We estimated the GRM for the X-chromosome and parameterized it under three assumptions of dosage compensation10: 1) equal X-linked variance for males and females; 2) no dosage compensation i.e. both X-chromosomes are active for females; 3) full dosage compensation i.e. one of the X-chromosomes is completely inactive for females. We fitted the parameterized GRMs for the X-chromosome in an MLM whilst simultaneously estimating hG2 in the model to capture the genetic variation on the autosomes and variation due to possible population structure. For all the traits, the full-dosage compensation model fits the data best and the no-dosage compensation model is the worst with the equal-variance model in between (Supplementary Table 5). However, the differences in estimates are relatively small and none of them is statistically significant. Larger datasets will be required to distinguish such small differences. Under the assumption of full dosage compensation, the variance attributable to the X-chromosome for females was 0.61% (s.e. = 0.32%), 0.82% (s.e. = 0.35%), 0.57% (s.e. = 0.52%) and 0.0% (s.e. = 0.48%) for height, BMI, vWF and QTi, respectively. To verify that we
