Very interesting results. If true, it implies the existence of a mechanism of selection for certain imprinted genes in gametes or in early embryo that links sex-ratio bias to reproductive success (and likely gametic selection again) in subsequent generations. The data suggest that imprinted paternal contribution might be the driver. It was proposed some 22 years ago by Westoby and Haig (see http://www.sciencedirect.... for a review) that the paternal genomic contribution, when it dominates over the maternal contribution, tends to produce larger (more vigorous) embryos. Maternal imprinting usually suppresses these genes on the paternal genome, so as to reduce the embryo size (otherwise it competes against the maternal resources). Recent work links some of these imprinted loci to insulin-like-receptors and related processes, suggesting a metabolic link. Perhaps in those families with high male-to-female ratios the paternal contribution escapes the maternal suppression, and thus produce larger embryos and therefore more vigorous children, whose metabolic advantage in early life might translate to a higher reproductive success in later life. This makes me wonder whether human pedigrees with large sex-bias might show correlation (negative or positive) with diseases such as diabetes, and if true, whether a correction factor could be devised for better accuracy in GWAS studies for metabolic disorders where information on family pedigree for sex exists. There are other implications: which genes are involved in gametic selection in F1 in pedigrees with consistently high sex-ratio distortions, etc.