Our aim was to explore the association between alcohol consumption, before and during pregnancy, and the risk of preterm birth among 46,252 primiparous mothers.
We obtained information on alcohol consumption from questionnaire responses at pregnancy week 15 from the prospective, observational Norwegian Mother and Child Cohort Study. Data on preterm birth, categorized as delivery before gestation week 37, were retrieved from the Medical Birth Registry of Norway.
Among the participants, 91% consumed alcohol before pregnancy and fewer than 20% reported consuming alcohol during pregnancy. The adjusted odds ratio (aOR) for preterm birth associated with prepregnancy alcohol consumption was 0.81 (95% confidence interval [CI], 0.70-0.95). We did not find a risk reduction for overall drinking during pregnancy, aOR = 1.03 (95% CI, 0.90-1.19). However, dose-response analyses showed tendencies toward adverse effects when drinking 1-3 times per month during the first 15 weeks of pregnancy, aOR = 1.51 (95% CI, 1.14-2.00).
We did not find any effects of alcohol consumption during pregnancy, whereas pre-pregnancy drinking was associated with reduced risk of preterm birth. Residual confounding may have influenced the risk estimates, especially before pregnancy, as nondrinkers have lower socioeconomic status and well-being than drinkers.
This study examined potential self-selection bias in a large pregnancy cohort by comparing exposure-outcome associations from the cohort to similar associations obtained from nationwide registry data. The outcome under study was specialist-confirmed diagnosis of autism spectrum disorders (ASDs).
The cohort sample (n = 89 836) was derived from the population-based prospective Norwegian Mother and Child Cohort Study and its substudy of ASDs, the Autism Birth Cohort (ABC) study. The nationwide registry data were derived from the Medical Birth Registry of Norway (n = 507 856). The children were born in 1999–2007, and seven prenatal and perinatal exposures were selected for analyses.
ASDs were reported for 234 (0.26%) children in the cohort and 2072 (0.41%) in the nationwide population. Compared with the nationwide population, the cohort had an under-representation of the youngest women (
Prenatal folic acid supplements reduce the risk of neural tube defects in children, but it has not been determined whether they protect against other neurodevelopmental disorders.
To examine the association between maternal use of prenatal folic acid supplements and subsequent risk of autism spectrum disorders (ASDs) (autistic disorder, Asperger syndrome, pervasive developmental disorder-not otherwise specified [PDD-NOS]) in children.
The study sample of 85,176 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study (MoBa). The children were born in 2002-2008; by the end of follow-up on March 31, 2012, the age range was 3.3 through 10.2 years (mean, 6.4 years). The exposure of primary interest was use of folic acid from 4 weeks before to 8 weeks after the start of pregnancy, defined as the first day of the last menstrual period before conception. Relative risks of ASDs were estimated by odds ratios (ORs) with 95% CIs in a logistic regression analysis. Analyses were adjusted for maternal education level, year of birth, and parity.
Specialist-confirmed diagnosis of ASDs.
At the end of follow-up, 270 children in the study sample had been diagnosed with ASDs: 114 with autistic disorder, 56 with Asperger syndrome, and 100 with PDD-NOS. In children whose mothers took folic acid, 0.10% (64/61,042) had autistic disorder, compared with 0.21% (50/24,134) in those unexposed to folic acid. The adjusted OR for autistic disorder in children of folic acid users was 0.61 (95% CI, 0.41-0.90). No association was found with Asperger syndrome or PDD-NOS, but power was limited. Similar analyses for prenatal fish oil supplements showed no such association with autistic disorder, even though fish oil use was associated with the same maternal characteristics as folic acid use.
Use of prenatal folic acid supplements around the time of conception was associated with a lower risk of autistic disorder in the MoBa cohort. Although these findings cannot establish causality, they do support prenatal folic acid supplementation.
Excessive gestational weight gain (GWG) is associated with pregnancy complications, and Norwegian Health Authorities have adopted the GWG recommendations of the US Institute of Medicine and National Research Council (IOM). The aim of this study was to evaluate if a GWG outside the IOM recommendation in a Norwegian population is associated with increased risk of pregnancy complications like hypertension, low and high birth weight, preeclampsia, emergency caesarean delivery, and maternal post-partum weight retention (PPWR) at 6 and 18 months.
This study was performed in 56 101 pregnant women included in the prospective national Norwegian Mother and Child Cohort Study (MoBa) in the years 1999 to 2008. Women who delivered a singleton live born child during gestational week 37 to 42 were included. Maternal prepregnant and postpartum weight was collected from questionnaires at 17th week of gestation and 6 and 18 months postpartum.
