Major psychiatric disorders (MPDs) and premenstrual disorders (PMDs) are often comorbid, with indications of shared genetic architecture. However, the specific genetic variants underlying this comorbidity remain elusive. The aim of this study was to identify genomic loci shared between MPDs and PMDs, and to assess the functional characteristics of genes mapped to these loci.

We used genome-wide association data for symptoms of PMDs (S-PMD, n = 67 068) from the Norwegian Mother, Father and Child Cohort Study (MoBa), and for MPDs (schizophrenia, n = 130 644; bipolar disorder, n = 827 335; major depression, n = 1 918 432) from the Psychiatric Genomic Consortium. Shared genetic loci were identified with the conjunctional false discovery rate (conjFDR). Genes mapped to the identified loci were included in functional and pharmacological gene-set enrichment analyses (GSEAs).

We identified 20 loci shared between S-PMD and the MPDs, including 19 novel loci for S-PMD (conjFDR<0.05). GSEA revealed genes involved in calcium signaling and neuronal projection pathways. The drug enrichment analysis identified 36 drugs, including riluzole and mianserin, significantly associated with the identified molecular pathways.

We identified 20 genetic loci shared between the S-PMD and MPDs, implicating calcium transmission in the pathogenesis of PMDs. Together with the drug enrichment results, this provides a biological basis for repurposing existing drugs in the treatment of PMD.

Multiple observational studies have reported associations between age at menarche (AAM) and mental health problems, yet their shared genetic architecture remains poorly characterized.

We leveraged genome-wide association study summary statistics for AAM and 15 mental health-related phenotypes. We conducted a multi-method integrative analysis encompassing linkage disequilibrium score regression, pleiotropic analysis under the composite null hypothesis, functional mapping and annotation, multi-marker analysis of genomic annotation, pathway enrichment, and bidirectional two-sample Mendelian randomization (MR) to explore shared genetic architecture and potential causal relationships.

Our study identified significant genetic correlations between AAM and eight mental health-related phenotypes (miserableness, fed-up feelings, nervous feelings, ever thought that life is not worth living, ever self-harmed, depression, ever smoker, and age started smoking in former smokers). A total of 155 pleiotropic loci, 18 colocalized loci (e.g., 6q16.3), and 203 pleiotropic genes (e.g., LIN28B) were identified. These genes are expressed in multiple regions, including the cerebral cortex and hypothalamus, and are involved in various biological processes and signaling pathways. Additionally, MR analysis revealed causal associations between AAM and 5 mental health-related phenotypes (mood swings, miserableness, fed-up feelings, and age at which smokers started smoking in former/current smokers).

Our study revealed extensive genetic associations between AAM and mental health-related phenotypes, and further explored the potential causal relationships between them. These findings enhance our understanding of the relationship from a genetic perspective and establish a foundation for future research to explore the biological pathways and environmental interactions contributing to these associations.

Network analysis was employed to test whether the overall pattern of depressive–anxious symptom connections remains stable or whether specific symptom-to-symptom links shift from pregnancy to postpartum.

In a perinatal sample (n = 4,461 pregnant women, n = 5,711 postpartum women), depressive and anxiety symptoms were assessed with the Edinburgh Postnatal Depression Scale (EPDS) and Generalized Anxiety Disorder-7 (GAD-7). Phase-specific polychoric Gaussian graphical models were estimated with EBICglass. We examined strength and bridge centrality, community structure, and nodewise predictability, and compared networks using the network comparison test.

Depression and anxiety formed four reproducible communities (one GAD-7 worry/arousal and three EPDS affective/anhedonic, anxious–cognitive distress, and depressed affect/sleep–suicidality modules) with identical partitions across phases. Global strength was similar, but postpartum networks showed higher edge density and more negative partial correlations, suggesting localized changes in which symptom pairs were directly linked—and how strongly—across phases. Across phases, Sadness, Crying, Uncontrollable worrying, and Trouble relaxing were most central and predictable. Worry-, arousal-, and sleep-related symptoms (e.g., hard to sleep) showed the strongest bridge centrality postpartum, and Self-harm was a prominent bridge during pregnancy; several edges shifted between phases, including stronger Enjoyment–Self-harm and weaker Hard to sleep–Self-harm postpartum.

