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In the present study, the authors investigated the role of the intrauterine environment in childhood adiposity by comparing the maternal-offspring body mass index (BMI) association with the paternal-offspring BMI association when the offspring were 3 years of age, using parental prepregnancy BMI (measured as weight in kilograms divided by height in meters squared). The parent-offspring trios (n = 29,216) were recruited during pregnancy from 2001 to 2008 into the Norwegian Mother and Child Cohort Study conducted by The Norwegian Institute of Public Health. Data from self-administered questionnaires were used in linear regression analyses. Crude analyses showed similar parental-offspring BMI associations; the mean difference in offspring BMI was 0.15 (95% confidence interval: 0.13, 0.16) per each 1-standard-deviation increase in maternal BMI and 0.15 (95% confidence interval: 0.13, 0.17) per each 1-standard-deviation increase in paternal BMI. After all adjustments, the mean difference in offspring BMI per each 1-standard-deviation increment of maternal BMI was 0.12, and the mean difference in offspring BMI per each 1-standard-deviation increment of paternal BMI was 0.13. There was no strong support for heterogeneity between the associations (P > 0.6). In conclusion, results from the present large population-based study showed similar parental-offspring BMI associations when the offspring were 3 years of age, which indicates that the maternal-offspring association may be explained by shared familial (environmental and genetic) risk factors rather than by the intrauterine environment.

Familial correlations in birth weight and gestational age have been explained by fetal and maternal genetic factors, mainly in studies on offspring of twins. The aim of the present intergenerational study was to estimate and compare fetal and maternal genetic effects and shared sibling environmental effects on birth weight and gestational age and also on crown-heel length and head circumference. The authors used path analysis and maximum likelihood principles to estimate these effects and, at the same time, to adjust for covariates. Parent-offspring data were obtained from the Medical Birth Registry of Norway from 1967 to 2004. For the analysis of birth weight and crown-heel length, 101,748 families were included; for gestational age, 91,617 families; and for head circumference, 77,044 families. Assuming no cultural transmission and random mating, the authors found that fetal genetic factors explained 31% of the normal variation in birth weight and birth length, 27% of the variation in head circumference, and 11% of the variation in gestational age. Maternal genetic factors explained 22% of the variation in birth weight, 19% of the variation in birth length and head circumference, and 14% of the variation in gestational age. Relative to the proportion of explained variation, fetal genes were most important for birth length and head circumference.

Infants with congenital malformations have on average lower birth weight than do infants without malformations. Preterm delivery and low birth weight are known to recur in sibships. The aim of the study was to compare the birth weight of siblings to malformed infants with the birth weight of infants in families without malformed infants. Data were from the Medical Birth Registry in Norway from 1967 to 1998. Births were linked to their mothers through the unique personal identification number, providing sibship files with the mother as the observation unit. The study was based on 551,478 mothers with at least two singleton infants and 209,423 mothers with at least three singletons. The authors grouped the families according to whether and in which birth order an infant had a registered congenital malformation and compared birth weight and gestational age between infants of the same birth order in families with malformations and without. Overall, in families where one or two infants had a congenital malformation, the crude and adjusted mean birth weight of nonmalformed siblings did not differ from that of infants in unaffected families, whereas it was significantly reduced for the malformed infant itself. We conclude that reduced birth weight associated with congenital anomalies is specific to the affected pregnancy.

Knowledge of stillbirth recurrence risk is of clinical interest and may give etiological insight. The authors studied "gestational age-" and "weight-by-gestation-specific" stillbirth recurrence, and evaluated time trends in a population-based cohort study from the Medical Birth Registry of Norway, from 1967 to 2004. Singleton births, including stillbirths from 20 weeks' gestation, were linked to their mothers by national identification numbers. Stillbirth rates in second pregnancies among mothers with (N = 5,091) and without (N = 562,057; the reference group) a stillbirth in first pregnancies were compared across 4 gestational age and 3 weight-by-gestation groups. A remarkable symmetric pattern of gestational age-specific recurrence of stillbirth was found, with highest odds of stillbirth in the same age group. The adjusted odds ratio values associated with preterm stillbirth recurrence were high, for example, 25.7 (95% confidence interval: 19.8, 33.3) for stillbirth at 20-27 weeks' gestation (73/1,511 vs. 1,021/ 562,057), while lower for term stillbirth: adjusted odds ratio = 2.3 (95% confidence interval: 1.2, 4.7) (9/1,844 vs. 1,021/538,499). The proportion of second early stillbirths in the population attributable to previous early stillbirth was 6.4%, compared with 0.5% for second term stillbirth. Over time, recurrence of early stillbirth decreased, whereas that of mid/late stillbirth did not change significantly. A symmetric pattern of recurring stillbirth in similar weight-by-gestation groups was not found.

