In this prospective cohort study, more-rapid increases in WFL in the first 6 months of life were associated with sharply increased risk of obesity and adiposity (measured as the sum of skinfold thicknesses) at 3 years of age. We found the predicted probability of obesity at age 3 to be 40% among infants in the highest quartiles of both birth and 6-month WFL. These effects were independent of a number of potential confounders, including socioeconomic status and maternal smoking, gestational weight gain, and prepregnancy BMI. Birth WFL was only minimally associated with our anthropometric outcomes, which suggests that early interventions to prevent rapid increase in weight status in the first months of life may help reduce children’s risk of obesity later in childhood. Furthermore, the observed associations between rapid increases in weight status in the first 6 months of life and later obesity did not vary according to gender.
Our study was unique in 3 ways. First, we had research- level measures of length at birth and 6 months; most previous studies in this area were limited by their reliance on weight alone. Second, we were able to compare the effect of birth WFL adjusted for gestational age (“fetal growth”), as opposed to simply birth weight, with changes in WFL from birth to 6 months of age. Third, we were able to adjust for several prenatal and postnatal confounders, some of which were not available for previous longitudinal birth cohorts (eg, paternal BMI). Our findings are consistent with previous studies of both contemporary9,10
cohorts and confirm the findings of 2 systematic reviews of infant growth and obesity that concluded that infants at the highest end of the weight or BMI distribution and infants who grew most rapidly (usually measured as weight gain) were more likely to be obese later in life.7,8
In the review by Baird et al,7
relative risks of later obesity ranged from 1.17 to 5.70 among infants with more-rapid weight gain in the first year of life. Our observed magnitudes of effect were larger than previously reported values, possibly because we were able to use measures of length in addition to weight, which together reflect adiposity better than weight alone. It is also possible that the relatively close measurement of exposures and outcomes contributed to our observed magnitudes of effect.
In contrast to a previous study that examined changes in length in infancy,6
we found that changes in LFA from birth to 6 months were not associated with later obesity. Changes in WFA and changes in WFL from birth to 6 months were associated with later obesity and higher adiposity, which suggests that it is rapid weight gain in infancy that puts children at risk.
In this study, we were able to examine a wide range of factors that might confound the relationship between changes in WFL in infancy and later obesity. Parental body habitus, maternal smoking during pregnancy, and gestational weight gain all confounded the relationship between changes in WFL in infancy and later obesity. Although previous studies found that gestational diabetes and glucose tolerance were associated with offspring obesity, especially for older children and adolescents,25
we did not find maternal glucose tolerance to be associated with 6-month WFL or to be a confounder of the relationship between changes in WFL in infancy and later obesity. In addition, although previous studies raised the possibility that increased maternal intake of n
−3 polyunsaturated fatty acids during pregnancy might be associated with reduced adiposity in children,26–29
we did not find this factor to be a confounder.
Although breastfeeding was independently associated with a lower prevalence of obesity at age 3,30
the mode of infant feeding was not a confounder in this study. We were not able to assess fully whether breastfeeding was an intermediate of the relationship between changes in WFL in infancy and later obesity. It is possible that the quality of the infant diet after weaning also may mediate the relationship between infant weight gain and later obesity. Finally, we were not able to examine social and behavioral interactions regarding infant feeding. Hodges et al31
suggested that overfeeding and low caregiver responsiveness to child feeding cues might contribute to early infant weight gain and later obesity. Future studies should examine whether the mode of infant feeding, the quality of the infant diet after weaning, and overfeeding because of lack of parental responsiveness to infants’ satiety cues might explain the association of infant weight gain with later obesity.
When our study results are being interpreted, several limitations should be considered. First, although mothers in the study had diverse racial/ethnic backgrounds, their educational and income levels were relatively high. Our results may not be generalizable to more socioeconomically disadvantaged populations. Second, most of our measures were from self-reports, including prepregnancy weight, smoking, breastfeeding, and infant sleep, and loss to follow-up monitoring was not random. These factors might have introduced bias. Finally, our main outcome was obesity at age 3. Obesity at this age does not predict adult consequences as well as obesity later in childhood32
but can presage serious adverse health consequences in childhood itself.33