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Women with psychiatric diagnoses are at increased risk of preterm birth (PTB), with potential life-long impact on offspring health. Less is known about the risk of PTB in offspring of fathers with psychiatric diagnoses, and for couples where both parents were diagnosed. In a nationwide birth cohort, we examined the association between psychiatric history in fathers, mothers, and both parents and gestational age. We included all infants live-born to Nordic parents in 1997 to 2016 in Sweden. Psychiatric diagnoses were obtained from the National Patient Register. Data on gestational age were retrieved from the Medical Birth Register. Associations between parental psychiatric history and PTB were quantified by relative risk (RR) and two-sided 95% confidence intervals (CIs) from log-binomial regressions, by psychiatric disorders overall and by diagnostic categories. We extended the analysis beyond PTB by calculating risks over the whole distribution of gestational age, including \"early term\" (37 to 38 weeks). Among the 1,488,920 infants born throughout the study period, 1,268,507 were born to parents without a psychiatric diagnosis, of whom 73,094 (5.8%) were born preterm. 4,597 of 73,500 (6.3%) infants were born preterm to fathers with a psychiatric diagnosis, 8,917 of 122,611 (7.3%) infants were born preterm to mothers with a pscyhiatric diagnosis, and 2,026 of 24,302 (8.3%) infants were born preterm to both parents with a pscyhiatric diagnosis. We observed a shift towards earlier gestational age in offspring of parents with psychiatric history. The risks of PTB associated with paternal and maternal psychiatric diagnoses were similar for different psychiatric disorders. The risks for PTB were estimated at RR 1.12 (95% CI [1.08, 1.15] p < 0.001) for paternal diagnoses, at RR 1.31 (95% CI [1.28, 1.34] p < 0.001) for maternal diagnoses, and at RR 1.52 (95% CI [1.46, 1.59] p < 0.001) when both parents were diagnosed with any psychiatric disorder, compared to when neither parent had a psychiatric diagnosis. Stress-related disorders were associated with the highest risks of PTB with corresponding RRs estimated at 1.23 (95% CI [1.16, 1.31] p < 0.001) for a psychiatry history in fathers, at 1.47 (95% CI [1.42, 1.53] p < 0.001) for mothers, and at 1.90 (95% CI [1.64, 2.20] p < 0.001) for both parents. The risks for early term were similar to PTB. Co-occurring diagnoses from different diagnostic categories increased risk; for fathers: RR 1.10 (95% CI [1.07, 1.13] p < 0.001), 1.15 (95% CI [1.09, 1.21] p < 0.001), and 1.33 (95% CI [1.23, 1.43] p < 0.001), for diagnoses in 1, 2, and ≥3 categories; for mothers: RR 1.25 (95% CI [1.22, 1.28] p < 0.001), 1.39 (95% CI [1.34, 1.44] p < 0.001) and 1.65 (95% CI [1.56, 1.74] p < 0.001). Despite the large sample size, statistical precision was limited in subgroups, mainly where both parents had specific psychiatric subtypes. Pathophysiology and genetics underlying different psychiatric diagnoses can be heterogeneous. Paternal and maternal psychiatric history were associated with a shift to earlier gestational age and increased risk of births before full term. The risk consistently increased when fathers had a positive history of different psychiatric disorders, increased further when mothers were diagnosed and was highest when both parents were diagnosed.

Incidence of gestational diabetes (GDM) has increased rapidly. It poses significant risks for both mother and fetus affecting also negatively their longer-term metabolic heath. We asked whether early pregnancy maternal hemoglobin (Hb) levels, indicative for tissue oxygenation, would affect mother’s metabolic health and fetal outcome. We assessed in FinnGeDi, a Finnish multicenter case–control study for GDM (n = 1828), association of maternal 1st trimester Hb levels with metabolic parameters and perinatal outcome. Our data show that mothers with GDM had higher Hb levels compared to controls (mean difference 1.746 g/L). Hb levels associated positively with pre-pregnancy body mass index (BMI), fasting glucose levels and glucose levels in a glucose tolerance test and systolic and diastolic blood pressure (bp) levels. When assessed in quartiles the highest Hb quartile had more chronic and gestational hypertension and the most adverse outcome of the metabolic parameters, dose-dependency seen in bp, BMI and glucose levels. In a multivariable regression analysis Hb levels remained an independently associated parameter for GDM after adjusting for key covariates (OR 1.019, 95% CI [1.007; 1.031]). In conclusion, higher maternal Hb levels within the normal variation are an independent risk factor for GDM in this population but have little effect on perinatal outcome.

