Table 1.
Study | RS2/RS2 | RS1/RS1 | RS2/RS1 | Pa | Mb | RS1 Effect Group | Effect Estimate (g) | 95% CI (g) | p value |
---|---|---|---|---|---|---|---|---|---|
Moore | 193 | 4 | 66 | 22 | 24 | 28 | 122 | −43–286 | 0.15 |
UCL-FGS | 292 | 5 | 88 | 20 | 11 | 16 | 68 | −196–332 | 0.61 |
ALSPAC | 6,649 | 128 | 2,008 | 465 | 51 | 179 | 88 | 6–170 | 0.03∗ |
Combinedc | 7,134 | 137 | 2,162 | 507 | 86 | 223 | 93 | 22–163 | 0.01∗ |
The RS1 effect group consists of babies with maternally inherited RS1. RS1/RS2 heterozygous babies with heterozygous parents are uninformative for the parental origin of RS1 and were therefore removed from the analysis. All effect estimates (g) have been adjusted for the following covariates: gender, parity, maternal weight, gestational age, maternal smoking, diabetes, and hypertension. The observed genotype frequency had no evidence of deviation from the Hardy-Weinberg equilibrium. Asterisks represent p < 0.05. Three further alleles with different numbers of repeats were identified at the PHLDA2 RS locus in an extremely small number of individuals (n = 25) from the ALSPAC cohort and were thus excluded from the statistical analysis.
The number of heterozygous babies with paternally inherited RS1.
The number of heterozygous babies with maternally inherited RS1.
The meta-analysis of all three cohorts.