform decisions about serotonergic antidepressant use during pregnancy. [ABSTRACT FROM AUTHOR]

Background: Prenatal exposure to serotonin reuptake inhibitor (SRI) antidepressants increases risk for adverse neurodevelopmental outcomes, yet little is known about whether effects are present before birth. In relation to maternal SRI pharmacokinetics, this study investigated chronic and acute effects of prenatal SRI exposure on third-trimester fetal heart rate variability (HRV), while evaluating confounding effects of maternal depressed mood. Methods: At 36-weeks' gestation, cardiotocograph measures of fetal HR and HRV were obtained from 148 pregnant women [four groups: SRI-Depressed (n = 31), SRI-Non-Depressed (n = 18), Depressed (unmedicated; n = 42), and Control (n = 57)] before, and ~5-h after, typical SRI dose. Maternal plasma drug concentrations were quantified at baseline (pre-dose) and four time-points post-dose. Mixed effects modeling investigated group differences between baseline/pre-dose and post-dose fetal HR outcomes. Post hoc analyses investigated sex differences and dose-dependent SRI effects. Results: Maternal SRI plasma concentrations were lowest during the baseline/pre-dose fetal assessment (trough) and increased to a peak at the post-dose assessment; concentration-time curves varied widely between individuals. No group differences in fetal HR or HRV were observed at baseline/pre-dose; however, following maternal SRI dose, short-term HRV decreased in both SRI-exposed fetal groups. In the SRI-Depressed group, these post-dose decreases were displayed by male fetuses, but not females. Further, episodes of high HRV decreased post-dose relative to baseline, but only among SRI-Non-Depressed group fetuses. Higher maternal SRI doses also predicted a greater number of fetal HR decelerations. Fetuses exposed to unmedicated maternal depressed mood did not differ from Controls. Conclusions: Prenatal SRI exposure had acute post-dose effects on fetal HRV in late gestation, which differed depending on maternal mood response to SRI pharmacotherapy. Importantly, fetal SRI effects were sex-specific among mothers with persistent depressive symptoms, as only male fetuses displayed acute HRV decreases. At trough (pre-dose), chronic fetal SRI effects were not identified; however, concurrent changes in maternal SRI plasma levels suggest that fetal drug exposure is inconsistent. Acute SRI-related changes in fetal HRV may reflect a pharmacologic mechanism, a transient impairment in autonomic functioning, or an early adaption to altered serotonergic signaling, which may differ between males and females. Replication is needed to determine significance with postnatal development. [ABSTRACT FROM AUTHOR]

Women at the lower end of the socioeconomic distribution have higher rates of depression in pregnancy and lower rates of treatment. In this study, we investigate relationships between income and the use of psychotropic mediciness in pregnancy. This retrospective cohort study using population-based administrative datasets included all women who delivered a live infant in the province of British Columbia, Canada (population of 4.6 million), between April 1, 2000, and December 31, 2009. We compared the socioeconomic distribution in use of psychotropic mediciness in pregnancy. We included 305,984 deliveries among 217,721 women. Women at the low end of the income distribution were significantly more likely to have a diagnosis for all mental health conditions, except anxiety, which was more common in women of highest socioeconomic status. The adjusted odds ratios for psychotropic medicine use indicate that women in the lowest income quintile have lower odds of filling a prescription for a psychotropic medicine after controlling for covariates and diagnoses of mental health conditions. However, they were more likely to fill a prescription for an antipsychotic and were more likely to fill psychotropic medicines from three or more different drug categories during pregnancy. Our findings suggest that women of lower socioeconomic status are less likely to fill a prescription for a psychotropic medicine in pregnancy, a finding largely driven by their decreased likelihood of filling an antidepressant. This is despite overall higher rates of mental illness among women of lower socioeconomic status, suggesting a gap in treatment by socioeconomic status. [ABSTRACT FROM AUTHOR]

