In this study, the predicted probability of overweight in childhood varied from 6 to 29%, depending on the levels of four potentially modifiable risk factors in pregnancy and infancy— maternal smoking during pregnancy, gestational weight gain, breastfeeding duration, and daily sleep duration during infancy. This wide range of risk of childhood overweight implies that developmentally appropriate interventions to modify these factors may have substantial impact on preventing childhood obesity and its consequences.
Research into developmental origins of health and disease suggests that factors operating before and soon after birth can alter occurrence of chronic disease throughout the lifecourse (29
). Some critics, however, have questioned the magnitude of public health impact of modifying the pre- and postnatal environment. A previous attempt at quantifying long-term effects invoked birth weight as the single perinatal factor (30
). But birth weight, though easily measured, is unfortunately a poor proxy for true etiologic factors operating before and after birth (31
). Likewise, although several studies implicate rapid infant weight gain in the genesis of later obesity (12
), its modifiability is debatable beyond the potential effect of infant feeding, which we included as a risk factor in our analysis. In this study, we focused on four factors that are likely to be causal and potentially modifiable through clinical or public health interventions.
In most populations, the number of children with extreme risk factor profiles, e.g., those resulting in a 29% risk in this study, is likely to be small. Nevertheless, many mother–infant pairs in the intermediate categories would have room for substantial risk reduction. Consider, for example, a 3-year-old whose mother had smoked and gained an excessive amount of weight during pregnancy, and who had been breastfed for <12 months, but slept for at least 12 h/day during infancy. The estimated probability of overweight for such a child would be 19% (), which is likely to approximate the prevalence of overweight in US children by 2010 (32
). If the mother had not smoked or gained excessive weight during pregnancy and had breastfed for at least 12 months, the probability of overweight at 3 would be only 6%, assuming sleep duration did not change.
These are potentially achievable changes. In the developed world, smoking rates among pregnant women have risen and then declined in the past several decades (33
), and smoking cessation before or even during pregnancy is attainable (34
). Although no randomized controlled trials exist to show that moderating gestational weight gain is feasible, one trial with historical controls showed reduction in risk of excessive weight gain among low-income women (35
). In addition, wide fluctuations have occurred over the past 50 years in the amount of weight women gain during pregnancy, likely due to health professionals changing their recommendations over time (36
). After falling in the early to mid 20th century, breastfeeding rates have now risen from their nadir >30 years ago (37
), and a large randomized trial of breastfeeding promotion resulted in substantial increases in duration and exclusivity of breastfeeding (38
). Sleep duration during infancy appears modifiable as well (39
This study has several strengths. They include prospective data collection and the ability to adjust for several important confounding factors. The study also has several potential limitations. Gestational diabetes is associated with offspring overweight in some studies (40
), but was not prevalent enough in our cohort (n
= 42, 3.8%) to include as a risk factor. Including gestational diabetes status as a covariate hardly changed the estimated range of probabilities (from 0.06−0.29 to 0.06−0.30). Our main outcome was overweight at age 3. Overweight at this age does not predict adult consequences as well as overweight later in childhood (41
) but can nevertheless presage serious adverse health consequences in childhood itself (42
Some of our exposure–outcome associations were not “statistically significant” according to the common but arbitrary standard of a P
value <0.05. Nonetheless, as detailed in the Methods and Procedures section, other studies and meta-analyses have shown similar magnitudes of association with more precision than was possible in our single study, and the imprecision of our estimates is manifest in the width of the CIs (). As in other studies (43
), maternal BMI was a strong predictor of childhood obesity. Prevention of maternal obesity entering pregnancy is a public health priority, but was not the focus of this study, in which we evaluated modifiable factors once pregnancy begins.
Most measures were from self-report, including prepregnancy weight, smoking, breastfeeding, and infant sleep, and loss to follow-up was not random. These factors could have introduced bias. We obtained results from one cohort of mothers and children from Massachusetts. The quantitative results may not be directly applicable to other populations, chiefly because the frequencies of risk factors or overweight may differ. That is not a true limitation of the study, rather just a reminder that absolute risks differ across populations as covariate frequencies do. For example, in our calcuations of predicted probabilities if we had chosen as a “typical” participant, a woman with BMI of 30 instead of the sample population mean of 24.5 kg/ m2, the range of predicted probabilities would have been 0.11− 0.43 instead of 0.06−0.29. Regardless, more important than the exact probabilities is the message that varying levels of potentially modifiable early developmental factors predict a wide range of probabilities of childhood overweight.
In summary, we found that combinations of four modifiable factors in pregnancy and infancy can predict quite low or quite high risk of childhood overweight, in this cohort from well under 10 to almost 30%. Given the short- and long-term adverse consequences of childhood obesity, these findings suggest how crucial early developmental factors may be in determining obesity-related consequences across the life course. They also provide a strong rationale for testing developmentally appropriate pre- and postnatal interventions to prevent childhood overweight.