Abstract P229: Prenatal Development and Obesity: Two Distinct Pathways to Diabetes in Adulthood
Background: Adverse prenatal development, often indicated by low birthweight, is associated with elevated risk of cardiometabolic disease, but the mediating role of obesity is not well understood.
Methods: We used data from the National Longitudinal Study of Adolescent to Adult Health, a nationally representative sample of adolescents followed 14 years over 4 waves into adulthood (1994-95, 1995-96, 2001-02, 2008-09; n=14,180). In gender-stratified path analysis, we examined pathways from birth weight [BW (kg); linear (BW) and quadratic (BW2)], to latent trajectories in body mass index (BMI) from adolescence to adulthood, to prevalent diabetes or prediabetes (DM; HbA1c, diagnosis, medication) in adulthood (Figure), adjusting for sociodemographic characteristics.
Results: Direct associations between BW and DM (not through BMI) indicated that increasing BW was associated with non-significantly lower likelihood of DM in women [coeff (95% CI): BW: -0.30 (-1.23, 0.63); BW2: 0.01 (-0.14, 0.16)] and unrelated to DM in men. We identified distinct, gender-specific indirect pathways from greater BW to higher BMI and DM. In girls, the association between BW and BMI in adolescence was J-shaped, by which girls born lower and higher BW exhibited elevated BMI in adolescence [coeff (95% CI): BW: -2.10 (-3.96, -0.24); BW2: 0.44 (0.13, 0.75)]; higher BW predicted marginally faster BMI gain from adolescence to adulthood. Higher adolescent BMI and faster BMI gain was associated with diabetes in women [coeff (95% CI): BMI intercept: 0.09 (0.06, 0.12); BMI slope: 0.12 (0.08, 0.17)]. In boys, BW was not associated with BMI at adolescence or BMI gain thereafter; in turn, adolescent BMI was unrelated to diabetes, while faster BMI gain was associated with higher likelihood of adult DM [coeff (95% CI): 0.29 (0.20, 0.37)].
Conclusions: Findings suggest that in girls, slowing BMI gain prior to adolescence and from adolescence to adulthood is critical for diabetes prevention, yet may not address distinct pathology stemming from early life.
Author Disclosures: J. Boone-Heinonen: None. R.M. Sacks: None. E. Hooker: None. N.F. Dieckmann: None. C.S. Harrod: None. K.L. Thornburg: None.
- © 2017 by American Heart Association, Inc.