Depression in pregnancy negatively affects maternal-child health. Transcranial direct current stimulation (tDCS), a non-invasive brain stimulation treatment for depression, has not been evaluated in pregnancy. To conduct a pilot randomized controlled trial (RCT) to evaluate tDCS for antenatal depression. In this pilot RCT in Toronto, Ontario (October 2014 to December 2016), adult pregnant women 14–32 weeks gestation with major depressive disorder who had declined antidepressant medication were considered for inclusion. Participants were randomly assigned 1:1 to tDCS or sham-control. Active tDCS comprised 30-min sessions of 2 mAmp direct current delivered over the dorsolateral prefrontal cortex, 5 days per week, for 3 weeks. Sham was administered similarly, but with current turned off after 30 s. Main outcomes were feasibility, acceptability, and protocol adherence. Maternal Montgomery Asperg Depression Rating Scale (MADRS) was measured post-treatment and at 4 and 12 weeks postpartum. Of 20 women randomized, 16 completed treatment and provided data (124 tDCS, 122 sham sessions). Views of treatment were positive with no serious adverse events. Post-treatment estimated marginal mean MADRS scores were 11.8 (standard error, SE 2.66) for tDCS and 15.4 (SE 2.51) for sham (p = 0.34). At 4 weeks postpartum, 75.0% of tDCS women were remitted versus 12.5% sham-control (p = 0.04). Results support proceeding to a definitive RCT to evaluate tDCS for antenatal depression. The preliminary efficacy estimates immediately post-treatment and in the postpartum, are encouraging with respect to the potential use of tDCS to improve treatment rates in this population. The trial was registered at: clinical trials.gov (NCT02116127). • Evaluation of transcranial direct current stimulation (tDCS) for depression in pregnancy is feasible. • Views of treatment were positive with no adverse effects. • Results support proceeding to a definitive randomized controlled trial to evaluate tDCS for antenatal depression. • Preliminary efficacy estimates are encouraging with respect to the potential use of tDCS in this under-treated population. [ABSTRACT FROM AUTHOR]

The effect of perinatal selective serotonin reuptake inhibitors (SSRIs) on brain-derived neurotrophic factor (BDNF) and S100 calcium binding protein B (S100B) has not been investigated. Using a cohort of 86 pregnant women, we found that SSRIs significantly increase BDNF levels in late pregnancy and that S100B, but not BDNF, is associated with maternal depression in SSRI-treated women only. This shows that serum S100B could be a unique biomarker to determine efficacy of SSRIs during gestation. [ABSTRACT FROM AUTHOR]

Women at the lower end of the socioeconomic distribution have higher rates of depression in pregnancy; however, we know little about the role of socioeconomic status (SES) in determining their treatment. Herein, we investigate the relationships between income and the use of health services for depression in pregnancy. This retrospective cohort study using population-based administrative datasets included all women who delivered a live infant in the province of British Columbia, Canada (population of 4.3 million) between April 1st, 2000 and December 31st, 2009. We restricted to women with an indication of depression during pregnancy and examined their use of health services to treat depression by income quintile. Women in the highest income quintile were significantly more likely to see a psychiatrist for depression during pregnancy and to fill prescriptions for serotonin reuptake inhibitor (SRI) antidepressants than women in the lowest income quintile. Women at the lower end of the income distribution were more likely to have a GP visit for depression. Women at the low end of the income distribution were more likely to end up in hospital for depression or a mental health condition during pregnancy and more likely to receive a benzodiazepine and/or an antipsychotic medication. Our findings suggest a critical gap in access to health services for women of lower income suffering from depression during pregnancy, a time when proper access to effective treatment has the most potential to improve the long-term health of the developing child and the whole family unit. [ABSTRACT FROM AUTHOR]

Mood disorders and treatment with selective serotonin reuptake inhibitor (SSRI) antidepressants during pregnancy are common and both pose neurodevelopmental risks. This often makes the decision to treat prenatal depression with pharmacotherapy (i.e., antidepressants) challenging for clinicians and mothers. SSRIs block the reuptake of the neurotransmitter serotonin (5HT) and given its developmental role, it is not inconceivable that early changes in 5HT signaling could have an impact on early brain development. Identifying long-term neurodevelopmental effects of prenatal SSRI exposure is challenging in humans due to difficulties in distinguishing the effect of the drug from mother’ôs mood during pregnancy and everyday environment in which the child lives, all of which contribute to shaping emotional, cognitive, and social development long after birth. In this review, we focus on the long-term neurobehavioral effects in childhood illustrating wide variations in outcomes revealing that some, but not all children appear to be affected by prenatal SSRI exposure. Emerging research reports findings that are beginning to distinguish the impact of genetic factors and the environment from prenatal medication exposure. Future research is needed to identify genetic, maternal, and environmental factors that put some children at developmental risk and others who may even benefit from maternal SSRI treatment. [ABSTRACT FROM AUTHOR]

The article discusses a research study for the impact of the intake of selective serotonin reuptake inhibitor (SSRIs) in pregnancy to manage mood disorder. Developmental programming is used to report parental exposures and developmental outcomes, influences of SSRI in early brain development is studied through setting pathways via serotonergic fetal programming, and a risk of affective disturbances is noted. It also presents a conclusion of the study.

