A more pointed argument against the infinitesimal nature of effects is that it predicts less granularity in the distribution of risk and phenotypic trait variation than is often observed, though I am not aware of a quantitative assessment of this claim. In the infinitesimal model, disease risk ought to blend smoothly when unrelated people have children. The larger the number of alleles affecting a trait, the lower the among-individual variance should be under random mating since most individuals will share similar numbers of risk alleles. However, disease incidence and complex phenotypes generally cluster in families. A possible resolution of this conundrum is that the observed clustering of disease in families could be explained by stochastic variation in the number of susceptibility alleles: if two people happen to have more than the average number of small variants, so will their children. Furthermore, homophily, the tendency for couples to pair on the basis of shared attributes (including sub-clinical disease indicators), will tend to enrich for variants that promote those attributes104. Granularity of traits is difficult to document, but facial features provide a
