“…Most saliently, a paper published earlier this year integrated a great deal of research on social epistasis, i.e., interorganismal gene-gene interactions, and mutation load in humans, mice, and other organisms to develop the novel thesis that the fitness costs of the accumulation of certain kinds of deleterious mutations under conditions of relaxed negative selection in humans are externalized onto noncarrier individuals and thereby amplified via the damage that these mutations do to populations’ “group-level extended phenotype[s]” (Woodley of Menie et al, 2017). This theory, which was termed the social epistasis amplification model, is based partly on the biological literature concerning eusocial insects, in which the term “social epistasis” was coined (e.g., Linksvayer, 2007).…”