Purpose To identify specific quantitative and qualitative factors that govern the decision to adhere or decline antidepressant medication in antenatal women with moderate-to-severe mood and anxiety disorders. Methods Fifty women (30 adherers, 20 decliners) were recruited between 18 and 34 weeks gestation in a tertiary care clinic for perinatal mothers. They were prospectively monitored 4 weeks apart up to 1-month postpartum on the: Hamilton Anxiety Scale, Hamilton Depression Scale, Mood Disorders Insight Scale, Antidepressant Compliance Questionnaire, Penn State Worry Questionnaire, and NEO Personality Inventory. Qualitative interviews were conducted at baseline. Hierarchical linear modeling determined illness trajectories of the two groups. Results Significantly different course of illness was observed in adherers versus decliners. Adherers had healthier attitudes toward depression and compliance with medication ( P < .005). Decliners had less illness insight ( P < .001) and cited fear of fetal exposure, and thought medication was unwarranted. Conclusions Pregnant women experienced significantly divergent illness trajectories depending on if they accepted antidepressant medication therapy for their illness. Risk perception, attitudes, and illness insight impacted decisions surrounding adherence and decline. [ABSTRACT FROM AUTHOR]

Prenatal serotonin reuptake inhibitor exposure is common and neonatal outcomes vary greatly, often leading to confusion about whether to use or even continue antenatal use of these antidepressants. Importantly, some but not all infants are affected, which raises questions about how maternal drug metabolism contributes to fetal drug exposure. To address this key question, our paper reviews the role of key maternal, fetal, and placental pharmacokinetic, metabolic, and genetic factors that affect the extent of fetal drug exposure. Considering the role of these factors may further our understanding of variables that may assist in optimizing maternal psychopharmacotherapy during pregnancy and neonatal outcomes. [ABSTRACT FROM AUTHOR]

An introduction is presented in which the author discusses various reports within the issue on topics including risks associated with maternal depression during pregnancy, prenatal exposure to selective serotonin reuptake inhibitors (SSRIs) and molecular factors that influences hydroxytryptamine levels during gestation.

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Aims To compare the disposition of fluoxetine and norfluoxetine enanantiomers in the mother, foetus and infant. Methods Blood from pregnant women taking fluoxetine ( n = 9), during pregnancy was sampled in the third trimester and at delivery (maternal and cord venous blood), and from the infants 48 h after delivery. The subset of these women who were breastfeeding, plus additional subjects recruited in the postpartum period, were studied further, and maternal and infant blood, and breast milk was sampled between 6 days and 11 months ( n = 23). Drug and metabolite concentrations were measured using gas chromatography/mass spectrometry or liquid chromatography, tandem mass spectrometry. Results There was a high correlation between maternal and foetal (cord blood) fluoxetine and norfluoxetine enantiomers ( r2−0.9), the mean foetal/maternal ratios (95% confidence intervals) being 0.91 (0.61, 1.02) and 1.04 (0.93, 1.05), for fluoxetine and norfluoxetine, respectively. In 2 day old infants exposed to the drug in utero, the fluoxetine and norfluoxetine plasma concentrations were the same as in cord blood at delivery. Over the next 2 months, the plasma concentrations in the infants fell progressively. Stereoselective disposition of both the drug and metabolite in the mother, foetus, infant and breast milk was observed. The S : R ratios in the foetus and newborn (∼3) were significantly higher than in the serum (∼2) or breast milk (∼1.9) of the mothers, resulting in greater exposure of the foetus and infants to the biologically active enantiomers, particularly S-norfluoxetine. Conclusions Foetal and infant exposure to fluoxetine and norfluoxetine is enhanced by their stereoselective disposition in the mother, foetus, breast milk and infant. Increased exposure may also result from decreased metabolism of the drug in the foetus and neonate. [ABSTRACT FROM AUTHOR]