Perinatal depression and anxiety organize into cohesive yet partially distinct symptom networks that remain globally stable but show localized shifts in direct symptom-to-symptom connections from pregnancy to postpartum. Central affective and arousal nodes, particularly sadness, pathological worry, and sleep disturbance, may be high-yield targets for phase-tailored screening and intervention.

Peripartum depression (PPD) is one of the most common pregnancy complications; nevertheless, it often goes underdiagnosed. Pinpointing important correlates is crucial for early risk identification and pathophysiology understanding. We aimed to investigate the association between self-reported mood swings during oral contraceptive (OC) use and peripartum depressive symptoms (PPDS).

We used data from the Swedish longitudinal cohort study Mom2B. 3829 women who had reported previous usage of OCs were included. Self-reported mood swings during OC use were assessed through a single question, and PPDS were evaluated using established cut-offs of the Edinburgh Postnatal Depression Scale (EPDS).

Self-reported mood swings during OC use were associated with PPDS at gestational weeks 12–22 (OR = 1.30, 95% CI, 1.01–1.66), 24–34 (OR = 1.37, 95% CI, 1.10–1.71) and 36–42 (OR = 1.39, 95% CI, 1.05–1.82) as well as at postpartum weeks 6–13 (OR = 1.46, 95% CI, 1.12–1.92) and 24–35 (OR = 2.07, 95% CI, 1.43–2.99). Interestingly, self-reported mood swings during OC use were associated with higher odds for newly developed PPDS in early postpartum (OR for weeks 6–13 = 1.92, 95% CI: 1.19–3.08).

Women with self-reported mood swings during OC use have higher risk of experiencing depressive symptoms across the peripartum period and twice the risk of newly developed PPDS during the early postpartum, adding to current evidence of a hormonal sensitive subgroup of women and the opportunity to use this simple question in future predictive efforts.

Maternal depressive symptoms can influence brain development in offspring, prenatally through intrauterine programming, and postnatally through caregiving related mother–child interaction.

The participants were 5-year-old mother–child dyads from the FinnBrain Birth Cohort Study (N = 68; 28 boys, 40 girls). Maternal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale (EPDS) at gestational week 24, 3 months, 6 months, and 12 months postnatal. Children’s brain imaging data were acquired with task-free functional magnetic resonance imaging (fMRI) at the age of 5 years in 7-min scans while watching the Inscapes movie. The derived brain metrics included whole-brain regional homogeneity (ReHo) and seed-based connectivity maps of the bilateral amygdalae.

We found that maternal depressive symptoms were positively associated with ReHo values of the left amygdala. The association was highly localized and strongest with the maternal depressive symptoms at 3 months postnatal. Seed-based connectivity analysis did not reveal associations between distal connectivity of the left amygdala region and maternal depressive symptoms.

These results suggest that maternal depressive symptoms soon after birth may influence offspring’s neurodevelopment in the local functional coherence in the left amygdala. They underline the potential relevance of postnatal maternal distress exposure on neurodevelopment that has received much less attention than prenatal exposures. These results offer a possible thus far understudied pathway of intergenerational effects of perinatal depression that should be further explored in future studies.

Knowledge of the impact of perimenopause on women with attention-deficit/hyperactivity disorder (ADHD) is lacking. We compared levels of perimenopausal symptoms and prevalence of severe perimenopausal symptoms among women with and without ADHD across age groups.

In this cohort study, we used data from the population-based Stress-and-Gene-Analysis cohort study. ADHD diagnosis was self-reported at baseline and 5-year follow-up. At follow-up, we assessed ADHD symptoms using the Adult ADHD Self-Report Scale, perimenopausal symptoms (psychological, somatic, and urogenital) using Menopause Rating Scale (MRS), and general physical symptoms using Patient Health Questionnaire. We described mean scores and mean difference on MRS among women with and without ADHD with linear regression models and contrasted the prevalence of severe perimenopausal symptoms among women with and without ADHD, calculating prevalence ratios (PRs) with 95% confidence intervals (CIs) using modified Poisson regression models.

