Cryosat-2-specific errors are equivalent to more than 50% of the sea surface height variability over 40% of the oceans.
Height was closely correlated with serum IGF1 (P = 6 × 10−15), so that the variability of circulating IGF1 accounts for 27% of height variability in the current cohort.
Heritability of height, defined as the portion of height variability due to genetic factors, was estimated at around 80% (Macgregor et al., 2006; Visscher, 2008; Visscher et al., 2008) while the tens of specific single nucleotide polymorphisms (SNPs) identified by large-scale GWASs account for only 10% of the heritability (Gudbjartsson et al., 2008; Lettre et al., 2008; Weedon et al., 2008).
Many questions are left unanswered by the present study, including the epigenetic participation of the P2 promoter to the 'missing heritability/causality' of human height variability [ 68, 69] and to the phenotypic plasticity of growth physiology [ 70].
Genetics thus seems to explain a major but limited part of height variability across individuals.
After merging the two cohorts, the inverse correlation with height was confirmed for 6/8 CGs of the P2 promoter and was maximal for CG-137 methylation (P = 4 × 10−7), so that CG-137 methylation accounted for 13% of height variability.
This factor had no strong loadings, but is associated with shrub density, canopy height variability and tree density, all of which also affect ground cover, and can be considered macrohabitat variables.
When the heights of these sites that have been corrected for the effects of non-tidal atmospheric and ocean loading are adjusted by the hydrological loading deformation, more than one third of the root-mean-square (RMS) values of the GPS height variability become larger.
Any diurnal pattern of intervertebral disc height variability would have once again introduced non-differential misclassification into the study, reducing the chances of finding statistically significant results.