Objective: To examine the relation between the mood and anxiety of pregnant, psychiatrically treated women and neonatal health outcomes after birth.Method: We prospectively assessed 46 women treated with psychotropic medications for anxiety and depression during pregnancy. We compared measures of maternal mental health with infant outcomes, in particular, the outcomes of infants with symptoms of poor neonatal adaptation.Results: The mothers of babies who demonstrated poor neonatal adaptation reported higher levels of anxiety and depression at study entry than did the mothers of healthy babies. This relation was not related to the presence or absence of treatment with clonazepam, an anxiolytic used to treat symptoms of anxiety. Further, increased psychiatric comorbidity in the mother was associated with a greater likelihood of transient symptoms in the newborn.Conclusions: Despite psychiatric treatment, the intensity and degree of comorbid symptoms appear to be related to poor transient neonatal health outcome. Our data suggest that, in addition to the impact of pharmacologic factors, maternal psychiatric status influences infant outcomes. [ABSTRACT FROM AUTHOR]

Background: The severity and treatment of depression/anxiety during pregnancy and postpartum has important implications for maternal and child well-being. Yet, little is known about prenatal SSRI use and early child socioemotional development. This study explores effects of prenatal SSRI exposure, and pre- and postnatal internalizing symptoms on trajectories of infant temperament, identifying potential differences for boys and girls.Methods: Using latent growth models, sex differences in infant temperament trajectories from 3- to 10-months were examined in relation to prenatal and postpartum internalizing symptoms and prenatal SSRI exposure among 185 mother-infant dyads.Results: For girls, prenatal internalizing symptoms were associated with greater initial distress to limitations, and lower duration of orienting, smiling/laughter, and soothability. Postnatal symptoms predicted slower decreases in girls' duration of orienting. SSRI exposure predicted decreases in distress to limitations and slower increases in smiling and laughter. For boys, maternal internalizing symptoms did not generally affect temperament profiles. SSRI exposure was associated with higher initial activity level and slower declines in distress to limitations.Limitations: Only parent-report indicators of infant temperament across 10 months of infancy were provided. Maternal internalizing symptoms were measured at discrete times during pregnancy and postpartum, with no analysis of changes in symptoms across time.Conclusions: Prenatal SSRI treatment, and both prenatal and postpartum internalizing symptoms, exert unique effects on infant temperament. Overall, the present study suggests sex-dependent fetal programming effects that should be further evaluated in future research. Results have implications for perinatal mental health treatment and perceived impacts on child socioemotional development. [ABSTRACT FROM AUTHOR]

Motor development underlies many aspects of education and learning. There has been uncertainty about the impact of exposure of antidepressant medication in pregnancy on child motor outcomes. This paper examines whether exposure to antidepressants in utero increases the risk of poorer motor development in two areas: sensorimotor and visuospatial processing. Data were obtained from 195 women and children across 3 groups: women with untreated depression in pregnancy, women treated with antidepressants and control women. Data were collected across pregnancy, postpartum and until 4 years for mother and child. Maternal depression was established at baseline with the Structured Clinical Interview for DSM-IV. Antidepressant exposure, including type, dose and timing, was measured through repeated self-report across pregnancy and the postpartum, medical records at delivery and in cord blood samples collected at delivery. Child sensorimotor and visuospatial outcomes were assessed at 4 years of age with four subtests from the NEPSY-II. Our study found for sensorimotor development, visuomotor precision completion time was associated with better performance for antidepressant-exposed children compared to those with mothers with untreated depression. Yet another measure of sensorimotor development, motor manual sequences, was poorer in those exposed to antidepressants. One subtest for visuospatial processing, block construction, was associated with poorer performance in antidepressant-exposed children who had poor neonatal adaptation and those exposed to a higher dose of antidepressant. These findings suggest an inconsistent association between sensorimotor development and antidepressant use in pregnancy. However, the findings for visuospatial processing would support further exploration of antidepressant associated poor neonatal adaption and later motor development. [ABSTRACT FROM AUTHOR]

• Perinatal SSRIs differentially impact offspring affective behaviors. • Maternal mood symptoms are important to consider in addition to SSRIs. • Sex/gender and age of offspring are important factors affecting outcomes. • Environmental and genetic factors need to be considered. • Further research is needed to determine perinatal SSRI effects on offspring. The developmental impact of selective serotonin reuptake inhibitor (SSRI) and other antidepressant treatments during gestation and postpartum on anxiety and depression behaviors in offspring is unclear. This review focuses on how perinatal exposure to SSRI and other antidepressant may have long term consequences for these affective behaviors during early childhood and beyond. Outcomes vary and consideration is given to methodological factors related to how early SSRI exposure affects developments studied in rodent models such as: a) between pre- and early post-natal SSRI exposure, b) sex, c) experimental models of gestational maternal stress and d) impact of non-SSRI antidepressant medications. We will also review how multiple contextual factors (maternal caregiving and gene x environment interactions) may contribute to the effects of perinatal SSRI exposure and maternal mental illness on affective behaviors in children. [ABSTRACT FROM AUTHOR]

