SSRIs in Pregnancy
- First-lineSertraline is the preferred agent for de novo treatment — most safety data, lowest placental passage (cord:maternal ~0.29–0.45).
- Frame itCounsel as risk of medication vs. risk of untreated illness — never "medication vs. no risk." Untreated moderate-to-severe depression carries real obstetric and neonatal harms.
- MalformationsNo class-wide teratogenic signal. The historical paroxetine–cardiac association largely attenuates after confounding adjustment. Avoid paroxetine for de novo use; don't reflexively switch a stable patient.
- PPHNVery low absolute risk (~2–3 extra cases per 1,000), likely overstated by confounding (adjusted OR 1.10, non-significant).
- NeonatePNAS occurs in ~25–30% but is mild and self-limiting (resolves 2–4 weeks). Highest with fluoxetine & escitalopram. Do not taper before delivery to "protect" the baby — notify the neonatal team instead.
- DosingNo blanket third-trimester dose increase. Paroxetine & fluvoxamine levels fall (watch for relapse); sertraline levels rise (watch for side effects, not relapse).
- At deliveryNotify, don't modify. Tell the pediatric team the agent and dose so they can monitor — the single highest-yield action at birth.
SSRIs (sertraline, fluoxetine, escitalopram, citalopram, paroxetine, fluvoxamine) are the first-line pharmacological treatment for moderate-to-severe perinatal depression and anxiety. Most are not considered major teratogens, and sertraline remains the preferred first-line agent owing to its extensive safety record and low placental passage.
Roughly 25–30% of neonates exposed in late pregnancy experience Poor Neonatal Adaptation Syndrome (PNAS), which is typically mild and self-limiting. Every decision must weigh the known risks of medication against the well-documented risks of untreated maternal illness — including poor prenatal care, preterm birth, and postpartum depression. The recurring theme of the modern literature is that many apparent "SSRI risks" are substantially explained by confounding by indication: the depression, not the drug, is frequently the true driver.
The Two-Risks Framework
Every counseling conversation should be framed as risk of medication vs. risk of untreated illness — never medication vs. no risk. This single reframe is the most important conceptual tool in perinatal psychopharmacology, because the comparator a patient instinctively reaches for ("if I just stop, the baby is safe") does not exist.
Untreated moderate-to-severe antenatal depression is not a neutral state. It is independently associated with poor prenatal self-care and nutrition, reduced attendance at antenatal visits, substance use, preterm birth, low birth weight, impaired maternal–infant bonding, and a markedly elevated risk of postpartum depression and, in severe cases, postpartum psychosis. Untreated maternal illness also elevates fetal cortisol exposure, which has its own implications for fetal growth and stress-axis programming.
The decision is never "drug vs. nothing." It is "treated illness vs. untreated illness," and both arms carry risk. A woman presenting on an SSRI is, by definition, someone whose clinician once judged her depression severe enough to warrant pharmacotherapy. That history should anchor the conversation — it is evidence about her baseline risk of relapse, not a generic population statistic.
Major Congenital Malformations
Evidence: Convincing — no class-wide increaseThe baseline major congenital malformation (MCM) rate in the general population is approximately 3%. As a class, SSRIs are not associated with a clinically meaningful increase in overall malformations once confounding by indication and lifestyle factors are addressed.
The Paroxetine Exception
Paroxetine was historically linked to cardiac defects, specifically ventricular and atrial septal defects (VSD/ASD). However, the largest and most rigorously adjusted study to address this — Huybrechts et al. (NEJM 2014, n = 949,504) — found no significant association after full confounding adjustment, including for right ventricular outflow tract (RVOT) defects (RR 1.07, 95% CI 0.59–1.93). A 2025 umbrella review classified the paroxetine–cardiac association as no stronger than "suggestive" evidence (pooled OR ~1.24–1.28). The signal, if real, is small in absolute terms.
Despite this reassurance, paroxetine is still generally avoided for de novo treatment in pregnancy because of the historical signal, the residual FDA advisory, its pronounced third-trimester concentration decline, and the availability of better-studied alternatives. This is a "why start here when sertraline exists?" argument, not a statement that paroxetine is a proven teratogen.