Women with ADHD (n = 535) had higher total perimenopausal symptom scores (18.0 vs. 13.0, p < 0.01) than women without ADHD (n = 4,857). The difference was most pronounced among women aged 35–39 years (19.0 vs. 12.5, p < 0.01). The prevalence of severe perimenopausal symptoms was significantly higher among women with ADHD compared to those without, both overall (54.2% vs. 30.1%, PR = 1.80, 95% CI = 1.64–1.98) and on all subdimensions (psychological: 58.6% vs. 36.0%, PR = 1.63, 95% CI = 1.51–1.76; somatic: 30.4% vs. 13.9%, PR = 2.20, 95% CI = 1.88–2.57; uro-genital: 43.2% vs. 27.5%, PR = 1.57, 95% CI = 1.40–1.77).

Women with ADHD have higher prevalence of severe perimenopausal symptoms. These symptoms present at an earlier age than among women without ADHD, indicating an earlier onset age of perimenopause in ADHD.

Certain prescription drugs used during pregnancy are associated with offspring autism spectrum disorder (ASD). Nonetheless, ASD risk following prenatal exposure to most drugs remains unknown. Furthermore, methodological challenges and ethical concerns hinder the scope for causal inference.

We used a case-cohort study design of a nationally representative sample from Israel to examine the associations between maternal prescription drug use during pregnancy and offspring ASD. To scrutinize these associations, the analyses were (a) adjusted for indication proxy (level 2 Anatomical Therapeutic Chemical (ATC) codes), (b) repeated using shared pharmacological targets as exposures, and (c) inspected further through target-enrichment analysis.

The sample included 1,400 individuals with and 94,713 without an ASD diagnosis. Among all drugs prescribed during pregnancy, five were statistically significantly associated with increased offspring ASD risk after adjustment for indication proxy (e.g., hazard ratio [95% confidence interval] cyproterone = 2.71 [1.17–6.25] and prednisolone = 2.10 [1.27–3.49]), and two with decreased risk (ferrous sulfate = 0.82 [0.68, 0.99] and lynestrenol = 0.43 [0.2, 0.93]). Further analysis revealed four pharmacological targets shared by these drugs, which were themselves associated with ASD (e.g., neuronal acetylcholine receptor α4β4 = 1.45 [1.05–1.99] and serotonin 2b receptor = 1.31 [1.04–1.61]). Enrichment analysis suggested the association between ASD and medications affecting cholinergic and serotonergic signaling.

Increased ASD risk followed prenatal exposure to five prescription drugs, and decreased risk followed exposure to two. Subsequent analyses suggested no confounding by indication in these associations, but further studies are warranted.

Antenatal depression symptom is a global health concern, but the trajectories of antenatal depression symptom vary across different studies. Additionally, the influencing factors and adverse pregnancy outcomes of antenatal depression symptom may differ across heterogeneous subtypes, which requires further exploration.

A prospective cohort study was conducted in Hubei province, China, from July 2022 to September 2023. Pregnant women (<14 weeks) were enrolled and followed up at 16, 21, 28, and 37 gestational weeks, with depressive symptom measured using the Edinburgh Postnatal Depression Scale (EPDS). Latent class growth modeling and logistic regression were used for data analysis.

Of 1034 women enrolled, 725 completed all follow-ups. Four depressive symptom trajectories were identified: no depression group (32.13%), persistent subclinical depression group (42.48%), persistent moderate depression group (19.17%), and persistent high depression group (6.21%). Risk factors of depressive symptom trajectories included low social capital, unplanned pregnancy, primiparity, mental illness history, high perceived stress, and low resilience (p < 0.05). Compared to the no depression group, gestational diabetes mellitus (GDM) risk was 1.90 times higher in the persistent moderate group and 2.59 times higher in the persistent high group; small for gestational age (SGA) risk was 2.42 times higher in the persistent moderate group and 3.98 times higher in the persistent high group.