Gestational diabetes (GDM) is often accompanied by maternal overweight. Our aim was to evaluate the separate and concomitant effects of GDM and maternal overweight/obesity on perinatal outcomes. We used the Finnish Medical Birth Register to identify all 24,577 women with a singleton pregnancy who delivered in 2009 in Finland and underwent an oral glucose tolerance test (OGTT). Women were divided into groups according to the result of OGTT (GDM/no GDM) and pre-pregnancy body mass index (BMI): normal weight (≤24.9 kg/m2), overweight (25.0-29.9 kg/m2), and obese (≥30.0 kg/m2). Primary outcomes included macrosomia, caesarean delivery, and treatment at neonatal ward. Normal weight women without GDM constituted the reference group. Compared to reference group, overweight or obese women without GDM had an increased risk of macrosomia [odds ratio adjusted for age, parity, smoking and socio-economic status (aOR)1.18 (95% CI 1.09-1.28) and 1.50 (95% CI 1.19-1.88)], and caesarean delivery [aORs 1.17 (95% CI 1.07-1.28) and 1.52 (95% CI 1.37-1.69)], respectively. In normal weight GDM women the risk of macrosomia [aOR 1.17 (95% CI 0.85-1.62)] and caesarean delivery [aOR 1.10 (95% CI 0.96-1.27)] was not significantly increased as compared to normal weight women without GDM. GDM increased the risk of treatment at neonatal ward in all BMI categories and maternal obesity without GDM was also a risk factor for treatment at neonatal ward. Interaction p values between BMI and GDM on these outcomes were <0.001. Maternal overweight and obesity without GDM increased the risk of macrosomia and caesarean delivery when compared to the reference group. These risks were amplified when overweight/obesity was accompanied by GDM. Obesity without GDM was a risk factor for treatment at neonatal ward; GDM increased this risk in all BMI categories. Our results suggest that especially maternal obesity should be considered as a risk factor for adverse pregnancy outcomes and GDM further amplifies this risk.

Importance Corticosteroids administered to women at risk of imminent preterm birth is one of the most effective ways to improve the prognosis of infants born preterm. Scant data about long-term neurodevelopmental and neurosensory outcomes among the treatment-exposed children are mixed, suggesting that not all domains of neurodevelopmental and neurosensory function may be equally affected. Moreover, the long-term outcomes may vary according to whether the treatment-exposed children are being born preterm (<37 weeks and 0 days) or term (≥37 weeks and 0 days). Objectives To study whether antenatal corticosteroid treatment is associated with psychological developmental and neurosensory disorders in children born term and preterm and whether the associations persist in a sibling-comparison design. Design, Setting, and Participants This population-based retrospective register-linkage study comprised all singleton live births in Finland between January 1, 2006, and December 31, 2017, followed up until December 31, 2018, as well as a sibling comparison among term sibling pairs. Data were analyzed from March 21, 2021, to July 7, 2022. Exposures Antenatal corticosteroid treatment. Main Outcomes and Measures Cox proportional hazards regression models were used to estimate the associations between antenatal corticosteroid treatment and physician-diagnosed specific developmental disorders of speech and language, scholastic skills, and motor function; pervasive developmental disorder; other or unspecified psychological developmental disorder; disorders of vison and hearing; epilepsy; and cerebral palsy. Results The study population comprised 670 097 singleton children (342 562 boys [51.1%]) followed up for a median of 5.8 years (IQR, 3.1-8.7 years). Of the 14 868 treatment-exposed children (2.2%; 53.9% boys), 6730 (45.3%) were born term, and 8138 (54.7%) were born preterm, and of the 655 229 nonexposed children (97.8%; 51.1% boys), 634 757 (96.9%) were born term, and 20 472 (3.1%) were born preterm. Of the 241 621 eligible maternal sibling pairs born term, 4128 (1.7%) were discordant for treatment exposure. Compared with nonexposure in the entire population, treatment exposure was significantly associated with higher adjusted hazard ratios (aHRs) for specific developmental disorders of speech and language (aHR, 1.38 [95% CI, 1.27-1.50];P < .001), specific developmental disorders of scholastic skills (aHR, 1.32 [95% CI, 1.13-1.54];P = .004), specific developmental disorder of motor function (aHR, 1.32 [95% CI, 1.18-1.49];P < .001), pervasive developmental disorder (aHR, 1.35 [95% CI, 1.17-1.56];P < .001), other or unspecified disorder of psychological development (aHR, 1.88 [95% CI, 1.58-2.25];P < .001), and vision or hearing loss (aHR, 1.22 [95% CI, 1.04-1.43];P = .02). Compared with nonexposure in the term-born group, treatment exposure was significantly associated with higher aHRs for specific developmental disorders of speech and language (aHR, 1.47 [95% CI, 1.31-1.66];P < .001), specific developmental disorders of scholastic skills (aHR, 1.28 [95% CI, 1.01-1.63];P = .04), specific developmental disorder of motor function (aHR, 1.38 [95% CI, 1.12-1.70];P < .001), pervasive developmental disorder (aHR, 1.42 [95% CI, 1.16-1.75];P < .001), other or unspecified disorder of psychological development (aHR, 1.92 [95% CI, 1.51-2.43];P < .001), epilepsy (aHR, 1.57 [95% CI, 1.22-2.01];P < .001), and cerebral palsy (aHR, 2.18 [95% CI, 1.47-3.23];P < .001). The hazard for any psychological developmental and neurosensory disorder was significantly higher for the treatment-exposed sibling compared with the nonexposed cosibling (absolute difference, 1.2% [95% CI, 0.03%-2.4%];P < .001; aHR, 1.22 [95% CI, 1.04-1.42];P = .01). Antenatal corticosteroids were not associated with either significant benefit or risk in the preterm group. Conclusions and Relevance This study suggests that the possible long-term psychological developmental and neurosensory harms warrant careful consideration of risks and benefits when deciding on maternal antenatal corticosteroid treatment.