If a patient is already stable on paroxetine when she becomes pregnant, do not automatically switch. Switching SSRIs mid-pregnancy introduces a new variable, a washout-and-titration window, and a real period of mood instability — all to avoid a small, largely confounding-explained absolute cardiac risk. Reserve the "avoid paroxetine" rule for de novo prescribing.
Persistent Pulmonary Hypertension of the Newborn
Evidence: Evolving — very low absolute riskPPHN is a rare but serious neonatal condition. Older meta-analyses reported an adjusted OR of roughly 1.8–2.1 for SSRI exposure after 20 weeks' gestation. However, the largest and most rigorously adjusted study — Huybrechts et al. (JAMA 2015, n ≈ 3.8 million) — found the association attenuated to non-significance after full confounding adjustment (adjusted OR 1.10, 95% CI 0.94–1.29).
In absolute terms, registry data put the exposed rate at roughly 3 per 1,000 births vs. a background of about 1.2 per 1,000 — a number needed to harm on the order of 1,000. Even if the association is real, the excess is approximately 2 extra cases per 1,000 exposed pregnancies.
Unadjusted SSRI OR for PPHN was 1.51 (95% CI 1.35–1.69), falling to 1.10 (95% CI 0.94–1.29) after restricting to women with depression and adjusting for a high-dimensional propensity score. When the outcome was narrowed to primary PPHN, the adjusted OR was 1.28 (95% CI 1.01–1.64) — a residual signal that keeps the question open but small.
When a patient asks about PPHN, anchor the conversation in absolute, concrete terms: "For every 1,000 babies exposed, roughly 2 extra cases might occur — and even that small number may be explained by other factors rather than the medication itself." Relative risks frighten; absolute risks inform.
Poor Neonatal Adaptation Syndrome
Evidence: Convincing — common but transientPNAS (also called neonatal adaptation syndrome or neonatal behavioral syndrome) is the most common, clinically encountered consequence of late-pregnancy SSRI exposure, affecting roughly 25–30% of exposed neonates. Symptoms include irritability, jitteriness, tremor, weak or high-pitched cry, mild respiratory distress (tachypnea), temperature instability, and feeding difficulties.
The reassuring core message: symptoms are usually mild and resolve within 2–4 weeks (most within the first days to two weeks). A severe syndrome — seizures, dehydration, the need for intubation — is uncommon, and no neonatal deaths have been reliably attributed to SRI exposure. The pathophysiology is debated: it may reflect either serotonergic effects or a discontinuation/withdrawal phenomenon, and the distinction matters because it argues against pre-delivery tapering (see Section Five).
SSRI-Specific Differences
Escitalopram and fluoxetine are associated with the highest risk of delayed neonatal adaptation, in a dose-dependent manner (Cornet et al., 2024, n = 280,090). Fluoxetine's long half-life and its active metabolite norfluoxetine (t½ 7–15 days) lead to prolonged neonatal serotonin exposure, because the neonate's immature hepatic metabolism cannot efficiently clear the drug after delivery. Agents with the lowest placental passage — sertraline and paroxetine — are intuitively attractive when PNAS is a particular concern, although the clinical magnitude of this advantage is modest.
PNAS is transient, predictable, and rarely serious. The right response is anticipatory: ensure delivery occurs where the neonate can be observed, and brief the pediatric/neonatal team in advance. It is almost never a reason to destabilize the mother by altering her regimen before birth.
Tapering Before Delivery
Evidence: Mixed — not supported as routine practiceThe instinct to taper an SSRI in the weeks before delivery to "prevent" PNAS is widespread but poorly supported. The evidence is genuinely mixed: one small case series (n = 38) reported fewer NICU admissions with tapering, but a meaningful improvement in fetal and neonatal health from a late-pregnancy taper has not been established. ACOG's guidance is that observational data do not support pre-delivery tapering as a way to mitigate neonatal adaptation syndrome, and AAFP guidance similarly states that discontinuing SSRIs in the third trimester does not improve these outcomes.
The asymmetry of harms is the deciding factor. PNAS is transient and manageable; a postpartum depressive relapse triggered by a peri-delivery taper — at precisely the moment a woman is most vulnerable — is not. The taper trades a self-limiting neonatal problem for a potentially serious maternal one. The decision should be individualized through shared decision-making, but the default should be continuation.
Tapering before delivery feels protective but generally is not. PNAS is transient; postpartum relapse from destabilization is not. The superior strategy is to alert the neonatal team so they can monitor — keeping the mother stable through the highest-risk window of her life for relapse.