The authors studied the extent to which preterm birth and perinatal mortality are dependent on the gestational ages of previous births within sibships. The study was based on data collected by the Medical Birth Registry of Norway from 1967 to 1995. Newborns were linked to their mothers through Norway's unique personal identification number, yielding 429,554 pairs of mothers and first and second singleton newborns with gestational ages of 22-46 weeks, based on menstrual dates. Siblings' gestational ages were significantly correlated (r = 0.26). The risk of having a preterm second birth was nearly 10 times higher among mothers whose firstborn child had been delivered before 32 weeks' gestation than among mothers whose first child had been born at 40 weeks. However, perinatal mortality in preterm second births was significantly higher among mothers whose first infant had been born at term, compared with mothers whose firstborn child was delivered at 32-37 weeks. Since perinatal mortality among preterm infants is dependent on the gestational age in the mother's previous birth, a common threshold of 37 weeks' gestation for defining preterm birth as a risk factor for perinatal death may not be appropriate for all births to all mothers.

To describe trends in low birth weight (less than 2,500 g), the authors analyzed 1.7 million live births and stillbirths registered between 1967 and 1995 in the Medical Birth Registry of Norway. The proportion of low birth weight infants declined from 5.3% in 1967 to 4.5% in 1979 and was followed by a steady increase that reached 5.3% in 1995. Similar trends were observed in the proportion of preterm births. Mean birth weight increased from 3,456 g in 1967 to 3,518 g in 1995. From 1979 to 1987, the increase in the prevalence of low birth weight was related to single births, and after 1987 it was related to multiple births, which increased from 2.3% of all births in 1987 to 3.1% in 1995. The proportion of low birth weight in births occurring after 37 weeks of gestation declined continuously, resulting in low birth weight births' to an increasing extent being made up of births occurring before 37 weeks of gestation. In an ecologic analysis based on county of maternal residence, the increase in low birth weight among single births was accounted for by an increase in deliveries with induction of labor or cesarean section. The authors conclude that the overall proportion of low birth weight births is not a good indicator of health in a population with extensive use of obstetric procedures that affect gestational age or assisted fertilization, which increases the number of multiple births.

To investigate the recurrence of sudden infant death syndrome (SIDS) among siblings, the authors analyzed data for all 352,475 mothers whose first and second single births were reported to the Medical Birth Registry of Norway during 1967-1988. Recurrence of stillbirths from the 16th week of gestation onward and infant deaths other than SIDS were also studied. Relative risk of recurrence for SIDS was 5.8 (95% confidence interval (CI) 2.1-13.2); for asphyxia- and immaturity-related infant deaths, 12.5 (9.2-17.4); for congenital malformations, 7.2 (4.7-11.0); and for other causes of infant death, 8.0 (2.0-22.1). Deaths due to infections did not recur. Similar categories of infant deaths had higher overall relative risk, 9.1, compared with 1.6 for dissimilar categories. Previous early stillbirth (16-27 weeks) had a high recurrence (relative risk (RR) = 21.8, 95% CI 17.5-26.9), while late stillbirth (> or = 28 weeks) had lower recurrence (RR = 4.6, 95% CI 3.7-5.8). Previous SIDS was associated with an increased risk of all other types of loss. In contrast, previous late stillbirth and previous asphyxia- and immaturity-related infant deaths were associated with a reduced risk of subsequent SIDS (RR = 0.31, 95% CI 0.08-0.84, and RR = 0.23, 95% CI 0.01-1.13, respectively). In conclusion, as with other infant and fetal deaths, SIDS deaths showed strong sibship aggregation consistent with a genetic susceptibility in subsets of SIDS that may interact with environmental factors. The authors also suggest common pregnancy-specific risk factors for late stillbirths, asphyxia- and immaturity-related infant deaths, and SIDS.