Background: Decisions about antidepressant use in pregnancy are complex. We performed a pilot randomized controlled trial assessing the feasibility of a trial protocol for an online patient decision aid (PDA) for women deciding about antidepressant use in pregnancy.Methods: 96 preconception and pregnant Canadian women recruited from specialist (n = 51) and non-specialist (n = 45) settings with Decisional Conflict Scale (DCS, range 0-100) score of ≥25 signifying moderate-to-high decisional conflict were randomly allocated to either the PDA or a control condition that guided participants to publicly available resources for advice around antidepressants and pregnancy. Follow-up data were collected at 4 weeks post-randomization.Results: About 88.9% of eligible participants consented to participate. Women's views of the tool were positive; 88.7% of participants provided follow-up data. At follow-up, mean DCS score had decreased by 19.9 points in the PDA group vs. 13.3 in controls (adjusted mean difference, MD, 7.01, 95% CI -14.3 to 0.30). In the non-specialist setting, DCS scores decreased more for PDA users (25.5 points) than controls (10.5 points; adjusted MD -15.1, 95% CI -25.6 to -4.55); the MD was negligible in the specialist setting.Limitations: The main limitation is the highly educated, high-income nature of our sample.Conclusions: Evaluation of an online PDA for antidepressant use in pregnancy with national recruitment is feasible. Pilot results suggest that the tool is acceptable and reduces decisional conflict more than clinical care alone in a non-specialist setting. Evaluation of the PDA's impact on longer-term maternal and child clinical outcomes is a key next step. [ABSTRACT FROM AUTHOR]

The long-term impact of selective serotonin reuptake inhibitor (SSRI) antidepressant treatment during pregnancy and postpartum on offspring outcomes is still not clear. Specifically, perinatal SSRI exposure may have long-term consequences for body weight and related health outcomes in the newborn period and beyond. This review focuses on the impact of perinatal SSRI exposure on weight using human and animal findings. The impact of maternal mood is also explored. We propose potential mechanisms for weight changes, including how early alterations in serotonin signaling may have implications for weight via changes in metabolism and motor development. As the majority of serotonin is in the gastrointestinal (GI) system we also speculate that perinatal SSRI exposure might alter the brain-gut relationship, via the microbiome, leading to changes in feeding behavior and weight. [ABSTRACT FROM AUTHOR]

Recent research has linked early life exposure to selective serotonin reuptake inhibitor medications (SSRIs) to modifications of social behaviors in children. Serotonin is a key regulator of neurodevelopment, social behaviors and mental health, and with the growing use of SSRIs to treat maternal affective disorders during the perinatal period, questions have been raised about the benefits and risks of perinatal SSRI exposure on the developing child. This review will highlight how perinatal SSRIs affect maternal care and neurodevelopmental outcomes related to social affiliative behaviors in offspring; such as play behaviors, social interactions, reproductive behaviors, and maternal care of the next generation. We will also review how early life exposure to SSRIs can alter related neurobiology, and the epigenome. Both clinical research and findings from animal models will be discussed. Understanding the impact of perinatal SSRIs on neurobehavioral outcomes will improve the health and well-being of subsequent generations. [ABSTRACT FROM AUTHOR]