Neurodevelopment & Relapse Evidence
Two questions dominate patient conversations: "Will this affect my child's brain?" and "What happens if I stop?" The modern, confounding-controlled literature answers both with more reassurance than older studies suggested.
Neurodevelopment: Confounding, Not Causation
The pivotal study is Suarez et al. (JAMA Internal Medicine 2022), which drew on ~3.18 million pregnancies across two large U.S. claims databases (MAX, ~1.93 million; MarketScan, ~1.25 million). Crude analyses showed apparent associations — for example, ADHD with a crude HR of ~2.0 — but these collapsed toward the null in sibling-controlled analyses, which account for shared genetics and family environment. For any neurodevelopmental disorder, the sibling-controlled HR was 0.97 (95% CI 0.88–1.06); autism and ADHD were similarly null. The interpretation: the crude associations are driven by parental and environmental factors, not by the medication.
Relapse: Severity-Dependent, Not Universal
The widely quoted 68% relapse figure comes from Cohen et al. (JAMA 2006), in which 44/65 women (68%) who discontinued relapsed vs. 21/82 (26%) who maintained treatment (HR 5.0, 95% CI 2.8–9.1). Crucially, that cohort was recruited from specialist reproductive-psychiatry centers and enriched for severe, recurrent illness — it is not a general-population estimate. Bayrampour et al. (2020) put the pooled relapse RR at a non-significant 1.74 (95% CI 0.97–3.10) overall, rising to a significant 2.30 (95% CI 1.58–3.35) only in the severe/recurrent subgroup.
| Study / Source | Population | Outcome | Key Finding | Takeaway |
|---|---|---|---|---|
| Cohen et al. (JAMA, 2006) |
201 women, recurrent MDD; specialist centers | Relapse | 68% relapse on discontinuation vs. 26% on maintenance (HR 5.0, 95% CI 2.8–9.1) | High relapse risk — but in a high-recurrence subgroup, not all pregnant patients |
| Huybrechts et al. (NEJM 2014; JAMA 2015) |
~949,504 (cardiac); ~3.8 M (PPHN) | Cardiac / PPHN | No significant increase in cardiac defects or PPHN after full adjustment | Absolute risk of both is very low after adjustment |
| Suarez et al. (JAMA Intern Med, 2022) |
3.18 M pregnancies (MAX + MarketScan) | Neuro-development | No association with ASD, ADHD, or any NDD in sibling-controlled analysis (HR 0.97, 0.88–1.06) | Crude associations are confounding, not causation |
| Bayrampour et al. (J Clin Psychiatry, 2020) |
Meta-analysis, 8 studies | Relapse | Pooled RR 1.74 (0.97–3.10) overall; 2.30 (1.58–3.35) for severe/recurrent only | The 68% figure overstates risk in mild/first-episode cases |
| Trinh et al. (JAMA Psychiatry, 2023) |
57,934 pregnancies (Denmark + Norway) | Postpartum outcomes | Previously stable users who discontinued late showed a modestly higher probability of initiating psycholeptics post partum vs. continuers (HR 1.13, 95% CI 1.03–1.24) | Women with severe illness on stable treatment may benefit from continuation |
| Cesta et al. (JAMA Netw Open, 2024) |
27,773 women (Sweden) | Postpartum outcomes | No significant overall association between SSRI/SNRI discontinuation and adverse postpartum psychiatric outcomes in women without severe comorbid conditions | Reassuring for mild/moderate cases who choose to stop |
The 68% relapse rate applies to women with severe, recurrent MDD (≥3 episodes) recruited from specialist clinics. For a patient with a single mild-to-moderate episode, relapse risk is substantially lower. Tailor the number to the patient in front of you — do not deploy 68% as a universal statistic, or you will frighten low-risk women into over-treatment and exaggerate the stakes for everyone.
Maternal & Obstetric Risks
While patients fixate on fetal safety, several maternal and obstetric effects deserve the clinician's attention — though, as with the fetal outcomes, the recurring story is one of confounding by the underlying depression.
Hypertensive Disorders of Pregnancy
Evidence: NeutralOlder data suggested a modest link between SSRI use and preeclampsia (2018 meta-analysis: RR 1.21, 95% CI 1.05–1.40). A 2025 meta-analysis found that after adjusting for depression as a confounder, SSRIs carried no significant independent risk (adjusted OR 1.03, 95% CI 0.97–1.10). The association appears driven by maternal depression itself rather than the drug.