This study identified four antenatal depressive symptom trajectories. Persistent moderate and high depression groups were linked to GDM and SGA, highlighting the importance of mental health assessments and intervention for pregnant women, especially those with higher depression severity, to prevent adverse outcomes.

Maternal alcohol consumption can adversely affect children’s development, but the impact of paternal drinking is less understood. We aimed to investigate whether maternal or paternal alcohol consumption during pregnancy affected children’s mental health and behavior.

A total of 2,013 parent–child triads from the European Longitudinal Study of Pregnancy and Childhood cohort were used. Data on alcohol consumption was obtained from questionnaires during pregnancy and after the child’s birth. Mental health and behavior of children were assessed with Strength and Difficulties Questionnaire (SDQ). The associations were tested using linear regression, adjusting for socio-demographic and psychosocial covariates.

Increased maternal alcohol consumption was associated with higher total SDQ scores at ages 7, 11, and 18 years old when the outcomes were reported by mothers, but only at 11 years when reported by children. We did not observe any dose–response relationship, and the effect size did not change during the follow-up. The effects were observed across various domains of SDQ: in the emotional symptoms subscale at age 11, in the conduct problems subscale at ages 7 and 11, and in the hyperactivity/inattention subscale at age 18. Paternal alcohol consumption was not associated with SDQ.

Maternal alcohol consumption during pregnancy is associated with long-term effects on children’s mental health and behavior, particularly when reported by mothers. No association was found between paternal alcohol consumption, suggesting that the results may stem from biological effects of alcohol or other factors beyond the direct exposure, potentially encompassing broader maternal psychosocial or behavioral characteristics.

Postpartum anxiety (PPA) symptoms have harmful effects on child development and mother–infant interactions. Accordingly, in-depth knowledge of associated risk factors is crucial for prevention policies. This study aimed to estimate PPA symptom prevalence at 2 months and to identify associated risk factors in a representative sample of all women who gave birth in France in 2021, and in two subgroups: women with no postpartum depression (PPD) symptoms, and those with no history of mental health care.

Among the 12,723 women included in the representative French national perinatal survey 2021ENP, 7,133 completed the Edinburgh Postnatal Depression Scale (EPDS) self-administered questionnaire – including three anxiety-specific items (EPDS-3A) – at 2 months postpartum. We estimated the adjusted prevalence ratios (aPR) of PPA symptoms using Poisson regression models with robust variance.

PPA symptom prevalence at 2 months was 27.6% (95% CI [26.5–28.8]). Associated risk factors were: age ≤ 34 years (maximum aPR = 1.38 [1.22–1.58] obtained for persons aged 25–29 years vs. 35–39 years), poorer health literacy (1.15 [1.07–1.23]), a history of medical termination of pregnancy (1.32 [1.05–1.68]), psychological (1.31 [1.17–1.47]) or psychiatric (1.42 [1.24–1.63]) care history since adolescence, nulliparity (1.23 [1.12–1.35]), no weight gain or loss (1.29 [1.03–1.61] vs. 9–15 kg gain) or gain ≥23 kg (1.20 [1.00–1.43]) during pregnancy, ≥3 pregnancy-related emergency consultations (1.16 [1.03–1.31] vs. none), poor/good support during pregnancy, (1.16 [1.00–1.34] and 1.15 [1.05–1.26], respectively, vs. very good), sadness (1.52 [1.36–1.69]), anhedonia (1.48 [1.27–1.72]), or both (1.99 [1.79–2.21]) during pregnancy, not at all/not very satisfied with pain management during childbirth (1.16 [1.01–1.32] vs. quite/very satisfied). Similar risk factors were found in the ‘no PPD symptoms’ and ‘no history of mental health care’ subgroups.

