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1.  Gestational Age Patterns of Fetal and Neonatal Mortality in Europe: Results from the Euro-Peristat Project 
PLoS ONE  2011;6(11):e24727.
Background
The first European Perinatal Health Report showed wide variability between European countries in fetal (2.6–9.1‰) and neonatal (1.6–5.7‰) mortality rates in 2004. We investigated gestational age patterns of fetal and neonatal mortality to improve our understanding of the differences between countries with low and high mortality.
Methodology/Principal Findings
Data on 29 countries/regions participating in the Euro-Peristat project were analyzed. Most European countries had no limits for the registration of live births, but substantial variations in limits for registration of stillbirths before 28 weeks of gestation existed. Country rankings changed markedly after excluding deaths most likely to be affected by registration differences (22–23 weeks for neonatal mortality and 22–27 weeks for fetal mortality). Countries with high fetal mortality ≥28 weeks had on average higher proportions of fetal deaths at and near term (≥37 weeks), while proportions of fetal deaths at earlier gestational ages (28–31 and 32–36 weeks) were higher in low fetal mortality countries. Countries with high neonatal mortality rates ≥24 weeks, all new member states of the European Union, had high gestational age-specific neonatal mortality rates for all gestational-age subgroups; they also had high fetal mortality, as well as high early and late neonatal mortality. In contrast, other countries with similar levels of neonatal mortality had varying levels of fetal mortality, and among these countries early and late neonatal mortality were negatively correlated.
Conclusions
For valid European comparisons, all countries should register births and deaths from at least 22 weeks of gestation and should be able to distinguish late terminations of pregnancy from stillbirths. After excluding deaths most likely to be influenced by existing registration differences, important variations in both levels and patterns of fetal and neonatal mortality rates were found. These disparities raise questions for future research about the effectiveness of medical policies and care in European countries.
doi:10.1371/journal.pone.0024727
PMCID: PMC3217927  PMID: 22110575
2.  Mothers’ Negative Affectivity During Pregnancy and Food Choices for Their Infants 
Objective
To investigate whether maternal negative affectivity assessed in pregnancy is related to subsequent infant food choices.
Design
Cohort study.
Subjects
Mothers (N = 37, 919) and their infants participating in the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health.
Measurements
Maternal negative affectivity assessed pre-partum (SCL-5 at week 17 and 30 of pregnancy), introduction of solid foods by month 3, and feeding of sweet drinks by month 6 (by mothers’ reports).
Results
Mothers with higher negative affectivity were 64% more likely (95% CI 1.5–1.8) to feed sweet drinks by month 6, and 79% more likely (95% CI 1.6–2.0) to introduce solid foods by month 3. These odds decreased to 41% and 30%, respectively, after adjusting for mother’s age, body mass index, and education.
Conclusion
The maternal trait of negative affectivity is an independent predictor of infant feeding practices that may be related to childhood weight gain, overweight, and obesity.
doi:10.1038/ijo.2009.230
PMCID: PMC2822132  PMID: 19918247
maternal feeding practices; negative affectivity; solid foods; sweet drinks
3.  Pregnancy outcome in women before and after cervical conisation: population based cohort study 
Objectives To examine the consequences of cervical conisation in terms of adverse outcome in subsequent pregnancies.
Design Population based cohort study.
Data sources Data on cervical conisation derived from the Cancer Registry of Norway and on pregnancy outcome from the Medical Birth Registry of Norway, 1967-2003. 15 108 births occurred in women who had previously undergone cervical conisation and 57 136 who subsequently underwent cervical conisation. In the same period there were 2 164 006 births to women who had not undergone relevant treatment (control).
Results The proportion of preterm delivery was 17.2% in women who gave birth after cervical conisation versus 6.7% in women who gave birth before cervical conisation and 6.2% in women who had not undergone cervical conisation. The relative risk of a late abortion (<24 weeks’ gestation) was 4.0 (95% confidence interval 3.3 to 4.8) in women who gave birth after cervical conisation compared with no cervical conisation. The relative risk of delivery was 4.4 (3.8 to 5.0) at 24-27 weeks, 3.4 (3.1 to 3.7) at 28-32 weeks, and 2.5 (2.4 to 2.6) at 33-36 weeks. The relative risk of preterm delivery declined during the study period and especially of delivery before 28 weeks’ gestation.