Postpartum Hemorrhage
Evidence: Suggestive — small absolute riskSSRIs inhibit platelet serotonin uptake, which can mildly impair platelet aggregation. Studies show a small increase in PPH risk (OR ~1.2–1.5). The clinical action is communication, not discontinuation: flag SSRI use to the obstetric team. Most patients need no medication change, but those with additional risk factors (placenta previa, known bleeding disorders, anticoagulation) warrant closer monitoring.
Gestational Diabetes
Evidence: Inconclusive / mixedSSRIs as a class show no significant association with GDM after adjustment for maternal BMI and lifestyle. Some data suggest venlafaxine and amitriptyline may carry risk, but this does not extend to SSRIs.
Many headline "SSRI risks" in pregnancy — preeclampsia, GDM, preterm birth — overlap heavily with the known risks of untreated depression itself. When a patient raises these, explain that the best adjusted data point to the depression, not the medication, as the primary driver. This is both more accurate and more reassuring.
Pharmacokinetics & Dosing
Pregnancy substantially alters drug disposition, but the direction and magnitude differ by agent. The single most important practical message is that blanket dose increases are not supported — the approach must be symptom-driven and drug-specific.
The Mechanics of Change
Expanded plasma volume: total body water and plasma volume rise by 40–50% by the third trimester, contributing a hemodilution effect for many drugs. Selective hepatic induction: pregnancy induces enzymes at different rates — CYP2D6 and CYP3A4 activity increase (affecting fluoxetine and paroxetine), while CYP2C19 activity decreases, which can reduce clearance of agents that depend on it.
Agent-Specific Changes (Westin et al., PLoS One 2017)
- Paroxetine: concentrations decline by ~51% during pregnancy — maintain a high index of suspicion for sub-therapeutic levels in the third trimester.
- Fluvoxamine: concentrations decline by ~56% — similar concern for sub-therapeutic levels.
- Sertraline (the paradox): concentrations have been found to increase by ~68% (Westin 2017), likely reflecting its multi-enzyme metabolism and the pregnancy-related fall in CYP2C19 activity. Note that this is not universal — a later study (Stika et al., 2022) found sertraline concentration-to-dose ratios actually decreased by ~22% in pregnancy, a discrepancy that may be explained by CYP2C19 genotype. The practical message stands: do not assume sertraline levels are falling, and watch for toxicity/side effects rather than reflexively raising the dose.
- Fluoxetine: relatively stable, buffered by its long-acting metabolite norfluoxetine — though individual monitoring is still warranted.
An Individualized Titration Strategy
Paroxetine / Fluvoxamine
Watch for the "dosing dip." If subtle symptoms (early-morning awakening, rising rumination) return after ~week 28, a dose increase is likely appropriate.
Sertraline
Monitor for emergent toxicity / side effects (GI distress, tremor, agitation) rather than relapse, as levels may rise. Don't reflexively increase the dose.
Postpartum Reset
Plan to reassess — and likely reduce — the dose within 1–2 weeks of delivery, as pregnancy-related metabolic changes reverse rapidly.
Low-Dose Patients
Someone stable on a very low pre-pregnancy dose is more susceptible to relapse if levels dip, regardless of which SSRI is used. Monitor proactively.
Sertraline is the most commonly prescribed SSRI in pregnancy, yet it is the one whose levels may increase rather than decrease. If a patient on sertraline reports new GI symptoms, tremor, or agitation in the third trimester, consider toxicity before assuming relapse — and do not reflexively raise the dose.
