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ijpo69-sup-0001-suppl.doc34KTable S1. Number of missing body mass index (BMI) data at each assessment.
ijpo69-sup-0001-suppl.doc34KSection S1. The number of participants providing information about weight and height by telephone interview at age 19 years was n = 27 (8.8 %). A re-analysis at age 19 years was carried out with the reduced sample of which data about weight and height had been assessed objectively. Significant group differences supported the demonstrated effect of neuropeptide Y (NPY) rs16147 on BMI [C homozygotes vs. T allele carriers F {1, 276} = 5.01; P = 0.026].
ijpo69-sup-0001-suppl.doc34KSection S2. In total, 22 data points in 21 subjects were unavailable. Table S1 depicts the number of replaced data points at the different assessments. A repeated-measures analysis of covariance (ANCOVA) was carried out, including only those subjects with a complete data history to determine the effects of genotype and genotype by age interaction on variation in BMI. The significant main effect of NPY genotype [F {1, 282} = 4.73; P < 0.031], age [F {6, 1692} = 65.54; P < 0.001] and the interaction thereof [F {6, 1692} = 3.04; P < 0.042] was confirmed in the reduced sample of n = 285 participants.
ijpo69-sup-0001-suppl.doc34KSection S3. Additional analyses were conducted to explore the genotype effect on weight at different ages. In parallel to the results for BMI, post hoc comparisons showed that genotype effects on weight were significant in older age groups (15 years [F {1, 303} = 5.75; P = 0.017] and 19 years [F {1, 303} = 4.92; P = 0.027]). In addition, a significant group difference emerged at the age of 8 years [F {1, 303} = 4.22; P = 0.041], while there was no such effect in the younger age groups (3 months [F {1, 303} = 1.62; P = 0.205], 2 years [F {1, 303} = 3.56; P = 0.060], 4.5 years [F {1, 303} = 1.20; P = 0.274]), (see Fig. 1). However, differences according to NPY genotype failed to reach statistical significance at age 11 years [F {1, 303 = 1.70; P = 0.193].

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