Parameter | N1
| Genotype | N (%) | Mean ± SD | Additive genetic model2
|
---|
| | | | | Estimate | 95% CI | p-value3
|
---|
Δ BMI-SDS4,5
| 207 | TT | 53 (26) | 0.33 ± 0.40 | -0.032 | -0.091...0.027 | 0.287 |
| | AT | 86 (41) | 0.25 ± 0.27 | | | |
| | AA | 68 (33) | 0.27 ± 0.27 | | | |
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1 total number of individuals who participated in the obesity intervention program; 2 linear regression analyses for BMI-SDS http://www.mybmi.de including covariates age and sex- including baseline BMI-SDS did not substantially alter the result; the p-value for the sex main effect was 0.740; 3 two-sided p-value; 4 median time interval between repeated measurements 12 months; positive values for descriptive statistics indicate weight reduction in units of BMI-SDS; asymptotic two-sided p-value for Kruskal-Wallis Test 0.44; 5 A trend towards a deviation from Hardy-Weinberg equilibrium was observable for genotype frequencies for Δ BMI-SDS (exact p = 0.02). This finding, however, is not surprising and expected in case of a true genetic association and indeed the number of homozygotes for the at-risk A-allele was increased in these patients compared to controls.