A weight gain less than the IOM recommendations (GWG??IOM rec.) significantly increased the risk of pregnancy hypertension, a high birth weight baby, preeclampsia and emergency cesarean delivery in both nulliparous and parous normal weight women. Similar results were found for overweight women except for no increased risk for gestational hypertension in parous women with GWG?>?IOM rec. Seventy-four percent of the overweight nulliparous women and 66% of the obese women had a GWG?>?IOM rec. A GWG?>?IOM rec. resulted in increased risk of PPWR?>?2 kg in all weight classes, but most women attained their prepregnant weight class by 18 months post-partum.
For prepregnant normal weight and overweight women a GWG?>?IOM rec. increased the risk for unfavorable birth outcomes in both nulliparous and parous women. A GWG?>?IOM rec. increased the risk of a PPWR?>?2 kg at 18 months in all weight classes. This large study supports the Norwegian Health authorities' recommendations for normal weight and overweight women to comply with the IOM rec.
Cites: Am J Clin Nutr. 2009 Nov;90(5):1288-9419759164
Cites: Am J Clin Nutr. 2009 Dec;90(6):1552-819812177
Spontaneous preterm delivery (PTD) has a multifactorial etiology with evidence of a genetic contribution to its pathogenesis. A number of candidate gene case-control studies have been performed on spontaneous PTD, but the results have been inconsistent, and do not fully assess the role of how two genotypes can impact outcome. To elucidate this latter point we re-analyzed data from a previously published case-control candidate gene study, using a case-parent triad design and a hybrid design combining case-parent triads and control-mother dyads. These methods offer a robust approach to genetic association studies for PTD compared to traditional case-control designs.
The study participants were obtained from the Norwegian Mother and Child Cohort Study (MoBa). A total of 196 case triads and 211 control dyads were selected for the analysis. A case-parent triad design as well as a hybrid design was used to analyze 1,326 SNPs from 159 candidate genes. We compared our results to those from a previous case-control study on the same samples. Haplotypes were analyzed using a sliding window of three SNPs and a pathway analysis was performed to gain biological insight into the pathophysiology of preterm delivery.
The most consistent significant fetal gene across all analyses was COL5A2. The functionally similar COL5A1 was significant when combining fetal and maternal genotypes. PON1 was significant with analytical approaches for single locus association of fetal genes alone, but was possibly confounded by maternal effects. Focal adhesion (hsa04510), Cell Communication (hsa01430) and ECM receptor interaction (hsa04512) were the most constant significant pathways.
This study suggests a fetal association of COL5A2 and a combined fetal-maternal association of COL5A1 with spontaneous PTD. In addition, the pathway analysis implied interactions of genes affecting cell communication and extracellular matrix.
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated to infections and it has been suggested that vaccination can trigger the disease. However, little is known about the specific association between clinically manifest influenza/influenza vaccine and CFS/ME. As part of a registry surveillance of adverse effects after mass vaccination in Norway during the 2009 influenza A (H1N1) pandemic, we had the opportunity to estimate and contrast the risk of CFS/ME after infection and vaccination.
Using the unique personal identification number assigned to everybody who is registered as resident in Norway, we followed the complete Norwegian population as of October 1, 2009, through national registries of vaccination, communicable diseases, primary health, and specialist health care until December 31, 2012. Hazard ratios (HRs) of CFS/ME, as diagnosed in the specialist health care services (diagnostic code G93.3 in the International Classification of Diseases, Version 10), after influenza infection and/or vaccination were estimated using Cox proportional-hazards regression.
The incidence rate of CFS/ME was 2.08 per 100,000 person-months at risk. The adjusted HR of CFS/ME after pandemic vaccination was 0.97 (95% confidence interval [CI]: 0.91-1.04), while it was 2.04 (95% CI: 1.78-2.33) after being diagnosed with influenza infection during the peak pandemic period.
Pandemic influenza A (H1N1) infection was associated with a more than two-fold increased risk of CFS/ME. We found no indication of increased risk of CFS/ME after vaccination. Our findings are consistent with a model whereby symptomatic infection, rather than antigenic stimulation may trigger CFS/ME.
This study tested the hypothesis that moderate alcohol intake exerts its cardioprotective effect mainly through an increase in the serum level of high-density lipoprotein cholesterol.
In the Cohort of Norway (CONOR) study, 149 729 adult participants, recruited from 1994 to 2003, were followed by linkage to the Cause of Death Registry until 2006. At recruitment, questionnaire data on alcohol intake were collected, and the concentration of high-density lipoprotein cholesterol in serum was measured. Using Cox regression, we found that the adjusted hazard ratio for men for dying from coronary heart disease was 0.52 (95% confidence interval, 0.39-0.69) when consuming alcohol more than once a week compared with never or rarely. The ratio changed only slightly, to 0.55 (0.41-0.73), after the regression model included the serum level of high-density cholesterol. For women, the corresponding hazard ratios were 0.62 (0.32-1.23) and 0.68 (0.34-1.34), respectively.