[...]with advances in neonatal care, the survival for very preterm babies has improved, but longer-term risks in this group have not been comprehensively investigated. ASD has a male predominance, and size at birth is known to influence ASD risk, with increased risks in children born either small or large for GA [27–29]. [...]sex and size for GA should be considered in analyses of ASD risk by GA. To adjust for differences in birth weight, sex-specific size for GA was calculated as “small for GA” (below or equal to the 10th percentile), “appropriate for GA” (between the 11th and 90th percentile), and “large for GA” (above the 90th percentile) [36]. Cohort characteristics by gestational age (weeks) in 3,526,174 live births. https://doi.org/10.1371/journal.pmed.1003207.t001 Risk of ASD The risk of ASD by GA showed a gradual increase in risk of ASD from GA week 40 to GA week 24, and a small rise between GA week 40 and 44, with statistically significantly higher risk across the range of GA compared to the reference group of infants born week 40.

Overeating is a complex appetite trait, cross-sectionally linked to an elevated weight in children. However, little is known about longitudinal associations. Therefore, we studied how a tendency towards overeating predicts weight development between 8 and 16 years of age. In this study among 4517 children from the Finnish Health in Teens cohort, parents reported their child’s tendency to overeat when children were on average 11.2 (SD 0.8) years old. Children were then categorised as overeating, possibly overeating, or not overeating. Height and weight measurements from two data collection periods were combined with growth data from a national health register, and age- and sex-standardised body mass index z-scores (BMIz) were calculated using the International Obesity Task Force reference. Children also reported their lifestyle factors, including food consumption, physical activity, screen time, and sleep patterns. We examined the association between overeating and BMIz using a linear mixed model, adjusting for age, sex, specific food consumption frequencies, physical activity, screen time, and sleep duration. We further analysed whether associations differed by age, food consumption frequencies, or physical activity. The average BMIz in the overeating group was 1.18 (95% CI 1.10─1.26) units higher compared with those without overeating, but remained stable as age increased. Among those without overeating, BMIz increased 0.043 units per year of age ( p  < 0.001). Physical activity, but not food consumption, modified the association between overeating and BMIz ( p for interaction = 0.038). In the lowest third of physical activity (≤ 5 h/week), BMIz was 1.28 units higher (95% CI 1.15─1.41) in the overeating compared with the no overeating group, while in the highest third (≥ 9 h/week) the effect size was 1.08 (95% CI 0.93─1.24). In conclusion, children with a parent-reported tendency to overeat exhibited an elevated, but stable mean BMIz across adolescence. Public health programmes tackling the obesity epidemic should consider the differences in appetite self-regulation among children.