Conclusion Cervical conisation influences outcome in subsequent pregnancies in terms of an increased risk of preterm delivery, especially in the early gestational age groups in which the clinical significance is highest. A careful clinical approach should be taken in the selection of women for cervical conisation and in the clinical care of pregnancies after a cervical conisation.
doi:10.1136/bmj.a1343
PMCID: PMC2544429  PMID: 18801869
4.  The effects of smoking and hypertensive disorders on fetal growth 
Background
It is well known that smoking and pregnancy induced hypertension (PIH) are associated with decreased fetal growth. It has been reported that in preeclampsia the fetal growth deficit attributable to smoking is higher, which has been contradicted in other studies. We therefore evaluated the effects on fetal growth of early- and late onset PIH and chronic hypertension and how cigarette smoking modify these effects. We also quantified the proportion of small for gestational age (SGA) cases attributable to PIH, chronic hypertension, and smoking.
Methods
Population-based study based on record of 215598 singleton pregnancies from the Medical Birth Registry of Norway.
Results
In severe preeclampsia, mild preeclampsia, transient hypertension, and normotension in term birth, odds ratios (ORs) of SGA in smokers compared with non-smokers were 1.4 (95% confidence interval 0.9, 2.2), 1.6 (1.3, 1.9), 2.3 (1.8, 3.1), and 2.0 (1.9, 2.1), respectively. For preterm births, corresponding ORs were 1.3 (0.9, 2.0), 1.8 (1.1, 3.0), 4.1 (1.9, 9.0), and 1.7 (1.4, 2.0), respectively. The effect of early onset PIH was stronger than that in term births, while the effect of smoking was equal in preterm and term newborns. Only in non-smokers who delivered at term, the rates of SGA significantly increased with the severity of PIH (ORs = 1.3 (1.1, 1.5), 1.8 (1.7, 2.0), and 2.5 (2.2, 3.0) for transient hypertension, mild-, and severe preeclampsia, respectively). The combined effects of smoking and hypertension were generally not synergistic. The effect of smoking was not stronger in women who had chronic hypertension. Nor were the effects of chronic hypertension stronger in smokers. PIH explained 21.9 and 2.5% of preterm and term cases of SGA, respectively, while smoking explained 12% of SGA cases.
Conclusion
The effects of hypertensive disorder and smoking were generally not synergistic, which suggest that they may exert their main actions on separate sites or work through separate mechanisms within or outside the placenta. If smoking were eliminated in pregnant women, the number of SGA cases would be reduced by 12%.
doi:10.1186/1471-2393-6-16
PMCID: PMC1463005  PMID: 16630351
5.  Recurrence of pre-eclampsia across generations: exploring fetal and maternal genetic components in a population based cohort 
BMJ : British Medical Journal  2005;331(7521):877.
Objectives To assess the impact on risk of pre-eclampsia of genes that work through the mother, and genes of paternal origin that work through the fetus.
Design Population based cohort study.
Setting Registry data from Norway.
Participants Linked generational data from the medical birth registry of Norway (1967-2003): 438 597 mother-offspring units and 286 945 father-offspring units.
Main outcome measures Pre-eclampsia in the second generation.
Results The daughters of women who had pre-eclampsia during pregnancy had more than twice the risk of pre-eclampsia themselves (odds ratio 2.2, 95% confidence interval 2.0 to 2.4) compared with other women. Men born after a pregnancy complicated by pre-eclampsia had a moderately increased risk of fathering a pre-eclamptic pregnancy (1.5, 1.3 to 1.7). Sisters of affected men or women, who were themselves born after pregnancies not complicated by pre-eclampsia, also had an increased risk (2.0, 1.7 to 2.3). Women and men born after pre-eclamptic pregnancies were more likely to trigger severe pre-eclampsia in their own (or their partner's) pregnancy (3.0, 2.4 to 3.7, for mothers and 1.9, 1.4 to 2.5, for fathers).
Conclusions Maternal genes and fetal genes from either the mother or father may trigger pre-eclampsia. The maternal association is stronger than the fetal association. The familial association predicts more severe pre-eclampsia.
doi:10.1136/bmj.38555.462685.8F
PMCID: PMC1255793  PMID: 16169871
7.  Long term mortality of mothers and fathers after pre-eclampsia: population based cohort study 
BMJ : British Medical Journal  2001;323(7323):1213-1217.
Objective
To assess whether mothers and fathers have a higher long term risk of death, particularly from cardiovascular disease and cancer, after the mother has had pre-eclampsia.
Design
Population based cohort study of registry data.
Subjects
Mothers and fathers of all 626 272 births that were the mothers' first deliveries, recorded in the Norwegian medical birth registry from 1967 to 1992. Parents were divided into two cohorts based on whether the mother had pre-eclampsia during the pregnancy. Subjects were also stratified by whether the birth was term or preterm, given that pre-eclampsia might be more severe in preterm pregnancies.
Main outcome measures
Total mortality and mortality from cardiovascular causes, cancer, and stroke from 1967 to 1992, from data from the Norwegian registry of causes of death.
