Birth weight and obesity and fat distribution in later life


  • Imogen Rogers

    Corresponding author
    1. Unit of Paediatric and Perinatal Epidemiology, Division of Community-Based Medicine, University of Bristol, Bristol, UK
    • Unit of Paediatric and Perinatal Epidemiology, Division of Community-Based Medicine, University of Bristol, Bristol, UK
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Low birth weight, obesity and a central pattern of fat distribution are all related to a number of chronic diseases in adult life, including coronary heart disease, hypertension and non–insulin-dependent diabetes mellitus. The relationship between birth weight and obesity is therefore of interest as a possible mediator of the birth weight–disease association.

There is consistent evidence from studies in both adults and children that there is a positive association between birth weight and subsequent body mass index (BMI) and obesity. This association is linear in some studies (Rasmussen and Johansson, 1998; Parsons et al., 2001) or U-shaped in others (Curhan et al., 1996), with some excess of obesity in the lowest birth weight groups.

BMI is a measure of relative weight, and as such does not distinguish between lean and fat mass. The positive association between weight at birth and relative weight later on could be generated by increases in total adiposity, central adiposity, or lean body mass. Studies that have measured lean and fat body mass have tended to find a positive association between birth weight and lean body mass and an inverse association with relative adiposity (Phillips, 1995; Gale et al., 2001), although the data are more consistent for adults than for children. There is a lack of studies that have assessed lean and fat mass by accurate methods such as dual-energy X-ray absorptiometry (DXA) scans or deuterium dilution.

Several studies have related birth weight to subsequent fat distribution, but their interpretation is made difficult by the wide range of indices of fat distribution used, including waist circumference, waist:hip ratio (WHR), and skinfold ratios such as the subscapular:triceps ratio. These are all of disputed validity, particularly for children, and there is a lack of studies with direct measures of intraabdominal or peripheral fat, for example, by computerized tomography or DXA scan. Most studies of children have tended to use skinfold ratios, whereas those in adults have tended to use WHR. Although there does not appear to be a direct association between birth weight and fat distribution on controlling for BMI, there is fairly consistent evidence that low birth weight is associated with a more central pattern of fat distribution. This evidence is more consistent for skinfold ratios (Byberg et al., 2000; Okosun et al., 2000) than for WHR (Yarbrough et al., 1998; Bavdekar et al., 1999).

The associations that have been observed between birth weight and subsequent body habitus could be genetic in origin or could be a result of programming by the intrauterine environment. Birth weight differences between the members of monozygotic twin pairs must be environmentally determined, so if these were to be associated with differences in adult BMI, this would suggest a long-term programming effect on subsequent ponderosity. Data from the largest twin study of 1440 twin pairs in Minnesota found that intrapair birth weight differences were associated with differences in adult height and weight but not BMI (Allison et al., 1995), and a smaller twin study in the United Kingdom reported similar findings (Baird et al., 2001). Other twin studies have been less conclusive, finding no associations between intrapair birth weight differences and differences in adult body habitus in most cases, but some evidence that large birth weight differences (>15%) are associated with some differences in adult BMI or lean body mass. Studies that control for parental BMI also go some way toward controlling for genetic predisposition to obesity. Among adults the relationship between birth weight and obesity is largely removed on controlling for BMI; however, in children an independent positive association seems to remain.

Studies of the offspring of women exposed to famine during pregnancy or of the offspring of diabetic pregnancies could be considered to provide proxy measures of the intrauterine environment, the former representing intrauterine undernutrition and the latter intrauterine overnutrition. Information on the effects of exposure to famine is available from studies of the offspring of women exposed to the Dutch famine and the siege of Leningrad. Among 19-year-old men, exposure to famine in utero in the first trimester was associated with increased rates of obesity, whereas exposure in the third trimester was associated with reduced rates of obesity (Ravelli et al., 1976). A second study of 50-year-old subjects found exposure to famine in early gestation to be associated with increased BMI among women but not men, whereas exposure in late gestation was associated with reduced birth weight but no differences in adult BMI. Among subjects born around the time of the siege of Leningrad (Stanner et al., 1997), exposure to famine in utero was associated with increased subscapular:triceps ratio, but no difference in BMI, despite large birth weight differences. Studies of the Pima Indians of Arizona, a group with exceptionally high rates of diabetes, have found that the offspring of diabetic mothers are heavier than the offspring of nondiabetic mothers, and that this applies even among siblings discordant for maternal diabetes in pregnancy (Pettitt et al., 1983). Maternal diabetes in pregnancy seems to override the correlation between maternal and offspring BMI. Studies of other groups of diabetic women are less conclusive. In the “Growing Up Today” study in the United States, the risk of obesity associated with maternal diabetes was attenuated on controlling for BMI and, in a study of women with mild diabetes in pregnancy, there was no association with BMI in their offspring.

Pregnancy weight gain could be viewed as a measure of nutrient availability in utero, and is positively correlated with weight and skinfold thickness at birth. Most of the published studies have found no association between pregnancy weight gain and later BMI and/or obesity (Maffeis et al., 1994; Stettler et al., 2000), possibly because pregnancy weight gain is generally self-reported. The one study to find a significant association found that BMI and percentage body fat of 10- to 11-year-old Italian children was inversely associated with pregnancy weight gain (Esposito-Del Puente et al., 1994).

Catch-up growth, that is, an increase in weight or height sd score of >0.67, normally occurs in the first 2 years of life and may be a sign that fetal growth has been constrained. Catch-up growth appears to be driven by increased food intake by the infant and may be regulated by programming of appetite, possibly via alterations in leptin levels. Catch-up growth has been associated with increased BMI, percentage body fat, and waist circumference in childhood (Ong et al., 2000).