People who were born prematurely have high risks of many individual diseases and conditions in the early part of the life course. However, our knowledge of the burden of multiple diseases (multimorbidity) among prematurely born individuals is limited. We aimed to investigate the risk and patterns of chronic disease multimorbidity in adolescence and early adulthood among individuals born across the spectrum of gestational ages, comparing preterm and full-term born individuals. We used individual-level data from linked nationwide registers to examine the associations of gestational age at birth with specialised healthcare records of ≥2 chronic diseases (multimorbidity) in adolescence (age 10-17 years) and early adulthood (age 18-30 years). Our study population comprised 951,116 individuals (50.2% females) born alive in Finland between 1st January 1987 and 31st December 2006, inclusive. All individuals were followed from age 10 years to the onset of multimorbidity, emigration, death, or 31 December 2016 (up to age 30 years). We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for multimorbidity using flexible parametric survival models. During 6,417,903 person-years at risk (median follow-up: 7.9 years), 11,919 individuals (1.3%) had multimorbidity in adolescence (18.6 per 10,000 person-years). During 3,967,419 person-years at risk (median follow-up: 6.2 years), 15,664 individuals (1.7%) had multimorbidity in early adulthood (39.5 per 10,000 person-years). Adjusted HRs for adolescent multimorbidity, comparing preterm to full-term born individuals, were 1.29 (95% CI: 1.22 to 1.36) and 1.26 (95% CI: 1.18 to 1.35) in females and males, respectively. The associations of preterm birth with early adult multimorbidity were less marked, with the adjusted HRs indicating 1.18-fold risk in females (95% CI: 1.12 to 1.24) and 1.10-fold risk in males (95% CI: 1.04 to 1.17). We observed a consistent dose-response relationship between earlier gestational age at birth and increasing risks of both multimorbidity outcomes. Compared to full-term born males, those born at 37-38 weeks (early term) had a 1.06-fold risk of multimorbidity in adolescence (95% CI: 0.98 to 1.14) and this risk increased in a graded manner up to 6.85-fold (95% CI: 5.39 to 8.71) in those born at 23-27 weeks (extremely premature), independently of covariates. Among females, the same risks ranged from 1.16-fold (95% CI: 1.09 to 1.23) among those born at 37-38 weeks to 5.65-fold (95% CI: 4.45 to 7.18) among those born at 23-27 weeks. The corresponding risks of early adult multimorbidity were similar in direction but less marked in magnitude, with little difference in risks between males and females born at 36-37 weeks but up to 3-fold risks observed among those born at 23-27 weeks. Our findings indicate that an earlier gestational age at birth is associated with increased risks of chronic disease multimorbidity in the early part of the life course. There are currently no clinical guidelines for follow-up of prematurely born individuals beyond childhood, but these observations suggest that information on gestational age would be a useful characteristic to include in a medical history when assessing the risk of multiple chronic diseases in adolescent and young adult patients.

Recent research in economics emphasizes the role of in utero conditions for the health endowment at birth and in early childhood and for social as well as economic outcomes in later life. This paper analyzes the relation between maternal mental health during pregnancy and birth outcomes of the child. In particular, we analyze the relationship between maternal mental health during pregnancy and the probability of giving birth preterm (PT), having a newborn at low birth weight (LBW) or being small for gestational age (SGA). Based on large population-representative data from the German Socio-Economic Panel (SOEP) and cohort data from the National Educational Panel Study (NEPS), we present extensive descriptive evidence on the relationship between maternal mental health and preterm birth by carrying out OLS estimates controlling for a wide range of socioeconomic characteristics. In addition, we apply matching estimators and mother fixed effects models, which bring us closer toward a causal interpretation of estimates. In summary, the results uniformly provide evidence that poor maternal mental health is a risk factor for preterm birth and low birth weight in offspring. In contrast, we find no evidence for an relationship between maternal mental health and small for gestational age at birth.

Early life stress (ELS) may increase the risk of anxiety throughout the life course. Whether this effect extends to late adulthood is poorly known. In our study comprising 1872 participants from the Helsinki Birth Cohort Study born in 1934–1944, we investigated the association of various forms of ELS and their accumulation with self-reported anxiety symptoms at the age of 65–77 years. Data on childhood socioeconomic status and separation from parents were based on national registers for all participants. Information on self-reported emotional and physical trauma, parental divorce, and death of a family member in childhood was obtained from 1277 participants. We found that experiencing emotional trauma, physical trauma, and low socioeconomic status in childhood were associated with increased anxiety symptoms in late adulthood [B = 0.44 (95% CI = 0.31–0.58); B = 0.33 (95% CI = 0.20–0.46); B = 0.10 (95% CI = 0.01–0.19), respectively]. These associations remained significant even after controlling for other forms of ELS. Accumulation of early life stress also increased the levels of late-adulthood anxiety symptoms and the risk of anxiety regarded as clinically significant. Screening for potentially stressful childhood experiences in elderly populations may help identifying individuals with increased anxiety symptoms and planning preventive and therapeutic interventions for those exposed to ELS.