These results show an inverse but moderate association of birthweight with adult mortality from all-causes and a stronger inverse association with cardiovascular mortality. For men, higher birthweight was strongly associated with increased risk of cancer deaths. The findings suggest that birthweight can be a useful indicator of processes that influence long-term health.

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The objective of this study was to examine a possible association between maternal smoking in pregnancy and childhood overweight. From a population-based cohort of 5722 women from Trondheim, Bergen (Norway) and Uppsala (Sweden) enrolled in early pregnancy during 1986-92, a random sample of 482 women was selected for participation. They were followed up throughout pregnancy, and their children from birth until 5 years of age. Data on maternal smoking and diet, socio-economic determinants and breast feeding were recorded prospectively. During pregnancy and childhood, anthropometric measures were also recorded. Maternal smoking status was based on reported number of cigarettes smoked in week 17 of pregnancy. Child overweight was defined by body mass index (BMI) and sum of skinfold thickness (SFT) >or= 85th percentile at 5 years of age. Children of mothers who smoked in pregnancy had increased risk of overweight at 5 years of age (RR 2.5, 95% CI 1.5, 4.2 for BMI; and RR 1.8, 95% CI 1.1, 3.0 for SFT). Adjusting for maternal diet, breast feeding, maternal obesity and socio-economic status did not suggest confounding. However, adjustment for birthweight increased the observed risk. A linear increase in BMI and SFT was observed with increasing number of cigarettes smoked. In conclusion, smoking during pregnancy may be a risk factor for development of childhood overweight. This study may support the hypothesis of 'fetal origin of adult disease', but the risk of overweight associated with smoking during pregnancy was independent of intrauterine growth retardation, and may thus be attributed to specific effects of cigarette smoke.

To study the etiology and consequences of intrauterine growth retardation (IUGR), a prospective study was organized by the National Institute of Child Health and Human Development, NIH, with the Universities of Trondheim and Bergen in Norway, Uppsala in Sweden, and Alabama in the United States. This paper reports on the Scandinavian portion of the study. 6,354 women were referred to the study and 5,722 women, who were expecting their second or third child between January 1986 and March 1988, were eligible and made their first appointment for the study. Of these, 1,945 women and their births were selected for follow-up at four prenatal visits, delivery, and during the first year of life. This report analyzes the relative impact of various maternal pre-pregnancy risk factors associated with SGA birth. For example, mothers who smoked cigarettes around the time of conception, but who had none of the other major risk factors, nearly doubled their risk of SGA birth. A previous low birth weight (LBW) delivery increased the risk nearly two and a half times among non-smokers. If a mother both smoked and had a previous LBW, the relative risk rose to nearly five and a half. Low maternal pre-pregnancy weight (< 50 kg) increased the risk of SGA birth almost twofold among non-smokers, while low pre-pregnancy weight and smoking together increased the risk of SGA birth fourfold. A low weight mother who smoked and also had a previous LBW delivery, had a risk of SGA birth that was nearly six times that of a mother without those characteristics.

BackgroundMaternal smoking during pregnancy is linked to reduced birth weight but the gestation at onset of this relationship is not certain. We present a systematic review of the literature describing associations between maternal smoking during pregnancy and ultrasound measurements of fetal size, together with an accompanying meta-analysis.MethodsStudies were selected from electronic databases (OVID, EMBASE and Google Scholar) that examined associations between maternal smoking or smoke exposure and antenatal fetal ultrasound measurements. Outcome measures were first, second or third trimester fetal measurements.ResultsThere were 284 abstracts identified, 16 papers were included in the review and the meta-analysis included data from eight populations. Maternal smoking was associated with reduced second trimester head size (mean reduction 0.09 standard deviation (SD) [95% CI 0.01, 0.16]) and femur length (0.06 [0.01, 0.10]) and reduced third trimester head size (0.18 SD [0.13, 0.23]), femur length (0.27 SD [0.21, 0.32]) and estimated fetal weight (0.18 SD [0.11, 0.24]). Higher maternal cigarette consumption was associated with a lower z score for head size in the second (mean difference 0.09 SD [0, 0.19]) and third (0.15 SD [0.03, 0.26]) trimesters compared to lower consumption. Fetal measurements were not reduced for those whose mothers quit before or after becoming pregnant compared to mothers who had never smoked.ConclusionsMaternal smoking during pregnancy is associated with reduced fetal measurements after the first trimester, particularly reduced head size and femur length. These effects may be attenuated if mothers quit or reduce cigarette consumption during pregnancy.