Results
Women who had pre-eclampsia had a 1.2-fold higher long term risk of death (95% confidence interval 1.02 to 1.37) than women who did not have pre-eclampsia. The risk in women with pre-eclampsia and a preterm delivery was 2.71-fold higher (1.99 to 3.68) than in women who did not have pre-eclampsia and whose pregnancies went to term. In particular, the risk of death from cardiovascular causes among women with pre-eclampsia and a preterm delivery was 8.12-fold higher (4.31 to 15.33). However, these women had a 0.36-fold (not significant) decreased risk of cancer. The long term risk of death was no higher among the fathers of the pre-eclamptic pregnancies than the fathers of pregnancies in which pre-eclampsia did not occur.
Conclusions
Genetic factors that increase the risk of cardiovascular disease may also be linked to pre-eclampsia. A possible genetic contribution from fathers to the risk of pre-eclampsia was not reflected in increased risks of death from cardiovascular causes or cancer among fathers.
What is already known on this topicMaternal and fetal genes (including those inherited from the father) may contribute to pre-eclampsia, which occurs in 3-5% of pregnanciesOne set of candidate genes for pre-eclampsia is the maternal genes for thrombophilia, which may increase the mother's risk of death from cardiovascular diseaseWhat this study addsWomen who have pre-eclampsia during a pregnancy that ends in a preterm delivery have an eightfold higher risk of death from cardiovascular disease compared with women who do not have pre-eclampsia and whose pregnancy goes to termFathers of pregnancies in which pre-eclampsia occurred have no increased risk of death from cardiovascular diseaseThese results are compatible with maternal genes for thrombophilia having an effect on the risk of pre-eclampsia and of death from cardiovascular disease
PMCID: PMC59993  PMID: 11719411
9.  Fetal and maternal contributions to risk of pre-eclampsia: population based study 
BMJ : British Medical Journal  1998;316(7141):1343-1347.
Objective: To use familial patterns of recurrence of pre-eclampsia to investigate whether paternal genes expressed in the fetus contribute to the mother’s risk of pre-eclampsia and whether mother’s susceptibility to pre-eclampsia is related to maternal inheritance by mitochondrial DNA.
Design: Linked data on pregnancies of different women who had children with the same father, and subsequently linked data on pregnancies of half sisters who either had same mother and different fathers or had same father and different mothers.
Setting: Population based data from the Medical Birth Registry of Norway covering all births since 1967 (about 1.7 million) and the Norwegian Central Population Register.
Main outcome measures: Relative risk of pre-eclampsia after a previous pre-eclamptic pregnancy in the family. Relative risks approximated by odds ratios.
Results: If a woman becomes pregnant by a man who has already fathered a pre-eclamptic pregnancy in a different woman her risk of developing pre-eclampsia is 1.8 (95% confidence interval 1.2 to 2.6). If the woman has a half sister who had pre-eclampsia and with whom she shares the same mother but different fathers the risk of pre-eclampsia is 1.6 (0.9 to2.6). If the two sisters have the same father but different mothers the risk is 1.8 (1.01 to 2.9).
Conclusions: Both the mother and the fetus contribute to the risk of pre-eclampsia, the contribution of the fetus being affected by paternal genes. Mitochondrial genes, which are transmitted by mothers, do not seem to contribute to the risk.
Key messages Paternal genes in the fetus may contribute substantially to a pregnant woman’s risk of pre-eclampsia The role of the fetus may be as important as that of the mother Purely maternal inheritance (specifically by mitochondrial DNA) is probably not involved in pre-eclampsia Search for specific genes that predispose for pre-eclampsia should include the fetus as well as the mother
PMCID: PMC28531  PMID: 9563982
10.  Cardiovascular mortality after pre-eclampsia in one child mothers: prospective, population based cohort study 
Objective To assess the association of pre-eclampsia with later cardiovascular death in mothers according to their lifetime number of pregnancies, and particularly after only one child.
Design Prospective, population based cohort study.
Setting Medical Birth Registry of Norway.
