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In this nationwide study involving preterm infants in Sweden, Apgar scores at 5 and 10 minutes and the change in the Apgar score between 5 and 10 minutes provided prognostic information about neonatal survival across gestational-age strata.

The prevalence of smoking during pregnancy varies markedly across countries. In many industrialized countries, prevalence rates appear to have peaked and begun to decline, whereas in other countries smoking is becoming increasingly common among young women. Randomized controlled trials have shown that smoking interventions during pregnancy have had limited success. Smoking during pregnancy is in many countries recognized as the most important preventable risk factor for an unsuccessful pregnancy outcome. Smoking is causally associated with fetal growth restriction, and increasing evidence also suggests that smoking may cause stillbirth, preterm birth, placental abruption, and possibly also sudden infant death syndrome. Smoking during pregnancy also is generally associated with increased risks of spontaneous abortions, ectopic pregnancies, and placenta previa and may increase risks of behavioral disorders in childhood. Smoking during pregnancy will continue to be an important risk factor for maternal and fetal outcomes during pregnancy.

Maternal overweight and obesity are risk factors for stillbirth and infant mortality. Whether temporal changes in maternal weight affect these risks is not clear. We aimed to assess whether change of BMI between first and second pregnancies affects risks of stillbirth and infant mortality in the second-born offspring. In a Swedish population-based cohort of women who gave birth to their first and second child between Jan 1, 1992, and Dec 31, 2012, we investigated associations between change in maternal body-mass index (BMI) during early pregnancy from first to second pregnancies and risks of stillbirth and neonatal, postneonatal, and infant mortality after the second pregnancy. Relative risks (RRs) for each outcome according to BMI change categories were calculated with binomial regression. Complete information was available for 456 711 (77·7%) of 587 710 women who had their first and second single births in the study period. Compared with women with a stable BMI (change between −1 kg/m2 and <1 kg/m2) between pregnancies, the adjusted RRs for women who gained at least 4 BMI units between pregnancies were 1·55 (95% CI 1·23–1·96) for stillbirth and 1·29 (1·00–1·67) for infant mortality. Stillbirth risks increased linearly with increased BMI gain. Risks of infant mortality in second pregnancy only increased with BMI gain in women with healthy BMI (<25 kg/m2) during first pregnancy; the adjusted RR for healthy weight women who gained 2 to less than 4 BMI units was 1·27 (1·01–1·59) and for those who gained 4 BMI units or more the adjusted RR was 1·60 (1·16–2·22). In overweight women (BMI ≥25 kg/m2), weight loss before pregnancy reduced risk of neonatal mortality. Our findings emphasise the need to prevent weight gain before pregnancy in healthy and overweight women and that weight loss should be promoted in overweight women. Swedish Research Council for Health, Working Life and Welfare, and Karolinska Institutet.

Objective To estimate the risks of major congenital malformations in the offspring of mothers who are underweight (body mass index (BMI) <18.5), overweight (BMI 25 to <30), or in obesity classes I (BMI 30 to <35), II (35 to <40), or III (≥40) compared with offspring of normal weight mothers (BMI 18.5 to <25) in early pregnancy.Design Population based cohort study.Setting Nationwide Swedish registries.Participants 1 243 957 liveborn singleton infants from 2001 to 2014 in Sweden. Data on maternal and pregnancy characteristics were obtained by individual record linkages.Exposure Maternal BMI at the first prenatal visit.Main outcome measures Offspring with any major congenital malformation, and subgroups of organ specific malformations diagnosed during the first year of life. Risk ratios were estimated using generalised linear models adjusted for maternal factors, sex of offspring, and birth year.Results A total of 43 550 (3.5%) offspring had any major congenital malformation, and the most common subgroup was for congenital heart defects (n=20 074; 1.6%). Compared with offspring of normal weight mothers (risk of malformations 3.4%), the proportions and adjusted risk ratios of any major congenital malformation among the offspring of mothers with higher BMI were: overweight, 3.5% and 1.05 (95% confidence interval 1.02 to 1.07); obesity class I, 3.8% and 1.12 (1.08 to 1.15), obesity class II, 4.2% and 1.23 (1.17 to 1.30), and obesity class III, 4.7% and 1.37 (1.26 to 1.49). The risks of congenital heart defects, malformations of the nervous system, and limb defects also progressively increased with BMI from overweight to obesity class III. The largest organ specific relative risks related to maternal overweight and increasing obesity were observed for malformations of the nervous system. Malformations of the genital and digestive systems were also increased in offspring of obese mothers.Conclusions Risks of any major congenital malformation and several subgroups of organ specific malformations progressively increased with maternal overweight and increasing severity of obesity. For women who are planning pregnancy, efforts should be encouraged to reduce adiposity in those with a BMI above the normal range.

