Secular trends of sudden infant death syndrome and other causes of post perinatal mortality in Norwegian birth cohorts 1967-1984

Lack of positive diagnostic criteria and increasing professional concern, probably causing increasing ascertainment, have rendered reported increases in SIDS-rates controversial. However, these problems related to cause specific mortality do not apply to the total mortality. Due to the exceptional age-at-death distribution of SIDS cases, the SIDS fraction of all deaths increases during the first year of life to reach a maximum, in the present study of 56%, from the 105th through the 125th day of life. During these days, the total mortality rate in Norway increased from 0.24 per 1,000 in 1971-72 to 0.46 in 1983-84. Thus, the observed trend, with an increase in the SIDS rate from 1.02 per 1,000 in 1971-72 to 2.34 in 1983-84, is considered true. Observed in a country where perinatal and neonatal mortality have decreased for a long period of time and still remain very low in a global perspective, the increasing SIDS rate is a matter of great concern.     

Placental abruption and long-term maternal cardiovascular disease mortality: a population-based registry study in Norway and Sweden

Women with preeclamptic pregnancies have increased long-term cardiovascular disease (CVD) mortality. We explored this mortality risk among women with placental abruption, another placental pathology. We used linked Medical Birth Registry and Death Registry data to study CVD mortality among over two million women with a first singleton birth between 1967 and 2002 in Norway and 1973 and 2003 in Sweden. Women were followed through 2009 and 2010, respectively, to ascertain subsequent pregnancies and mortality. Cox regression analysis was used to estimate associations between placental abruption and cardiovascular mortality adjusting for maternal age, education, year of the pregnancy and country. There were 49,944 deaths after an average follow-up of 23 years, of which 5453 were due to CVD. Women with placental abruption in first pregnancy (n = 10,981) had an increased risk of CVD death (hazard ratio 1.8; 95 % confidence interval 1.3, 2.4). Results were essentially unchanged by excluding women with pregestational hypertension, preeclampsia or diabetes. Women with placental abruption in any pregnancy (n = 23,529) also had a 1.8-fold increased risk of CVD mortality (95 % confidence interval 1.5, 2.2) compared with women who never experienced the condition. Our findings provide evidence that placental abruption, like other placental complications of pregnancy, is associated with women’s increased risk of later CVD mortality.     

Birth outcomes among offspring of adult cancer survivors: A population‐based study

Do cancer and cancer treatment influence patients' subsequent pregnancies and outcomes for the offspring? In this study, we compared birth outcomes in 3,915 female and male survivors and 144,653 controls from the general population with similar parity, by merging data from the Cancer Registry and the Medical Birth Registry of Norway. The cancer survivors were diagnosed at age 16–45 in the period 1967–2004. Subgroups of nulliparous survivors (childless before cancer) and primiparous (one pregnancy before and one after cancer) were analyzed, using logistic regression to compare birth outcomes with controls, focusing perinatal death, congenital anomalies, preterm birth (<37 gestational weeks) and low birth weight (LBW, <2,500 g). We adjusted for maternal age, birth period and educational level. Nulliparous female survivors' offspring had increased risk of preterm birth (OR = 1.30 [95% CI 1.05–1.61]) but similar risks of LBW and perinatal death as their controls. Primiparous female survivors differed from their controls, with higher frequency of preterm birth (OR = 1.89 [95% CI 1.40–2.56]) and LBW at term (OR = 2.02 [95% CI 1.15–3.55]). A borderline significant increase of perinatal death was seen among offspring of primiparous female survivors, with OR = 1.92 (95% CI 0.98–3.76). Offspring of male survivors did not differ from their controls. For all cancer types combined, no increased risk of congenital anomalies was seen among either female or male survivors' offspring. Pregnant female cancer survivors should be offered close follow‐up, as there is an increased risk of adverse birth outcomes, in particular among those with higher parities.     

FTO, type 2 diabetes, and weight gain throughout adult life: a meta-analysis of 41,504 subjects from the Scandinavian HUNT, MDC, and MPP studies

OBJECTIVE

FTO is the most important polygene identified for obesity. We aimed to investigate whether a variant in FTO affects type 2 diabetes risk entirely through its effect on BMI and how FTO influences BMI across adult life span.

