Genome-wide association (GWA) studies have identi[[Unable to Display Character: &#64257;]]ed nearly 50 common variants for obesity, many of which influence body mass index (BMI), a common proxy for obesity assessed in large epidemiological studies. The associations of these variants with change in BMI across the life course are not well understood, but are of particular interest during the transition from adolescence to young adulthood, a high risk period for weight gain. The current study assessed the association of 41 established obesity SNPs with change in BMI during the period between adolescence and young adulthood in an ethnically diverse, nationally representative cohort, the National Longitudinal Study of Adolescent Health, followed for 13 years. Race/ethnicity-stratified linear mixed models accounted for sampling design, family relatedness, and repeated measures of BMI. Models included a SNP-by-year interaction term and adjusted for sex, age at baseline, current smoking, and geographic region. Analyses included 6383 European American (EA), 2252 African American (AA) and 1700 Hispanic American (HA) participants with measurements from 1996 (ages 12-21 y) to 2008 (ages 24-34 y), with an average of 2.6 observations per individual. For analyses in AA we excluded SNPs (n=14) that failed to capture signal of functional variant in a recent African American population genome-wide association study (Monda et al 2012). Average BMI gain over the 13-year period was 4.9 (SD=5.0) kg/m 2 , with higher increases in AA 5.8 (SD=5.7) kg/m 2 and HA 5.5 (SD=5.6) kg/m 2 . Model results for the 41 SNPs in EA and HA and 27 SNPs in AA suggest that SNP by year interactions show nominal significance (p<0.05) for 12 SNPs in EA, 2 SNPs in HA and 1 SNP in AA. After correction for multiple testing (n=41 tests, p<0.0012), 1 SNP remained significant for EA (rs2287019, near QPCTL ) and none in AA or HA. Each effect allele for rs2287019 contributed an increase of 0.030(SE=0.009) kg/m 2 per year to BMI in EA. These findings suggest that the locus near QPCTL and possibly other obesity loci play a role in the trajectory of BMI across the period from adolescence to young adulthood, a period with high risk for subsequent adult obesity. These findings may help inform the biological processes that influence weight gain at this vulnerable period of the life cycle and may provide information that is useful for the design of effective interventions to prevent weight gain.