Comparative SSRI Table
The two variables that most often differentiate agents in clinical decision-making are placental passage (relevant to fetal exposure and PNAS) and half-life (relevant to neonatal washout). Sertraline's combination of the most data and the lowest placental passage is what earns it first-line status.
| Medication | MCM Risk (baseline ~3%) | Primary Clinical Note | Placental Passage (cord:maternal) | Half-Life |
|---|---|---|---|---|
| Sertraline | ~Baseline (no significant increase after adjustment) | Gold standard. Most safety data; preferred first-line. Levels may rise in pregnancy. | Lowest (~0.29–0.45) | ~26 hours |
| Escitalopram | ~Baseline (no significant increase) | Strong alternative first-line. High fetal AUC; higher PNAS risk. | High (F:M AUC ~0.91) | 27–32 hours |
| Fluoxetine | ~Baseline (unadjusted signal attenuates) | Higher PNAS risk; long half-life complicates neonatal washout. | High (~0.60–0.89) | 2–4 days (metabolite 7–15 days) |
| Citalopram | ~Baseline (unadjusted signal attenuates) | Highest placental passage; minimal drug–drug interactions. Note QTc/dose ceiling. | Highest (~0.70–0.89) | ~35 hours |
| Paroxetine | Slightly elevated for cardiac defects (attenuates after adjustment) | Avoid for de novo use. Historical cardiac signal; weight gain; marked 3rd-trimester decline (−51%). | Low–moderate (~0.38–0.58) | ~21 hours |
| Fluvoxamine | ~Baseline (limited data) | Limited perinatal data; pronounced 3rd-trimester decline (−56%). | Low (amniotic ratio ~0.10) | 15–22 hours |
Cord:maternal ratios are pooled approximations from placental-passage and ex-vivo perfusion studies; individual values vary by gestational age and assay. Citalopram's dose ceiling reflects its QTc-prolongation advisory, independent of pregnancy.
Starting new? → Sertraline (best data, lowest placental passage). Already on something that works? → Continue it; switching mid-pregnancy adds risk. On paroxetine and newly pregnant? → Continue if stable; just avoid initiating it de novo. Especially worried about PNAS? → Sertraline or paroxetine have the lowest placental passage; escitalopram and fluoxetine carry the highest PNAS risk.
Selection Guide & Special Cases
Beyond the headline "start sertraline" rule, a handful of recurring scenarios benefit from a pre-formed answer.
The patient already stable on a non-preferred agent
Continuity usually beats theoretical optimization. A woman euthymic on paroxetine, citalopram, or fluoxetine generally should continue, because the destabilization risk of switching outweighs the small differential safety advantage of moving to sertraline.
Planning ahead — preconception
The ideal time to optimize an SSRI regimen is before conception, not during. If a switch to a preferred agent is ever going to happen, the preconception window — when there is time to establish stability on the new drug — is where it belongs.
Citalopram and the QTc ceiling
Citalopram carries a dose-related QTc-prolongation advisory (a general caution, not pregnancy-specific). It remains usable in pregnancy but is not a reason to exceed standard dose ceilings.
Watch for additive serotonergic load when an SSRI is combined with other serotonergic agents (e.g., triptans, tramadol, ondansetron, linezolid, or another antidepressant). Pregnancy does not change serotonin-syndrome physiology, but the obstetric setting introduces several of these drugs (notably ondansetron for hyperemesis), so review the full medication list rather than the SSRI in isolation.
Clinic-Ready Tools
The Patient Script — Shared Decision-Making
When we think about your treatment, we look at two sets of risks. We know a lot about these medications — they've been used in millions of pregnancies and don't show a pattern of birth defects. On the other hand, we also know the risks of not treating the depression.
Untreated, your body produces high levels of stress hormones like cortisol, which can affect the baby's growth and raise the chance of you becoming very unwell after the baby arrives. Our goal is the lowest effective dose to keep you stable — because a healthy, present mother is the most important thing for your baby's development.
EMR Documentation Template
Maternal risks of untreated illness: Reviewed — poor prenatal self-care, increased preterm-birth risk, elevated risk of postpartum depression/psychosis.
Fetal / neonatal risks: Discussed lack of association with structural malformations (for [sertraline / escitalopram]); low absolute PPHN risk (~0.3%); potential for transient neonatal adaptation syndrome (jitteriness, tachypnea) at birth.
Obstetric management: Discussed small potential increase in PPH risk; patient advised to notify OB provider.
Plan: [Continue / Initiate] [medication] at [dose]. Educated on agent-specific PK changes — e.g., paroxetine/fluvoxamine: likely need for 3rd-trimester dose increase; sertraline: monitor for increased side effects as levels may rise. Neonatal team to be notified at delivery of agent + dose.
The single highest-impact action at the point of delivery is ensuring the pediatric/neonatal team knows the mother is on an SSRI — the specific agent and dose. This enables proactive monitoring for PNAS without any medication change that could destabilize the mother.
