Growth in foetal life and infancy is associated with abdominal adiposity at the age of 2 years: The Generation R Study

The Generation R Study Group, Erasmus Medical Center, Rotterdam, The Netherlands.
Clinical Endocrinology (Impact Factor: 3.46). 09/2009; 72(5):633-40. DOI: 10.1111/j.1365-2265.2009.03708.x
Source: PubMed


Early weight gain is associated with an increased risk of obesity. It is not known whether rapid weight gain in foetal life and infancy is also associated with increased abdominal adiposity. We examined the associations of foetal and postnatal growth characteristics with abdominal fat mass at the age of 2 years.
This study was performed in 481 children participating in a prospective cohort study from early foetal life onward.
Foetal and postnatal growth characteristics in second and third trimester, at birth and at the age of 2 years were related to abdominal fat mass (subcutaneous distance and area, preperitoneal distance and area) measured by ultrasound at the age of 2 years.
Foetal and birth weight were not associated with abdominal subcutaneous fat mass. Estimated foetal weight in second trimester of pregnancy was inversely associated with preperitoneal fat area [-3.73% (95% confidence interval -7.23, -0.10)] per standard deviation score increase in weight. Weight gain from birth to the age of 2 years was positively associated with preperitoneal fat mass measures. These associations remained significant after adjustment for age, sex, breastfeeding and body mass index. Positive associations were found between catch-up growth in weight and abdominal fat mass measures.
Our results suggest that rapid growth rates during foetal life and infancy are associated with increased abdominal subcutaneous and preperitoneal fat mass in healthy children. Further studies need to explore whether these associations persist in later life and are related to metabolic syndrome outcomes.

38 Reads
  • Source
    • "This association has been seen for obesity in adults and children, in high-income and low-income countries [8] [9] [10] and is consistent for cohorts over the last 80 years [8]. The " critical window " for the effects of growth is not known, but slower weight gain in the first few weeks (regardless of gestation or birth weight) is associated with a lower risk of later obesity [11] [12], insulin resistance [13], endothelial dysfunction [5], and adult obesity [14]. Therefore, differences in weight gain between formula-and breast-fed infants in the first postnatal weeks, when breastfed babies often lose weight compared to weight gain in babies given formula [15] [16], could partially explain longterm programming advantages of breastfeeding [6]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Faster weight gain early in infancy may contribute to a greater risk of later obesity in formula-fed compared to breast-fed infants. One potential explanation for the difference in weight gain is higher macronutrient intake in formula-fed infants during the first weeks of life. A systematic review was conducted using Medline to assess the macronutrient and energy content plus volume of intake in breast-fed and formula-fed infants in early infancy. All studies from healthy, term, singleton infants reporting values for the composition of breast milk during the first month of life were included. The energy content of colostrum (mean, SEM: 53.6 ± 2.5 kcal/100 mL), transitional milk (57.7 ± 4.2 kcal/100 mL), and mature milk (65.2 ± 1.1 kcal/100 mL) was lower than conventional infant formula (67 kcal/100 mL) on all days analyzed. The protein concentration of colostrum (2.5 ± 0.2 g/100 mL) and transitional milk (1.7 ± 0.1 g/100 mL) was higher than formula (1.4 g/100 mL), while the protein content of mature milk (1.3 ± 0.1 g/100 mL) was slightly lower. Formula-fed infants consume a higher volume and more energy dense milk in early life leading to faster growth which could potentially program a greater risk of long-term obesity.
    Journal of nutrition and metabolism 09/2012; 2012:891201. DOI:10.1155/2012/891201
  • Source
    • "Several studies determined an association between weight gain in the first 2-3 years of life and central adiposity, mostly assessed by larger waist circumference , in both adulthood [7] and early childhood [8– 13]. Imaging techniques such as magnetic resonance imaging [7], ultrasonography [10] [11], or computed tomography have seldom or never been used to assess the association between postnatal growth and later central adiposity. While in these studies weight gain in the first years of life was studied, the importance of particularly the first 3 months of life in the development of central adiposity was addressed in other studies in children [14] and adults [15] [16] [17]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background. Increased childhood weight gain has been associated with later adiposity. Whether excess early postnatal weight gain plays a role in childhood abdominal fat is unknown. Design. In the ongoing Wheezing Illnesses Study Leidsche Rijn (WHISTLER), birth cohort weight and length from birth to age 3 months were obtained. In the first 316 five-year-olds, intra-abdominal and subcutaneous fat were measured ultrasonographically. Individual weight and length gain rates were assessed in each child. Internal Z-scores of weight for length gain (WLG) were calculated. Multiple imputation was used to deal with missing covariates. Results. Per-1-unit increase in Z-score WLG from birth to 3 months, BMI, waist circumference, and subcutaneous fat were significantly higher; 0.51 kg/m(2), 0.84 cm, and 0.50 mm, respectively. After multiple imputation, a trend towards significance was observed for intra-abdominal fat as well (0.51 mm/SD). In the associations with 5-year adiposity, no interaction between postnatal Z-score WLG and birth size was found. Conclusion. Excess early postnatal weight gain is associated with increased general and central adiposity, characterized by more subcutaneous and likely more intra-abdominal fat at 5 years of age.
    International Journal of Pediatrics 05/2012; 2012(7240):141656. DOI:10.1155/2012/141656
  • Source
    Clinical Endocrinology 06/2010; 72(6):856. DOI:10.1111/j.1365-2265.2010.03819_2.x · 3.46 Impact Factor
Show more