Background Postpartum depression (PPD) can result in negative personal and child developmental outcomes. Only a few large population‐based studies of PPD have used clinical diagnoses of depression and no study has examined how a maternal depression history interacts with known risk factors. The objective of this study was to examine the impact of a depression history on PPD and pre‐ and perinatal risk factors. Methods A nationwide prospective cohort study of all women with live singleton births in Sweden from 1997 through 2008 was conducted. Relative risk (RR) of clinical depression within the first year postpartum and two‐sided 95% confidence intervals were estimated. Results The RR of PPD in women with a history of depression was estimated at 21.03 (confidence interval: 19.72–22.42), compared to those without. Among all women, PPD risk increased with advanced age (1.25 (1.13–1.37)) and gestational diabetes (1.70 (1.36–2.13)). Among women with a history of depression, pregestational diabetes (1.49 (1.01–2.21)) and mild preterm delivery also increased risk (1.20 (1.06–1.36)). Among women with no depression history, young age (2.14 (1.79–2.57)), undergoing instrument‐assisted (1.23 (1.09–1.38)) or cesarean (1.64(1.07–2.50)) delivery, and moderate preterm delivery increased risk (1.36 (1.05–1.75)). Rates of PPD decreased considerably after the first postpartum month (RR = 0.27). Conclusion In the largest population‐based study to date, the risk of PPD was more than 20 times higher for women with a depression history, compared to women without. Gestational diabetes was independently associated with a modestly increased PPD risk. Maternal depression history also had a modifying effect on pre‐ and perinatal PPD risk factors.

Maternal obesity has been positively associated with risk of adverse pregnancy outcomes, but evidence of a causal relation is scarce. Causality would be lent support if temporal changes in weight affected risk of adverse pregnancy outcomes. We examined the associations between change in prepregnancy body-mass index (BMI) from the first to the second pregnancies, and the risk of adverse outcomes during the second pregnancy in a nationwide Swedish study of 151 025 women who had their first two consecutive singleton births between 1992 and 2001. Compared with women whose BMI changed between −1·0 and 0·9 units, the adjusted odds ratios for adverse pregnancy outcomes for those who gained 3 or more units during an average 2 years were: pre-eclampsia, 1·78 (95% CI 1·52–2·08); gestational hypertension 1·76 (1·39–2·23); gestational diabetes 2·09 (1·68–2·61); caesarean delivery 1·32 (1·22–1·44); stillbirth 1·63 (1·20–2·21); and large-for-gestational-age birth 1·87 (1·72–2·04). The associations were linearly related to the amount of weight change and were also noted in women who had a healthy prepregnancy BMI for both pregnancies. These findings lend support to a causal relation between being overweight or obese and risks of adverse pregnancy outcomes. Additionally they suggest that modest increases in BMI before pregnancy could result in perinatal complications, even if a woman does not become overweight. Our results provide robust epidemiological evidence for advocating weight loss in overweight and obese women who are planning to become pregnant and, to prevent weight gain before pregnancy in women with healthy BMIs.

In this study based on registry data, women with a history of bariatric surgery who were matched with women without this history had a reduced risk of gestational diabetes and excessive fetal growth, a shorter gestation, and an increased risk of small-for-gestational-age infants. In 2008, an estimated 300 million women worldwide were obese (body-mass index [BMI; the weight in kilograms divided by the square of the height in meters], ≥30). 1 In 2011–2012 in the United States, 36% of adult women were obese, 2 and the majority of women in early pregnancy were either overweight or obese (BMI, ≥25). 3 Maternal obesity is a risk factor for gestational diabetes, with attendant increased risks of macrosomia, delivery complications, obesity in the offspring, and later development of type 2 diabetes in the mother. 4 – 6 Maternal obesity is also associated with an increased risk of stillbirth, 7 preterm birth, 8 and . . .