References
- Huybrechts KF, et al. Antidepressant use in pregnancy and the risk of cardiac defects. N Engl J Med. 2014;370(25):2397–2407.
- Gao SY, et al. SSRI use during early pregnancy and congenital malformations: a systematic review and meta-analysis of cohort studies of more than 9 million births. BMC Med. 2018;16(1):205.
- Fabiano N, et al. Safety of psychotropic medications in pregnancy: an umbrella review. Mol Psychiatry. 2025;30(1):327–335.
- Huybrechts KF, et al. Antidepressant use late in pregnancy and risk of persistent pulmonary hypertension of the newborn. JAMA. 2015;313(21):2142–2151.
- Kieler H, et al. SSRIs during pregnancy and risk of persistent pulmonary hypertension in the newborn. BMJ. 2012;344:d8012.
- Masarwa R, et al. Prenatal exposure to SSRIs and SNRIs and risk for PPHN: a systematic review, meta-analysis, and network meta-analysis. Am J Obstet Gynecol. 2019;220(1):57.e1–57.e13.
- Cornet MC, et al. Maternal treatment with SSRIs during pregnancy and delayed neonatal adaptation: a population-based cohort study. Arch Dis Child Fetal Neonatal Ed. 2024;109(3):294–300.
- Moses-Kolko EL, et al. Neonatal signs after late in utero exposure to serotonin reuptake inhibitors. JAMA. 2005;293(19):2372–2383.
- Hu S, et al. Association of antidepressant use during pregnancy and pregnancy-induced hypertension: a systematic review and meta-analysis. BMC Pregnancy Childbirth. 2025;25(1):884.
- Skalkidou A, et al. SSRI use during pregnancy and risk for postpartum haemorrhage. BJOG. 2020;127(11):1366–1373.
- Suarez EA, et al. Association of antidepressant use during pregnancy with risk of neurodevelopmental disorders in children. JAMA Intern Med. 2022;182(11):1149–1160.
- Cohen LS, et al. Relapse of major depression during pregnancy in women who maintain or discontinue antidepressant treatment. JAMA. 2006;295(5):499–507.
- Bayrampour H, et al. The risk of relapse of depression during pregnancy after discontinuation of antidepressants: a systematic review and meta-analysis. J Clin Psychiatry. 2020;81(4):19r13134.
- Cesta CE, et al. Postpartum psychiatric outcomes and sick leave after discontinuing SSRI or SNRI in pregnancy. JAMA Netw Open. 2024;7(10):e2438269.
- Trinh NTH, et al. Timing of antidepressant discontinuation during pregnancy and postpartum psychiatric outcomes in Denmark and Norway. JAMA Psychiatry. 2023;80(5):441–450.
- Westin AA, et al. Selective serotonin reuptake inhibitors and venlafaxine in pregnancy: changes in drug disposition. PLoS One. 2017;12(7):e0181082.
- Stika CS, et al. Changes in sertraline plasma concentrations across pregnancy and the postpartum period. Clin Pharmacol Ther. 2022. (CYP2C19 genotype as a source of inter-individual variability.)
- Hendrick V, et al. Placental passage of antidepressant medications. Am J Psychiatry. 2003;160(5):993–996.
- Préta LH, et al. Prediction of maternal and fetal exposure to escitalopram, sertraline, and paroxetine by combining human ex vivo placenta perfusion data and PBPK modeling. Clin Pharmacokinet. 2025. doi:10.1007/s40262-025-01574-5.
- Schoretsanitis G, et al. Antidepressant transfer into amniotic fluid, umbilical cord blood & breast milk: a systematic review & combined analysis. Prog Neuropsychopharmacol Biol Psychiatry. 2021;107:110228.
- ACOG Clinical Practice Guideline No. 5: Treatment and management of mental health conditions during pregnancy and postpartum — psychiatric medication. Obstet Gynecol. 2023;141(6):1262–1288. (Current guideline; supersedes Committee Opinion No. 354.)
- ACOG Committee Opinion No. 354: Treatment with selective serotonin reuptake inhibitors during pregnancy. Obstet Gynecol. 2006;108(6):1601–1603. (Historical; superseded by CPG No. 5.)
- AHA Scientific Statement: Optimizing psychological health across the perinatal period. J Am Heart Assoc. 2025;14(5):e041369.
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