In the U.S., preterm birth affects 1 in 9 live births in the general population and 1 in 5 among African Americans. This study was the first to demonstrate the association between preterm birth and insulin levels during early developmental periods. The in utero and early childhood periods are critical windows for growth, development, and metabolic programming. Available studies in children and adults linked preterm birth with adverse metabolic alterations, but it is unclear whether the observed association between preterm birth, later insulin resistance and type 2 diabetes stems from the in utero period or early childhood.
“Our study lends further support to previous studies that have reported relationships between preterm birth and insulin resistance in childhood, young adulthood and middle-adulthood,” observed Xiaobin Wang, MD, MPH, ScD, Zanvyl Krieger Professor, and the Principal Investigator of the Boston Birth Cohort. “Our findings suggest that insulin resistance exhibited by adolescents and adults born preterm may originate in utero” and a continued follow-up of the study children into adolescence and adulthood will provide more definite answers.
In the U.S., preterm birth is a leading cause of infant mortality and is known to be linked with a spectrum of childhood morbidity such as neuro-developmental disorders (including cerebral palsy and autism), chronic lung disease (including asthma), and hearing and visual impairment. “Prevention of preterm birth is not only important to reduce infant mortality and childhood morbidity, but also has important implications for prevention of chronic disease in later life such as insulin resistance and type 2 diabetes,” as pointed out by Wang.
This study included 1,358 children from the Boston Birth Cohort, who were enrolled at birth and followed prospectively from birth onward. The study sought to examine if preterm birth is associated with elevated plasma insulin levels (indirect evidence of insulin resistance) at birth, and if elevated insulin levels persist into early childhood. The researchers compared four groups of children born with different length of gestation: full term (more than 39 weeks); early term (between 37 and 38 weeks); late preterm (between 34 and 36 weeks); and early preterm (less than 34 weeks). They found that the more severe the prematurity, the higher level of blood insulin. For example, at birth, insulin levels were 1.13, 1.45 and 2.05 folds higher for early term, late preterm and early preterm, respectively, than those born full term. This pattern persists in early childhood. Children ranked in the top insulin category at birth were more likely to remain in the top in early childhood relative to children ranked in the lowest category (41.2% vs. 28.6%).
Type 2 diabetes is a significant and growing public health challenge in the U.S. and worldwide, and can lead to multi-organ damages, including heart disease, kidney disease, stroke, vascular disease, and eye disease. Like many other chronic diseases, type 2 diabetes has a long latency before it is diagnosed clinically, and once developed, it is not reversible, and requires lifetime medical treatment. By recognizing that preterm birth may be a risk factor for the future development of insulin resistance and type 2 diabetes, health care providers and parents can initiate preemptive measures to reduce the risk at the youngest possible age, including optimal nutrition, close monitoring of growth trajectory and metabolic profiles, and physical activity.
“Preterm Birth and Random Plasma Insulin Levels at Birth and in Early Childhood” was written by Guoying Wang, Sara Divall, Sally Radovick, David Paige, Yi Ning, Zhu Chen, Yuelong Ji, Xiumei Hong, Sheila O. Walker, Deanna Caruso, Colleen Pearson, Mei-Cheng Wang, Barry Zuckerman, Tina L. Cheng and Xiaobin Wang.
The Boston Birth Cohort (the parent study) is supported in part by the March of Dimes PERI grants (20-FY02-56, #21-FY07-605), the Food Allergy Initiative, and the National Institutes of Health (NIH) grants (R21 ES011666, R01 HD041702, R21HD066471, R21AI088609, U01AI090727), and philanthropic support from The Ludwig Family Foundation.
Johns Hopkins Bloomberg School of Public Health media contact: Tim Parsons at 410-955-7619 or [email protected]