Citation

Norris, Shane A.; Osmond, Clive; Gigante, Denise; Kuzawa, Christopher W.; Ramirez-Zea, Manuel; Richter, Linda M.; Stein, Aryeh D.; Tandon, Nikhil; Fall, Caroline H. D.; & COHORTS group (2012). Size at Birth, Weight Gain in Infancy and Childhood, and Adult Diabetes Risk in Five Low- or Middle-Income Country Birth Cohorts. Diabetes Care, 35(1), 172-179.

Abstract

Objective: We examined associations of birth weight and weight gain in infancy and early childhood with type 2 diabetes (DM) risk in five cohorts from low- and middle-income countries. Research design and methods: Participants were 6,511 young adults from Brazil, Guatemala, India, the Philippines, and South Africa. Exposures were weight at birth, at 24 and 48 months, and adult weight, and conditional weight gain (CWG, deviation from expected weight gain) between these ages. Outcomes were adult fasting glucose, impaired fasting glucose or DM (IFG/DM), and insulin resistance homeostasis model assessment (IR-HOMA, three cohorts). Results: Birth weight was inversely associated with adult glucose and risk of IFG/DM (odds ratio 0.91[95% CI 0.84–0.99] per SD). Weight at 24 and 48 months and CWG 0–24 and 24–48 months were unrelated to glucose and IFG/DM; however, CWG 48 months–adulthood was positively related to IFG/DM (1.32 [1.22–1.43] per SD). After adjusting for adult waist circumference, birth weight, weight at 24 and 48 months and CWG 0–24 months were inversely associated with glucose and IFG/DM. Birth weight was unrelated to IR-HOMA, whereas greater CWG at 0–24 and 24–48 months and 48 months–adulthood predicted higher IR-HOMA (all P < 0.001). After adjusting for adult waist circumference, birth weight was inversely related to IR-HOMA. Conclusions: Lower birth weight and accelerated weight gain after 48 months are risk factors for adult glucose intolerance. Accelerated weight gain between 0 and 24 months did not predict glucose intolerance but did predict higher insulin resistance. Recently, Whincup et al. (1) concluded that birth weight is inversely associated with the development of type 2 diabetes (DM) and that this association is strengthened after adjusting for adult BMI. Studies from high-income countries have shown that rapid weight gain in childhood or adult life is associated with an increased incidence of DM and insulin resistance (2). Therefore, impaired fetal growth and excess postnatal weight gain are both potential precursors to adult DM. Four-fifths of all individuals with DM live in low- and middle-income countries (LMICs) (3). Many of these countries are undergoing swift nutritional and economic transitions, exposing individuals to environmental conditions that promote weight gain. The combination of early-life undernutrition and overnutrition in adulthood may be fueling the epidemic of DM in LMICs (4). Few studies have examined childhood weight gain in relation to adult diabetes in LMICs. Gestation and the first 2 postnatal years (the first “1,000 days”; http://www.thousanddays.org) are the time when children’s growth in LMICs falls most rapidly below international reference values (5) and, hence, provide a significant window of opportunity for improved infant survival, cognitive development, and adult economic status (6,7). A critical public health question for LMICs is whether promoting early-life weight gain to achieve improvements in human capital could have adverse effects on adult diabetes risk. Data from birth cohorts in the U.K. and Finland indicate that, as with birth weight, lower weight at 1 year is associated with an increased risk of DM (8,9). Other studies have shown that greater weight or weight gain at this age is associated with an increased risk of obesity (10,11), which could increase diabetes risk. To clarify relationships between early-weight dynamics and adult diabetes risk, we pooled data from five birth cohort studies in LMICs and investigated associations of weight at birth, 24 months, 48 months, and young adulthood and conditional weight gain (CWG) between these ages, with adult-fasting glucose concentrations, risk of glucose intolerance, and insulin resistance. We hypothesized that lower birth weight and infant CWG but higher CWG after infancy would predict increased risk.

URL

http://dx.doi.org/10.2337/dc11-0456

Reference Type

Journal Article

Year Published

2012

Journal Title

Diabetes Care

Author(s)

Norris, Shane A.
Osmond, Clive
Gigante, Denise
Kuzawa, Christopher W.
Ramirez-Zea, Manuel
Richter, Linda M.
Stein, Aryeh D.
Tandon, Nikhil
Fall, Caroline H. D.
COHORTS group