Small for gestational age (SGA) has been associated with increased risks of stillbirth and neonatal mortality, but data on long-term childhood mortality are scarce. Maternal antenatal care, including globally reducing the risk of SGA birth, may be key to achieving the Millennium Development Goal of reducing under-5 mortality. We therefore aimed to examine the association between SGA and mortality from 28 days to <18 years using a population-based and a sibling control design. In a Swedish population study, we identified 3,795,603 non-malformed singleton live births and 2,781,464 full siblings born from January 1, 1973, to December 31, 2012. We examined the associations of severe (<3rd percentile) and moderate (3rd to <10th percentile) SGA with risks of death from 28 days to <18 years after birth. Children born SGA were first compared to non-SGA children from the population, and then to non-SGA siblings. The sibling-based analysis, by design, features a better control for unmeasured factors that are shared between siblings (e.g., socioeconomic status, lifestyle, and genetic factors). Hazard ratios (HRs) were calculated using Cox proportional hazards and flexible parametric survival models. During follow-up (1973-2013), there were 10,838 deaths in the population-based analysis and 1,572 deaths in sibling pairs with discordant SGA and mortality status. The crude mortality rate per 10,000 person-years was 5.32 in children born with severe SGA, 2.76 in children born with moderate SGA, and 1.93 in non-SGA children. Compared with non-SGA children, children born with severe SGA had an increased risk of death in both the population-based (HR = 2.58, 95% CI = 2.38-2.80) and sibling-based (HR = 2.61, 95% CI = 2.19-3.10) analyses. Similar but weaker associations were found for moderate SGA in the population-based (HR = 1.37, 95% CI = 1.28-1.47) and sibling-based (HR = 1.38, 95% CI = 1.22-1.56) analyses. The excess risk was most pronounced between 28 days and <1 year of age but remained throughout childhood. The greatest risk increase associated with severe SGA was noted for deaths due to infection and neurologic disease. Although we have, to our knowledge, the largest study sample so far addressing the research question, some subgroup analyses, especially the analysis of cause-specific mortality, had limited statistical power using the sibling-based approach. We found that SGA, especially severe SGA, was associated with an increased risk of childhood death beyond the neonatal period, with the highest risk estimates for death from infection and neurologic disease. The similar results obtained between the population- and sibling-based analyses argue against strong confounding by factors shared within families.

AbstractObjectiveTo investigate associations between Apgar score at five and 10 minutes across the entire range of score values (from 0 to 10) and risks of childhood cerebral palsy or epilepsy, and to analyse the effect of changes in Apgar scores from five to 10 minutes after birth in infants born ≥37 completed weeks.Design, setting, and participantsPopulation based cohort study in Sweden, including 1 213 470 non-malformed live singleton infants, born at term between 1999 and 2012. Data on maternal and pregnancy characteristics and diagnoses of cerebral palsy and epilepsy were obtained by individual record linkages of nationwide Swedish registries.ExposuresApgar scores at five and 10 minutes.Main outcome measureCerebral palsy and epilepsy diagnosed up to 16 years of age. Adjusted hazard ratios were calculated, along with 95% confidence intervals.Results1221 (0.1%) children were diagnosed as having cerebral palsy and 3975 (0.3%) as having epilepsy. Compared with children with an Apgar score of 10 at five minutes, the adjusted hazard ratio for cerebral palsy increased steadily with decreasing Apgar score: from 1.9 (95% confidence interval 1.6 to 2.2) for an Apgar score of 9 to 277.7 (154.4 to 499.5) for an Apgar score of 0. Similar and even stronger associations were obtained between Apgar scores at 10 minutes and cerebral palsy. Associations between Apgar scores and epilepsy were less pronounced, but increased hazard ratios were noted in infants with a five minute Apgar score of 7 or less and a 10 minute Apgar score of 8 or less. Compared with infants with an Apgar of 9-10 at both five and 10 minutes, hazard ratios of cerebral palsy and epilepsy were higher among infants with a five minute Apgar score of 7-8 and a 10 minute Apgar score of 9-10.ConclusionRisks of cerebral palsy and epilepsy are inversely associated with five minute and 10 minute Apgar scores across the entire range of Apgar scores.

The aim of this study was to examine the validity of the Gender Dysphoria (GD) diagnoses in the Swedish National Patient Register (NPR), to discuss different register-based definitions of GD and to investigate incidence trends. We collected data on all individuals with registered GD diagnoses between 2001 and 2016 as well as data on the coverage in the NPR. We regarded gender confirming medical intervention (GCMI) as one proxy for a clinically valid diagnosis and calculated the positive predictive value (PPV) for receiving GCMI for increasing number of registered GD diagnoses. We assessed crude and coverage-adjusted time trends of GD during 2004–2015 with a Poisson regression, using assigned sex and age as interaction terms. The PPV for receiving GCMI was 68% for ≥ 1 and 79% for ≥ 4 GD-diagnoses. The incidence of GD was on average 35% higher with the definition of ≥ 1 compared to the definition of ≥ 4 diagnoses. The incidence of GD, defined as ≥ 4 diagnoses increased significantly during the study period and mostly in the age categories 10–17 and 18–30 years, even after adjusting for register coverage. We concluded that the validity of a single ICD code denoting clinical GD in the Swedish NPR can be questioned. For future research, we propose to carefully weight the advantages and disadvantages of different register-based definitions according to the individual study’s needs, the time periods involved and the age-groups under study.