Table 1. Clinical parameters of the study population stratified by genotypes.

		Genotype		Recessive model *	Additive model ¤
FSHB -211G>T	GG	GT	TT	GG+GT vs. TT	GG vs. GT vs. TT
n	650	290	22
Age (years)	10.8 (9.6–12.1)	10.8 (9.5–12.0)	11.1 (10.1–12.1)	p = 0.346	p = 0.416
BMI (kg/m2)	17.3 (15.0–19.8)	17.3 (15.0–19.9)	17.6 (15.8–19.6)	p = 0.560	p = 0.816
Age at pubertal onset	10.0 (9.8–10.1)	10.1 (9.8–10.3)	10.7 (10.5–10.9)	p = 0.246	p = 0.437
FSHR -29G>A	GG	GA	AA	GG+GA vs. AA	GG vs. GA vs. AA
n	512	368	74
Age (years)	10.8 (9.6–12.1)	10.8 (9.6–12.1)	10.8 (9.6–12.1)	p = 0.736	p = 0.898
BMI (kg/m2)	17.2 (15.1–19.5)	17.5 (15.1–20.2)	17.2 (14.7–20.0)	p = 0.660	p = 0.133
Age at pubertal onset (years)	10.0 (9.8–10.1)	10.0 (9.8–10.2)	10.6 (10.2–11.0)	p = 0.003	p = 0.031
FSHR 2039A>G	AA	AG	GG	AA+AG vs. GG	AA vs. AG vs. GG
n	242	504	218
Age (years)	10.8 (9.6–12.1)	10.8 (9.6–12.0)	10.9 (9.6–12.1)	p = 0.715	p = 0.443
BMI (kg/m2)	17.4 (15.0–20.3)	17.2 (15.1–19.7)	17.3 (15.2–19.7)	p = 0.960	p = 0.816
Age at pubertal onset	10.0 (9.7–10.2)	10.0 (9.9–10.2)	10.1 (9.8–10.3)	p = 0.527	p = 0.579

Age: mean (+/− SD), BMI: geometric mean (+/− SD), Age at pubertal onset: mean (95% CI).

In the recessive model, strong effects are expected only in minor allele homozygotes. These are compared with pooled wild-type and heterozygotes (e.g. FSHR -29GG+GA vs. AA).

Differences in ages and BMI levels between genotypes were assessed with independent samples t-test.

Differences in ages at pubertal onset between genotypes were assessed with probit analysis (categorical variable).

The additive model assumes a codominant effect of alleles in which the heterozygotes should exhibit intermediate levels; regressions are calculated over, for example, FSHR -29GG vs. GA vs. AA.

Differences in ages and BMI levels between genotypes were evaluated with One-way ANOVA.

Differences in ages at pubertal onset between genotypes were assessed with probit analysis (continuous variable).