Estimated PPA symptom prevalence at 2 months in our study sample was 27.6%. The risk factors we identified may guide future prevention policies.

This prospective study aimed to assess couples’ psychological status during the perinatal period to identify those at risk for postpartum depression.

Conducted at Lyon University Hospital from March to July 2022, the study enrolled pregnant women without progressive psychiatric disorders or obstetric risk factors, and their partners. Participants completed the Edinburgh Postnatal Depression Scale (EPDS) at three points: during the 9th month of pregnancy, immediate postpartum, and 6–8 weeks after delivery. A score ≥10 on the EPDS indicated depression risk. A score ≥10 on the EPDS indicate depression risk. The primary endpoint was EPDS scores throughout the perinatal period.

Ninety-five couples participated; 96% of patients and 68% of partners completed pre-delivery questionnaires, 81% and 71% during maternity stay, and 64% and 46% postpartum, respectively. Overall, 15% of patients and 1% of partners had EPDS scores >10 in the postpartum period. Psychiatric history and emergency cesarean sections were associated with higher immediate postpartum EPDS scores in patients [Beta 3.7 points, 95% CI 0.91; 6.4 and Beta 5.2 points, 2.2; 8.1, respectively]. Episiotomy was associated with higher EPDS scores in partners. No significant association between the different factors studied and the EPDS score was found at 6–8 weeks postpartum in patients nor their partners.

While specific risk factors for persistent perinatal depression in couples were not identified, a notable proportion of patients exhibited high EPDS scores. Screening all couples during prepartum and postpartum periods is crucial, regardless of identified risk factors.

There is growing concern regarding teratogenic effect of antipsychotics. Previous research assessing association between antipsychotics and congenital malformations (CMs) yielded mixed results and were all derived from Western countries. We aimed to examine risk of major and organ/system-specific CMs associated with prenatal antipsychotic exposure in Hong Kong.

This population-based study identified women aged 15–50 years who delivered their first/singleton child between 2003–2018 from public healthcare service database. Propensity score (PS)-weighted logistic-regression analyses were performed to examine risk of CMs following first-trimester exposure to antipsychotic classes (second- and first-generation antipsychotic; SGA and FGA) and six most frequently-prescribed individual antipsychotics.

Of 465,069 women, 419 and 420 redeemed ≥1 prescription of SGA and FGA during first-trimester, respectively. Prevalence of any CMs was 4.9% (95%CI:4.9–5.0%) in unexposed-infants, 9.1% (6.7–12.3%) in SGA-exposed infants, and 6.2% (4.3–9.0%) in FGA-exposed infants. SGA exposure (adjusted-odds-ratio: 2.11 [95%CI:1.19–3.86]) was associated with increased risk of CMs. This finding was consistent with sensitivity analyses addressing exposure misclassification and confounding by treatment indication, but not with PS-matched sensitivity analysis. Elevated risk of CMs was observed in infants exposed to high-dose olanzapine (7.50 [1.65–36.13]) and high-dose quetiapine (15.03 [4.86–56.72]), but with wide-CIs. Organ/system-specific malformations were not associated with SGA, FGA or individual antipsychotics.

We observed a small increased risk of major malformations associated with SGA, but was not consistently affirmed in sensitivity analyses, precluding firm conclusions. Research with large sample size clarifying comparative safety of individual antipsychotics on specific malformations is warranted.

Evidence on the negative outcomes of untreated mental disorders during pregnancy and in the first year after childbirth on women’s and children’s health has stimulated interest in how to develop and sustain high-quality mental health care during the perinatal period. In Italy, there is a lack of knowledge about how mental health services support women with perinatal mental disorders (PMDs). This study aims to describe the adoption of good practices for the prevention and care of PMDs by the Italian mental health departments (MHDs).

This is a nationwide cross-sectional survey conducted online using LimeSurvey. Starting from the Ministry of Health Registry’s 127 MHDs were invited to participate between February and March, 2023. Characteristics of the participating MHDs were reported as descriptive statistics.

