Objective: Gestational weight gain (GWG) is associated with childhood obesity. We analyzed whether this effect persists into adulthood and is mediated by effects in childhood. Design: The design of the study a prospective birth cohort study established in [1959][1960][1961]. Subjects: The subjects were offspring (n ¼ 4234 of whom 2485 had information from the last follow-up) of mothers included in 'The Copenhagen Perinatal Cohort' during pregnancy or at birth. Measurements: Information on maternal pre-pregnancy body mass index (BMI), GWG and several potential confounders were collected around delivery. Information on offspring BMI was available from various follow-up examinations from 1 to 42 years of age. The association of GWG with offspring BMI was analyzed by regression models including confounders. Using path analysis, the association of GWG with adult BMI was disentangled into an association mediated through childhood BMI and one independent hereof. Results: GWG was associated with offspring BMI at all ages. At the age of 42 years (n ¼ 1540), there was an increasing risk of obesity (odds ratio (OR) 1.08, 95% confidence interval (CI) 1.03-1.14 per kg GWG, P ¼ 0.003). Only half of the association of GWG on offspring adult BMI was mediated through birth weight and BMI up to 14 years of age. Conclusion: Greater GWG is associated with an increased BMI in childhood through adulthood and with an increased risk of obesity in adults. Only part of the association with adult BMI is mediated by childhood BMI, suggesting that excessive GWG induces a persisting susceptibility to obesogenic environments. As GWG is greater in women with small pre-pregnancy body weight, this implies a reinforcement of the obesity epidemic in the next generation. Our findings provide support for avoiding excessive GWG.

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The authors investigated the shape, sex- and age-dependency, and possible confounding of the association between birth weight and systolic blood pressure (SBP) in 197,954 adults from 20 Nordic cohorts (birth years 1910-1987), one of which included 166,249 Swedish male conscripts. Random-effects meta-regression analyses were performed on estimates obtained from age- and sex-stratified analyses within each of the cohorts. There was an inverse association between birth weight and SBP, irrespective of adjustment for concurrent body mass index. The association was linear for males, but for females with a birth weight greater than 4 kg, SBP increased with birth weight (p < 0.01). The association was stronger in the older age groups (p < 0.05), although this could have been a birth cohort effect. The association was stronger among females than among males (p = 0.005) when birth weight was less than or equal to 4 kg. The estimated effect of birth weight on SBP at age 50 years was -1.52 mmHg/kg (95% confidence interval: -2.27, -0.77) in men and -2.80 mmHg/kg (95% confidence interval: -3.85, -1.76) in women. Exclusion of the Swedish conscripts produced nearly identical results. This meta-analysis supports the evidence of an inverse birth weight-SBP association, regardless of adjustment for concurrent body size. It also reveals important heterogeneity in the shape and strength of the association by sex and age.

BackgroundPrenatal life exposures, potentially manifested as altered birth size, may influence the later risk of major chronic diseases through direct biologic effects on disease processes, but also by modifying adult behaviors such as physical activity that may influence later disease risk.Methods/Principal FindingsWe investigated the association between birth weight and leisure time physical activity (LTPA) in 43,482 adolescents and adults from 13 Nordic cohorts. Random effects meta-analyses were performed on categorical estimates from cohort-, age-, sex- and birth weight specific analyses. Birth weight showed a reverse U-shaped association with later LTPA; within the range of normal weight the association was negligible but weights below and above this range were associated with a lower probability of undertaking LTPA. Compared with the reference category (3.26–3.75 kg), the birth weight categories of 1.26–1.75, 1.76–2.25, 2.26–2.75, and 4.76–5.25 kg, had odds ratios of 0.67 (95% confidence interval: 0.47, 0.94), 0.72 (0.59, 0.88), 0.89 (0.79, 0.99), and 0.65 (0.50, 0.86), respectively. The shape and strength of the birth weight-LTPA association was virtually independent of sex, age, gestational age, educational level, concurrent body mass index, and smoking.Conclusions/SignificanceThe association between birth weight and undertaking LTPA is very weak within the normal birth weight range, but both low and high birth weights are associated with a lower probability of undertaking LTPA, which hence may be a mediator between prenatal influences and later disease risk.

Objective: To assess whether changes in the birth weight distribution or changes in the association of birth weight with the later risk of childhood overweight have contributed to the development of the obesity epidemic. Research Methods and Procedures: A Danish populationbased cohort study of 124,615 girls and 128,346 boys (ages 6 to 13 years), born between 1936 and 1983, were studied. Birth weight and annual measurements of height and weight were obtained from school health records. Overweight was defined by BMI in relation to internationally accepted criteria. The relative risk of being overweight by birth weight was calculated separately for each age, sex, and time period. Results: The birth weight distribution remained relatively stable over time. Compared with children with a birth weight of 3.0 to 3.5 kg, the risk of overweight increased consistently with each increase in birth weight category among girls and boys and at all ages between 6 and 13 years. Furthermore, the association between birth weight and increased risk of overweight in childhood remained stable across a 48-year period. Discussion: The increase in the prevalence of overweight could not be explained by time trends in the distribution of birth weight or by changes in the association between birth weight and the later risk of overweight over time. This implies that, unless the prenatal environment influences the later risk of overweight without increasing birth weight, the environmental influences contributing to the obesity epidemic in children of school age operate in the early postnatal period.