To evaluate the intrauterine growth potential of infants that die from sudden infant death syndrome (SIDS), the authors compared SIDS infants with their surviving siblings. The SIDS sibships themselves were also compared with sibships where all infants survived. Data from the population-based Medical Birth Registry of Norway, with 1.3 million births during 1967-1988, were used. From the birth cohorts, 1,984 SIDS cases were identified. All births were linked into sibships. The mean birth weight and gestational age were calculated across sibships of different sizes for first to fourth birth order. In a further analysis, birth weights were standardized to adjust for gestational age. Mothers of SIDS infants gave birth to smaller babies in general. SIDS infants weighed, on average, 85 g less at birth than their siblings and 164 g less compared with babies in nonaffected sibships. When birth weights were standardized for gestational age, most of the weight difference between SIDS infants and siblings was due to a shorter gestational age of SIDS infants, while the difference between surviving siblings of SIDS infants and births from nonaffected sibships remained. All births in sibships with a SIDS infant were intrauterine growth retarded. This may reflect factors that contribute to SIDS risk (such as maternal smoking). The factors that contribute to shorter gestational age and further slowing of growth in the SIDS infants may specifically influence the SIDS infant and not its siblings. Am J Epidemiol 1995 ;142 :84-90.

In Norway, external doses of radiation resulting from fallout from the Chernobyl nuclear accident were estimated from detailed measurements, including soil deposition patterns. Internal doses were estimated from measurements of radioactive cesium in meat and milk supplies. The doses were calculated as average monthly doses for each of 454 municipalities during 36 consecutive months after the accident in spring 1986. Prospectively collected data on all newborns listed in the Medical Birth Registry of Norway who were conceived in the period May 1983-April 1989 were used to assess possible dose-response relations between estimated external and food-based exposures and congenital malformations and some other conditions. A positive association was observed between total radiation dose (external plus food-based) and hydrocephaly, while a negative association was observed for Down's syndrome. However, an important conclusion of the study was that no associations were found for conditions previously reported to be associated with radiation, i.e., small head circumference, congenital cataracts, anencephaly, spina bifida, and low birth weight. Potential sources of bias, including exposure misclassification and incomplete ascertainment of cases, are discussed.

Data from the Medical Birth Registry of Norway, covering more than one million births for the period 1967-1984, were used to study the magnitude and effects of selective fertility, which is the tendency for a woman to replace a perinatal loss. Variation in fertility after the first three births is studied, controlling for perinatal outcome of previous births, maternal age, and year of birth. Even after the first birth, fertility is higher after a perinatal loss. Selective fertility is more strongly present at each successive birth order, and at each birth order it is stronger among older women. As the average number of births per woman decreases, the force of selective fertility increases; that is, its importance has increased over time. Perinatal mortality at the third and fourth birth orders is particularly distorted by the mechanism of selective fertility in studies based on cross-sectional data. Mortality at second birth is exaggerated by 1%, at third birth by 8% to 20%, and at fourth birth by 18% to 27%, with the largest effects seen in the later periods. A major portion of the increase in perinatal mortality from the second to fourth birth seen in most studies based on cross-sectional data can be explained by the mechanism of selective fertility.

Epidemiologic surveillance in Norway, the United States, Nigeria, Japan, Venezuela, India, and China, covering periods from 1851 to 1981, demonstrates a consistent decline in incidence rates of leprosy. At the same time, secular trends have been observed which imply an increasing age at onset, an increasing male excess, and an increasing fraction of new cases represented by multibacillary leprosy. Theoretically, an increasing age at onset may be caused by two mechanisms, namely postponement of infection to a later age and/or an increasing fraction of patients with long incubation periods. Cohort analyses have shown no increase in age at onset in subsequent birth cohorts, but rather have shown a decrease. The latter mechanism, the increasing importance of long incubation periods, is consistent with the shift toward multibacillary cases in which the incubation period is longer than that in paucibacillary cases. Apparently, this mechanism has also been present during the decline of tuberculosis. An increasing fraction of new patients with long incubation periods, resulting in an increasing age at onset, is proposed as a general principle to be expected in any disease in rapid decline which also has a long and varying incubation period. This theory offers a basis for assessment of secular trends.

Two five-year cohorts, 1967-1971 and 1977-1981, of the Medical Birth Registry of Norway, were utilized to analyze secular trends in early neonatal mortality rates, controlling simultaneously for birth weight, parity, maternal age, and sex. Improvement in the crude early neonatal mortality rate, from 6.5 to 2.9 per 1,000, was partitioned into one portion (18.4%) attributable to changes in the distribution of the birth weight or the other independent variables and another portion (81.6%) attributable to improved survival within each specific subgroup in the multivariate table. The early neonatal mortality rate was found to decrease in all subgroups, the low birth weight groups showing a significantly greater decline than the normal birth weight groups. Women with diabetes, epilepsy, or blood group antibodies were studied in separate analyses. For women with diabetes, the odds ratio of the early neonatal mortality rate between the first and the second periods was found to be three times the odds ratio for women without diabetes, and 2.9% of the total improvement of the crude early neonatal mortality rate was attributable to an improved survival in these infants.