BackgroundStudies on the health benefits from breastfeeding often rely on maternal recall of breastfeeding. Although short-term maternal recall has been found to be quite accurate, less is known about long-term accuracy. The objective of this study was to assess the accuracy of long-term maternal recall of breastfeeding duration.MethodsIn a prospective study of pregnancy and birth outcome, detailed information on breastfeeding during the child’s first year of life was collected from a cohort of Norwegian women who gave birth in 1986–88. Among 374 of the participants, data on breastfeeding initiation and duration were compared to recalled data obtained from mailed questionnaires some 20 years later. Intraclass correlation coefficient (ICC), Bland-Altman plot, and Kappa statistics were used to assess the agreement between the two sources of data. Logistic regression was used to assess predictors of misreporting breastfeeding duration by more than one month.ResultsRecorded and recalled breastfeeding duration were strongly correlated (ICC=0.82, p < 0.001). Nearly two thirds of women recalled their breastfeeding to within one month. Recall data showed a modest median overestimation of about 2 weeks. There were no apparent systematic discrepancies between the two sources of information, but recall error was predicted by the age when infants were introduced to another kind of milk. Across categories of breastfeeding, the overall weighted Kappa statistic showed an almost perfect agreement (κ = 0.85, 95% confidence interval [CI] 0.82 – 0.88).ConclusionBreastfeeding duration was recalled quite accurately 20 years after mothers gave birth in a population where breastfeeding is common and its duration long.

In epidemiologic studies of perinatal exposures, birth weight has been proposed as a proxy variable for intrauterine estrogen exposure. To assess the validity of this assumption, we performed analyses of the association between estriol levels in 188 women in the 17th, 25th, 33rd, and 37th weeks of pregnancy and the birth weights of their infants. We found a general increase in mean cumulative estriol dose with increasing birth weight category throughout pregnancy. In late pregnancy, mean pregnancy estriol level of mothers of infants in the highest birth weight category (>4,500 gm) was twice as high as that of mothers of infants in the lowest category (<2,500 gm), 775 nmol/liter and 392 nmol/liter, respectively. Smoking lowered the maternal estriol levels by 20% or more throughout pregnancy. With smoking and birth weight included in a regression analysis, maternal age, placental weight, and infant ponderal index did not add any explanatory power to the model. Our data suggest that, on an aggregate level, birth weight can be used as a proxy variable of intrauterine estriol exposure.

Objective: Animal studies have indicated that maternal androgen levels influence the intrauterine environment and development of the offspring. Human data are missing. We therefore investigated the possible association between maternal androgens and offspring size at birth in humans. Design: A random sample of parous Caucasian women (nZ147) was followed prospectively through pregnancy. Methods: Maternal serum levels of dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone and sex hormone-binding globulin (SHBG) were measured at gestational weeks 17 and 33. The main outcome measures were weight and length at birth. Associations between maternal androgen levels and offspring birth weight and length were investigated using multiple linear regression modeling adjusted for potential confounding by maternal height, pre-pregnancy body mass index, smoking, parity, offspring gender and gestational age at birth. Results: Elevated maternal testosterone levels at week 17 and 33 were both associated with lower birth weights and lengths. Accordingly, at week 17, an increase in maternal testosterone levels from the 25th to the 75th percentile was associated with a decrease in birth weight by 160 g (95% confidence interval (CI); 29-290 g), while at week 33 that estimate was 115 g (95% CI; 21-207 g). No similar associations were observed for DHEAS, androstenedione or SHBG. Conclusions: Elevated maternal testosterone levels during human pregnancy are associated with growth restriction in utero. Our results support animal studies, which have indicated that maternal androgen levels influence intrauterine offspring environment and development.