Participants We followed 836 147 Norwegian women with a first singleton birth between 1967 and 2002 for cardiovascular mortality through linkage to the national Cause of Death Registry. About 23 000 women died by 2009, of whom 3891 died from cardiovascular causes. Associations between pre-eclampsia and cardiovascular death were assessed by hazard ratios, estimated by Cox regression analyses. Hazard ratios were adjusted for maternal education (three categories), maternal age at first birth, and year of first birth
Results The rate of cardiovascular mortality among women with preterm pre-eclampsia was 9.2% after having only one child, falling to 1.1% for those with two or more children. With term pre-eclampsia, the rates were 2.8% and 1.1%, respectively. Women with pre-eclampsia in their first pregnancy had higher rates of cardiovascular death than those who did not have the condition at first birth (adjusted hazard ratio 1.6 (95% confidence interval 1.4 to 2.0) after term pre-eclampsia; 3.7 (2.7 to 4.8) after preterm pre-eclampsia). Among women with only one lifetime pregnancy, the increase in risk of cardiovascular death was higher than for those with two or more children (3.4 (2.6 to 4.6) after term pre-eclampsia; 9.4 (6.5 to 13.7) after preterm pre-eclampsia). The risk of cardiovascular death was only moderately elevated among women with pre-eclamptic first pregnancies who went on to have additional children (1.5 (1.2 to 2.0) after term pre-eclampsia; 2.4 (1.5 to 3.9) after preterm pre-eclampsia). There was little evidence of additional risk after recurrent pre-eclampsia. All cause mortality for women with two or more lifetime births, who had pre-eclampsia in first pregnancy, was not elevated, even with preterm pre-eclampsia in first pregnancy (1.1 (0.87 to 1.14)).
Conclusions Cardiovascular death in women with pre-eclampsia in their first pregnancy is concentrated mainly in women with no additional births. This association might be due to health problems that discourage or prevent further pregnancies rather than to pre-eclampsia itself. As a screening criterion for cardiovascular disease risk, pre-eclampsia is a strong predictor primarily among women with only one child—particularly with preterm pre-eclampsia.
doi:10.1136/bmj.e7677
PMCID: PMC3508198  PMID: 23186909
11.  Mediators of the association between pre-eclampsia and cerebral palsy: population based cohort study 
Objective To test the hypothesis that pre-eclampsia is a risk factor for cerebral palsy mediated through preterm birth and being born small for gestational age.
Design Population based cohort study.
Setting Clinical data from the Norwegian Cerebral Palsy Registry were linked with perinatal data prospectively recorded by the Medical Birth Registry of Norway.
Participants All singleton babies who survived the neonatal period during 1996-2006 (849 children with cerebral palsy and 616 658 control children).
Main outcome measures Cerebral palsy and cerebral palsy subtypes.
Results Children exposed to pre-eclampsia had an excess risk of cerebral palsy (unadjusted odds ratio 2.5, 95% confidence interval 2.0 to 3.2) compared with unexposed children. Among children born at term (≥37 weeks), exposure to pre-eclampsia was not associated with an excess risk of cerebral palsy in babies not born small for gestational age (1.2, 0.7 to 2.0), whereas children exposed to pre-eclampsia and born small for gestational age had a significantly increased risk of cerebral palsy (3.2, 1.5 to 6.7). Non-small for gestational age babies born very preterm (<32 weeks) and exposed to pre-eclampsia had a reduced risk of cerebral palsy compared with unexposed children born at the same gestational age (0.5, 0.3 to 0.8), although the risk was not statistically significantly reduced among children exposed to pre-eclampsia and born small for gestational age (0.7, 0.4 to 1.3). Exposure to pre-eclampsia was not associated with a specific cerebral palsy subtype.
Conclusions Exposure to pre-eclampsia was associated with an increased risk of cerebral palsy, and this association was mediated through the children being born preterm or small for gestational age, or both. Among children born at term, pre-eclampsia was a risk factor for cerebral palsy only when the children were small for gestational age.
doi:10.1136/bmj.f4089
PMCID: PMC3706637  PMID: 23838554
12.  International retrospective cohort study of neural tube defects in relation to folic acid recommendations: are the recommendations working? 
BMJ : British Medical Journal  2005;330(7491):571.
Objectives To evaluate the effectiveness of policies and recommendations on folic acid aimed at reducing the occurrence of neural tube defects.
Design Retrospective cohort study of births monitored by birth defect registries.
Setting 13 birth defects registries monitoring rates of neural tube defects from 1988 to 1998 in Norway, Finland, Northern Netherlands, England and Wales, Ireland, France (Paris, Strasbourg, and Central East), Hungary, Italy (Emilia Romagna and Campania), Portugal, and Israel. Cases of neural tube defects were ascertained among liveborn infants, stillbirths, and pregnancy terminations (where legal). Policies and recommendations were ascertained by interview and literature review.
Main outcome measures Incidences and trends in rates of neural tube defects before and after 1992 (the year of the first recommendations) and before and after the year of local recommendations (when applicable).
Results The issuing of recommendations on folic acid was followed by no detectable improvement in the trends of incidence of neural tube defects.
Conclusions Recommendations alone did not seem to influence trends in neural tube defects up to six years after the confirmation of the effectiveness of folic acid in clinical trials. New cases of neural tube defects preventable by folic acid continue to accumulate. A reasonable strategy would be to quickly integrate food fortification with fuller implementation of recommendations on supplements.
doi:10.1136/bmj.38336.664352.82
PMCID: PMC554029  PMID: 15722368

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