Several dietary substances have been hypothesized to influence the risk of preeclampsia. Our aim in this study was to estimate the association between dietary patterns during pregnancy and the risk of preeclampsia in 23,423 nulliparous pregnant women taking part in the Norwegian Mother and Child Cohort Study (MoBa). Women participating in MoBa answered questionnaires at gestational wk 15 (a general health questionnaire) and 17-22 (a FFQ). The pregnancy outcomes were obtained from the Medical Birth Registry of Norway. Exploratory factor analysis was used to assess the associations among food variables. Principal component factor analysis identified 4 primary dietary patterns that were labeled: vegetable, processed food, potato and fish, and cakes and sweets. Relative risks of preeclampsia were estimated as odds ratios (OR) and confounder control was performed with multiple logistic regression. Women with high scores on a pattern characterized by vegetables, plant foods, and vegetable oils were at decreased risk [relative risk (OR) for tertile 3 vs. tertile 1: 0.72; 95% CI: 0.62, 0.85]. Women with high scores on a pattern characterized by processed meat, salty snacks, and sweet drinks were at increased risk [OR for tertile 3 vs. tertile 1: 1.21; 95% CI: 1.03, 1.42]. These findings suggest that a dietary pattern characterized by high intake of vegetables, plant foods, and vegetable oils decreases the risk of preeclampsia, whereas a dietary pattern characterized by high consumption of processed meat, sweet drinks, and salty snacks increases the risk.

These findings are consistent with other reports of a protective effect of vitamin D on preeclampsia development. However, because vitamin D intake is highly correlated with the intake of long chain n-3 fatty acids in the Norwegian diet, further research is needed to disentangle the separate effects of these nutrients.

Human birth weight is subject to stabilizing selection; babies born too small or too large are less likely to survive. Particular combinations of maternal/fetal immune system genes are associated with pregnancies where the babies are ≤5th birth weight centile. Specifically an inhibitory maternal KIR AA genotype with a paternally derived fetal HLA-C2 ligand. We have now analysed maternal KIR and fetal HLA-C combinations at the opposite end of the birth weight spectrum. 1316 mother/baby pairs were genotyped for maternal KIR as well as fetal and maternal HLA-C. Presence of a maternal activating KIR2DS1 gene associated with increased birth weight, in linear or logistic regression analyses of all pregnancies >5th centile (p=0.005, n=1316). Effect of KIR2DS1 was most significant in pregnancies where its ligand, HLA-C2, was paternally but not maternally inherited by a fetus (p=0.005, OR=2.65). Thus maternal KIR are more frequently inhibitory with small babies but activating with big babies. At both extremes of birth weight the KIR associations occur when their HLA-C2 ligand is paternally inherited by a fetus. We conclude that the two polymorphic immune gene systems, KIR and HLA-C, contribute to successful reproduction by maintaining birth weight between two extremes with a clear role for paternal HLA.

Preeclampsia is a serious complication of pregnancy, affecting both maternal and fetal health. In genome-wide association meta-analysis of European and Central Asian mothers, we identify sequence variants that associate with preeclampsia in the maternal genome at ZNF831/20q13 and FTO/16q12. These are previously established variants for blood pressure (BP) and the FTO variant has also been associated with body mass index (BMI). Further analysis of BP variants establishes that variants at MECOM/3q26, FGF5/4q21 and SH2B3/12q24 also associate with preeclampsia through the maternal genome. We further show that a polygenic risk score for hypertension associates with preeclampsia. However, comparison with gestational hypertension indicates that additional factors modify the risk of preeclampsia.

Background During the 2009 influenza pandemic, pregnant women were at particular risk of serious influenza illness. This concern was further complicated by questions about vaccine safety in pregnant women raised by anecdotal reports of fetal deaths following vaccination. Methods We explored the safety of influenza vaccination of pregnant women by linking Norwegian national registries and medical consultation data to determine influenza diagnosis, vaccination status, birth outcomes, and background information for pregnant women before, during, and after the pandemic. We used Cox regression models to estimate hazard ratios of fetal death, with gestational day as the time metric and vaccination and pandemic exposure as time-dependent exposure variables. Results There were 117,347 eligible pregnancies in Norway in 2009–2010. Fetal mortality was 4.9/1000. 54% of pregnant women in their second or third trimester during the pandemic were vaccinated. Vaccination in pregnancy substantially reduced the risk of influenza diagnosis (adjusted hazard ratio, 0.30; 95% confidence interval [CI], 0.25 to 0.34). A clinical diagnosis of influenza in the mother increased the risk of fetal death (adjusted hazard ratio, 1.91; 95% CI, 1.07 to 3.41). Among pregnant women, the risk of fetal death was lower with vaccination, although this reduction was not statistically significant (adjusted hazard ratio, 0.88; 95% CI, 0.66 to 1.17). Conclusions Pandemic influenza in pregnancy was associated with increased risk of fetal death. Vaccination during pregnancy reduced the risk of influenza diagnosis. Vaccination itself did not increase fetal mortality, and may have reduced the risk of influenza-related fetal death during the pandemic.

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BackgroundThe aim of the current study was to estimate sex- and age-specific incidence rates of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) using population-based registry data. CFS/ME is a debilitating condition with large impact on patients and their families. The etiology is unknown, and the distribution of the disease in the general population has not been well described.MethodsCases of CFS/ME were identified in the Norwegian Patient Register (NPR) for the years 2008 to 2012. The NPR is nationwide and contains diagnoses assigned by specialist health care services (hospitals and outpatient clinics). We estimated sex- and age-specific incidence rates by dividing the number of new cases of CFS/ME in each category by the number of person years at risk. Incidence rate ratios were estimated by Poisson regression with sex, age categories, and year of diagnosis as covariates.ResultsA total of 5,809 patients were registered with CFS/ME during 2008 to 2012. The overall incidence rate was 25.8 per 100,000 person years (95% confidence interval (CI): 25.2 to 26.5). The female to male incidence rate ratio of CFS/ME was 3.2 (95% CI: 3.0 to 3.4). The incidence rate varied strongly with age for both sexes, with a first peak in the age group 10 to 19 years and a second peak in the age group 30 to 39 years.ConclusionsEarly etiological clues can sometimes be gained from examination of disease patterns. The strong female preponderance and the two age peaks suggest that sex- and age-specific factors may modulate the risk of CFS/ME.