Summary: Background: Serotonin influences the development of the hypothalamic–pituitary–adrenal (HPA) system; therefore prenatal exposure to selective serotonin reuptake inhibitor antidepressants (SSRIs) may alter HPA axis development and function. To address this, prenatal exposure to SSRIs and maternal mood were examined in relation to neonatal and infant levels of cortisol and its binding protein, corticosteroid-binding globulin (CBG). Methods: Serum cortisol and CBG levels were assayed from SSRI-exposed and non-exposed mothers and their neonates at delivery. Maternal mood symptoms were documented at 36 weeks gestation. To determine the long-term implications of changes in CBG, levels of salivary cortisol were assessed in infants at 3 months of age. Results: Prenatal SSRI exposure significantly increased serum CBG levels in neonates after vaginal delivery (p ≤0.038), even when controlling for maternal depression. Neonatal serum cortisol levels did not vary with SSRI exposure or antenatal maternal mood, but were significantly higher following vaginal delivery (p ≤0.003). Neonatal serum CBG levels were associated with infant salivary levels of evening cortisol (p ≤0.051). In SSRI-exposed infants, increased levels of neonatal CBG predicted a smaller diurnal change in infant salivary cortisol (p ≤0.028), regardless of maternal depression. Conclusions: Prenatal SSRI exposure affects the developing HPA system by altering serum CBG levels in neonates and infant salivary cortisol levels. Further research is warranted on the long-term functional implications of the effect of prenatal SSRI exposure on fetal hepatic CBG gene expression and the developing HPA system. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To address the maternal and neonatal risks of both depression and antidepressant exposure and develop algorithms for periconceptional and antenatal management. Method: Representatives from the American Psychiatric Association, the American College of Obstetricians and Gynecologists and a consulting developmental pediatrician collaborated to review English language articles on fetal and neonatal outcomes associated with depression and antidepressant treatment during childbearing. Articles were obtained from Medline searches and bibliographies. Search keywords included pregnancy, pregnancy complications, pregnancy outcomes, depressive disorder, depressive disorder/dt, abnormalities/drug-induced/epidemiology, abnormalities/drug-induced/et. Iterative draft manuscripts were reviewed until consensus was achieved. Results: Both depressive symptoms and antidepressant exposure are associated with fetal growth changes and shorter gestations, but the majority of studies that evaluated antidepressant risks were unable to control for the possible effects of a depressive disorder. Short-term neonatal irritability and neurobehavioral changes are also linked with maternal depression and antidepressant treatment. Several studies report fetal malformations in association with first trimester antidepressant exposure but there is no specific pattern of defects for individual medications or class of agents. The association between paroxetine and cardiac defects is more often found in studies that included all malformations rather than clinically significant malformations. Late gestational use of selective serotonin reuptake inhibitor antidepressants is associated with transitory neonatal signs and a low risk for persistent pulmonary hypertension in the newborn. Psychotherapy alone is an appropriate treatment for some pregnant women; however, others prefer pharmacotherapy or may require pharmacological treatment. Conclusions: Antidepressant use in pregnancy is well studied, but available research has not yet adequately controlled for other factors that may influence birth outcomes including maternal illness or problematic health behaviors that can adversely affect pregnancy. [Copyright &y& Elsevier]

• Maternal depression is associated with lower infant cortisol reactivity. • Early pregnancy depression is associated with reduced placental NR3C2 DNA methylation. • No association of maternal depression and cortisol with placental or infant buccal NR3C1 DNA methylation. • No association of antidepressant use with cortisol and placental or infant buccal NR3C1 and NR3C2 DNA methylation. • Association between infant cortisol reactivity and maternal depression was suppressed by placental NR3C2 DNA methylation. Understanding fetal programming pathways that underpin the relationship between maternal and offspring mental health necessitates an exploration of potential role of epigenetic variation in early development. Two genes involved in stress response regulation, the glucocorticoid and mineralocorticoid receptors (NR3C1 and NR3C2) have been a focus in understanding stressful exposures and mental health outcomes. Data were obtained from 236 pregnant women from the Mercy Pregnancy Emotional Wellbeing Study (MPEWS), a selected pregnancy cohort, recruited in early pregnancy. Depression was measured using the Structured Clinical Interview for DSM-IV (SCID-IV) and repeated measures of the Edinburgh Postnatal Depression Scale (EPDS). Antidepressant use, stressful events and anxiety symptoms were measured. NR3C1 and NR3C2 DNA methylation was measured in placental and infant buccal samples. Infant cortisol was measured in repeat saliva samples across a task. This study found maternal early pregnancy depressive disorder and symptoms were associated with lower DNA methylation at NR3C2 CpG_24 in placental tissue. There were no significant differences for depression or antidepressant use for DNA methylation of NR3C1. Antenatal depression was associated with lower infant cortisol reactivity at 12 months. DNA methylation in CpG_24 site in NR3C2 in placental samples suppressed the relationship between early maternal depressive symptoms and infant cortisol reactivity. These findings show a relationship between antenatal depression, NR3C2 DNA methylation and infant cortisol response providing support for a specific fetal programming pathway. Further research is required to examine the stability of this epigenetic mark across childhood and long-term mental health outcomes. [ABSTRACT FROM AUTHOR]

An abstract of the article "Neonatal S100B Protein Levels After Prenatal Exposure to Selective Serotonin Reuptake Inhibitors," by Jodi L. Pawluski and colleagues is presented.