One hundred nineteen MHDs participated, with a response rate of 93.7%. Regarding the prevention of PMDs, 69 (58.0%) MHDs offer preconception counseling, whereas only 6 (5.0%) have information material for this purpose. Written integrated care pathways for PMDs are not available in 94 (79.7%) MHDs. A reference professional for psychopharmacological treatment during pregnancy or breastfeeding is available in 55 (46.2%) MHDs, while a specific treatment plan for women with PMDs is adopted by 27 (22.7%) MHDs. Thirty-four (28.6%) MHDs have established an outpatient clinic for PMDs, whereas there are no inpatient psychiatric facilities designed for mothers and infants (mother-baby units).

There is a need to improve the care of women with PMDs in Italy. The provision of pre-conception counseling, integrated care pathways, and specialist skills and facilities for PMDs should be prioritized.

To identify the different factors associated with postpartum blues and its association with postpartum depression, from a large French cohort.

We conducted an analysis of the Interaction Gene Environment in Postpartum Depression cohort, which is a prospective, multicenter cohort including 3310 women. Their personal (according to the Diagnostic and Statistical Manual, fifth edition [DSM-5]) and family psychiatric history, stressful life events during childhood, pregnancy, and delivery were collected. Likewise, the French version of the Maternity Blues Scale questionnaire was administered at the maternity department. Finally, these women were assessed at 8 weeks and 1 year postpartum by a clinician for postpartum depression according to DSM-5 criteria.

The prevalence of postpartum blues in this population was 33%, and significant factors associated with postpartum blues were found as personal (aOR = 1.2) and family psychiatric history (aOR = 1.2), childhood trauma (aOR = 1.3), obstetrical factors, or events related to the newborn, as well as an experience of stressful life events during pregnancy (aOR = 1.5). These factors had a cumulative effect, with each additional factor increasing the risk of postpartum blues by 31%. Furthermore, adjustment for sociodemographic measures and history of major depressive episode revealed a significant association between postpartum blues and postpartum depression, mainly at early onset, within 8 weeks after delivery (aOR = 2.1; 95% CI = 1.6–2.7), but also at late onset (aOR = 1.4; 95% CI = 1.1–1.9), and mainly if the postpartum blues is severe.

These results justify raising awareness among women with postpartum blues, including reassurance and information about postpartum depression, its symptomatology, and the need for management in case of worsening or prolongation of postpartum blues.

Attention-deficit hyperactivity disorder (ADHD) is highly heritable, though environmental factors also play a role. Prenatal maternal stress is suggested to be one such factor, including exposure to highly distressing events that could lead to post-traumatic stress disorder (PTSD). The aim of this study is to investigate whether prenatal maternal PTSD is associated with offspring ADHD.

A register-based retrospective cohort study linking 553 766 children born in Sweden during 2006–2010 with their biological parents. Exposure: Prenatal PTSD. Outcome: Offspring ADHD. Logistic regression determined odds ratios (ORs) with 95% confidence intervals (CIs) for ADHD in the offspring. Adjustments were made for potential covariates, including single parenthood and possible indicators of heredity measured as parental ADHD and maternal mental disorders other than PTSD. Subpopulations, excluding children with indicators of heredity, were investigated separately.

In the crude results, including all children, prenatal PTSD was associated with offspring ADHD (OR: 1.79, 95% CI: 1.37–2.34). In children with indicators of heredity, the likelihood was partly explained by it. Among children without indicators of heredity, PTSD was associated with offspring ADHD (OR: 2.32, 95% CI: 1.30–4.14), adjusted for confounders.

Prenatal maternal PTSD is associated with offspring ADHD regardless of indicators of heredity, such as parental ADHD or maternal mental disorder other than PTSD. The association is partly explained by heredity and socioeconomic factors. If replicated in other populations, preferably using a sibling design, maternal PTSD could be identified as a risk factor for ADHD.

Postpartum depression affects around 12% of mothers in developed countries, with consequences for the whole family. Many women with depressive symptoms remain undetected and untreated. The aim of this study was to investigate to what extent women with depressive symptoms at 6 weeks postpartum are identified by the healthcare system, the interventions they received, and remission rates at 6 months postpartum.