Alcohol intake is related to a reduced risk of death from coronary heart disease in the follow-up of a large, population-based Norwegian cohort study with extensive control for confounding factors. Our findings suggest that the serum level of high-density cholesterol is not an important intermediate variable in the possible causal pathway between moderate alcohol intake and coronary heart disease.
Comment In: Circulation. 2011 Nov 22;124(21):2283-422105194
Hyperemesis gravidarum (hyperemesis), characterised by severe nausea and vomiting in early pregnancy, has an unknown aetiology. The aim of the present study was to investigate food and nutrient intake before pregnancy and the risk of developing hyperemesis in women participating in the Norwegian Mother and Child Cohort Study. From 1999 to 2002, a total of 7710 pregnant women answered a FFQ about their diet during the 12 months before becoming pregnant and a questionnaire about illnesses during pregnancy, including hyperemesis. Only women who were hospitalised for hyperemesis were included as cases. Nutrient intakes during the year before pregnancy did not differ between the ninety-nine women who developed hyperemesis and the 7611 who did not. However, the intake of seafood, allium vegetables and water was significantly lower among women who developed hyperemesis than among women in the non-hyperemesis group. Relative risks of hyperemesis were approximated as OR, and confounder control was performed with multiple logistic regression. Women in the upper tertile of seafood consumption had a lower risk of developing hyperemesis than those in the lower tertile (OR 0·56, 95 % CI 0·32, 0·98), and women in the second tertile of water intake had a lower risk of developing hyperemesis than those in the first tertile (OR 0·43, 95 % CI 0·25, 0·73). The findings suggest that a moderate intake of water and adherence to a healthy diet that includes vegetables and fish are associated with a lower risk of developing hyperemesis.
Observational studies show beneficial effects of moderate alcohol drinking on all-cause and cardiovascular disease (CVD) mortality, while binge drinking has been linked with increased mortality. The aim of this study was to assess the associations of alcohol use with mortality in a population with a hybrid of drinking patterns.
Participants in a population based cardiovascular health survey in Finnmark county in 1987-1988, aged 20-62 years, constituted the study cohort. Alcohol use was self-reported by use of questions on frequency of beer, wine and liquor intake, and one question on intake of around five drinks or more per occasion (binge drinking). Information on education, income and use of alcohol in an earlier and in a later survey was linked to the file. Mortality was assessed throughout 2009 by Cox regression, with adjustment for potential confounding factors. In the analysis of mortality by frequency of any alcohol use, we adjusted for binge consumption and vice versa.
Two opposite trends appeared: a higher all-cause mortality in both sexes, and higher CVD mortality in men, with increasing frequency of binge drinking, compared with non-bingers. Second, in both sexes low-frequent use of any alcohol was associated with lower all-cause and CVD mortality, compared with abstention. The combination of any use of alcohol at least weekly and binge consumption at least monthly was common, particularly in men.
Questions on drinking frequency and a specific question on binge drinking capture different effects of alcohol use on all-cause and CVD mortality.
Vaccine against human papillomavirus (HPV) has been offered free of charge to all 12-year-old girls in Norway since 2009. Nevertheless, the uptake of HPV vaccine is lower than for other childhood vaccines. The aim of this study was to examine whether parental education and income are associated with initiation and completion of HPV vaccination.
Nationwide register-based study.
Publicly funded childhood immunisation programme in Norway.
91,405 girls born between 1997 and 1999 and registered in the Norwegian Central Population Registry were offered HPV vaccine during the first 3 programme years. Of these, 84,139 had complete information on all variables and were included in the study.
Information on HPV-vaccination status was obtained from the Norwegian Immunisation Registry. Data on socioeconomic factors were extracted from Statistics Norway. Risk differences (RDs) and CIs were estimated with Poisson regression.
In the study sample, 78.3% received at least one dose of HPV vaccine and 73.6% received all three doses. High maternal education was significantly associated with lower probability of initiating HPV vaccination (multivariable RD=-5.5% (95% CI -7.0% to -4.0%) for highest compared with lowest education level). In contrast, high maternal income was significantly associated with higher probability of initiating vaccination (multivariable RD=10.1% (95% CI 9.0% to 11.3%) for highest compared with lowest quintile). Paternal education and income showed similar, but weaker, associations. The negative association between education and initiation was only seen for incomes below the median value.
In spite of the presumably equal access to HPV vaccine in Norway, we found socioeconomic disparities in vaccine uptake. More studies are needed to explain the underlying factors responsible for the observed socioeconomic differences. Insight into these factors is necessary to target information and increase vaccination coverage to ultimately reduce HPV-related disease across socioeconomic barriers.
Cites: Stat Methods Med Res. 2013 Dec;22(6):661-7022072596
Cites: J Epidemiol Community Health. 2014 Jan;68(1):57-6323986492
Cites: J Public Health (Oxf). 2014 Mar;36(1):36-4523620542
Cites: J Epidemiol Community Health. 2014 Jun;68(6):571-724567443