RESEARCH DESIGN AND METHODS

Through regression models, we assessed the relationship between the FTO single nucleotide polymorphisms rs9939609, type 2 diabetes, and BMI across life span in subjects from the Norwegian population-based HUNT study using cross-sectional and longitudinal perspectives. For replication and meta-analysis, we used data from the Malmö Diet and Cancer (MDC) and Malmö Preventive Project (MPP) cohorts, comprising a total sample of 41,504 Scandinavians.

RESULTS

The meta-analysis revealed a highly significant association for rs9939609 with both type 2 diabetes (OR 1.13; P = 4.5 × 10⁻⁸) and the risk to develop incident type 2 diabetes (OR 1.16; P = 3.2 × 10⁻⁸). The associations remained also after correction for BMI and other anthropometric measures. Furthermore, we confirmed the strong effect on BMI (0.28 kg/m² per risk allele; P = 2.0 × 10⁻²⁶), with no heterogeneity between different age-groups. We found no differences in change of BMI over time according to rs9939609 risk alleles, neither overall (∆BMI = 0.0 [−0.05, 0.05]) nor in any individual age stratum, indicating no further weight gain attributable to FTO genotype in adults.

CONCLUSIONS

We have identified that a variant in FTO alters type 2 diabetes risk partly independent of its observed effect on BMI. The additional weight gain as a result of the FTO risk variant seems to occur before adulthood, and the BMI difference remains stable thereafter.Genomewide association studies (GWAS) have identified a strong correlation between BMI and FTO single nucleotide polymorphisms (SNPs) (1–4), and the association has been confirmed in multiple populations (reviewed in 5). The FTO risk variants are also associated with obesity-related traits (6–8). However, these effects appear to be secondary to weight increase because the associations are attenuated after adjusting for BMI (2). In contrast, we and others have found that the association with type 2 diabetes may not be completely mediated through BMI, because it remains significant after BMI correction (9). This indicates that the relationship between sequence variation in FTO and type 2 diabetes is not fully mediated through BMI or that BMI in some populations does not reveal accurate estimates of the effect of FTO on adiposity.Various studies have investigated the effect of FTO variants on BMI and weight in a longitudinal perspective (10–18) but with diverging results. With access to extensive data from three large Scandinavian populations, through a meta-analysis approach using both cross-sectional and longitudinal data, we aimed to investigate whether the FTO risk allele affects type 2 diabetes risk after correction for BMI and whether it influences weight gain during adult life.     

Secular trends in the epidemiology of pre-eclampsia throughout 40 years in Norway: prevalence, risk factors and perinatal survival

Pre-eclampsia is a leading complication of pregnancy, associated with maternal and neonatal morbidity. The present study describes the epidemiology of pre-eclampsia in Norway, with data from the Medical Birth Registry of Norway, covering 40 years. We aimed at describing time trends in prevalence, selected risk factors and perinatal mortality. We also analysed time trends in recurrence risk of total pre-eclampsia and pre-eclampsia with preterm delivery. A total of 2,416,501 women giving birth during 1967-2008 were included. Prevalence of pre-eclampsia increased from 1967 to 1999 and decreased thereafter, with an overall prevalence of 3%. Rates increased more over time among younger than older women, resulting in a significantly lower excess risk of pre-eclampsia associated with high maternal age in later years. For example, relative risk (RR) of pre-eclampsia among primiparae aged ≥35 relative to <25 years changed from 2.4 [95% confidence interval (CI) 2.1, 2.7] in 1967-1976 to 1.2 [95% CI 1.1, 1.3] in 1999-2008. For recurrence risk, subsequent pregnancies to a mother were linked, with the mother being the unit of analysis. Recurrence risk of pre-eclampsia was high, particularly recurrence of preterm pre-eclampsia, with overall RR close to 50 of a second pregnancy with pre-eclampsia and preterm birth compared with women without pre-eclampsia in first pregnancies. Finally, stillbirth associated with pre-eclampsia decreased more than neonatal mortality over time, and in the last 5 years only a moderate excess risk of stillbirth and neonatal death was observed.