Postpartum women scoring 12–30 on the Edinburgh Postnatal Depression Scale (EPDS) at 6 weeks after delivery (n = 697) were identified from the longitudinal cohort study “Biology, Affect, Stress, Imaging and Cognition” (BASIC) in Uppsala, Sweden. A total of 593 women were included. Background and remission information at 6 months was collected from the BASIC dataset. Medical records were examined to identify interventions received.

Most women (n = 349, 58.7%) were not identified by the healthcare system as having depressive symptoms and 89% lacked any record of interventions. Remission rates at 6 months postpartum were 69% in this group. Among women identified by the healthcare system, 90% received interventions and about 50% were in remission at 6 months postpartum. The EPDS reduction during the study period was largest in the group identified by the child health services (CHS, −5.15) compared to the non-identified (−4.24, p < 0.001).

Despite screening guidelines, many women with depressive symptoms had no documentation of screening or interventions by the healthcare system. Furthermore, a significant proportion did not achieve remission despite interventions. Being identified by CHS was associated with the largest reduction of symptoms. Research is needed to understand gaps in the healthcare processes, to better identify peripartum depression.

There are few data on long-term neurological or cognitive outcomes in the offspring of mothers with type 1 diabetes (T1D). The aims of this study were to examine if maternal T1D increases the risk of intellectual disability (ID) in the offspring, estimate the amount of mediation through preterm birth, and examine if the association was modified by maternal glycated hemoglobin (HbA1c).

Population-based cohort study using population-based data from several national registries in Sweden.

All offspring born alive in Sweden between the years 1998 and 2015.

The risk of ID was estimated through hazard ratios with 95% confidence intervals (HR, 95% CI) from Cox proportional hazard models, adjusting for potential confounding. Risks were also assessed in mediation analyses and in subgroups of term/preterm births, in relation to maternal HbA1c and by severity of ID.

In total, 1,406,441 offspring were included. In this cohort, 7,794 (0.57%) offspring were born to mothers with T1D. The risk of ID was increased in offspring of mothers with T1D (HR; 1.77, 1.43–2.20), of which 47% (95% CI: 34–100) was mediated through preterm birth. The HRs were not modified by HbA1c.

T1D in pregnancy is associated with moderately increased risks of ID in the offspring. The risk is largely mediated by preterm birth, in particular for moderate/severe cases of ID. There was no support for risk-modification by maternal HbA1c.

Perinatal mental health disorders (PMHD) remain often undetected, undiagnosed, and untreated with variable access to perinatal mental health care (PMHC). To guide the design of optimal PMHC (i.e., coproduced with persons with lived experience [PLEs]), this qualitative participatory study explored the experiences, views, and expectations of PLEs, obstetric providers (OP), childcare health providers (CHPs), and mental health providers (MHPs) on PMHC and the care of perinatal depression.

We conducted nine focus groups and 24 individual interviews between December 2020 and May 2022 for a total number of 84 participants (24 PLEs; 30 OPs; 11 CHPs; and 19 MHPs). The PLEs group included women with serious mental illness (SMI) or autistic women who had contact with perinatal health services. We recruited PLEs through social media and a center for psychiatric rehabilitation, and health providers (HPs) through perinatal health networks. We used the inductive six-step process by Braun and Clarke for the thematic analysis.

We found some degree of difference in the identified priorities between PLEs (e.g., personal recovery, person-centered care) and HPs (e.g., common culture, communication between providers, and risk management). Personal recovery in PMHD corresponded to the CHIME framework, that is, connectedness, hope, identity, meaning, and empowerment. Recovery-supporting relations and peer support contributed to personal recovery. Other factors included changes in the socio-cultural conception of the peripartum, challenging stigma (e.g., integrating PMH into standard perinatal healthcare), and service integration.

This analysis generated novel insights into how to improve PMHC for all users including those with SMI or autism.