Reassessing the Evolution of Permanently Enlarged Human Breasts: A Critical Response to Pawłowski and Żelaźniewicz (2021)

Pawłowski and Żelaźniewicz (2021) argue that permanent female breast enlargement probably originated as a developmental by-product of selection on subcutaneous adiposity and endocrine changes, with sexual attraction arising through subsequent co-option. Their review is valuable in distinguishing present-day function from evolutionary origin and in challenging simplistic fertility-signalling accounts. Yet its comparative assessment relies on several mischaracterizations of primary evidence and on causal extrapolations that are not consistently subjected to the same evidentiary standard as competing hypotheses. Most notably, Ford and Beach's (1951) records of explicit preferences for particular breast morphologies in 13 societies are treated as evidence that breasts were sexually important in only 13 of approximately 190-191 societies. An earlier interpretation by Dettwyler (1995) makes a closely related error and further conflates recorded breast stimulation with the prevalence of sexual attraction. Other citations conflate conditional laboratory responses with general regional lipolysis, breast-cancer prognosis with incidence, human cell-line findings with chimpanzee receptor distributions, and tissue concentrations of DHEA with those of DHEAS. The proposed dietary-adrenal-neurodevelopmental-mammary sequence is biologically conceivable, but its key causal links are mechanistically underdetermined and the complete evolutionary sequence remains untested. We distinguish confirmed citation problems from defensible empirical claims, interpretive disagreements and unresolved questions. The available evidence weakens universal preferences for large breasts and strong honest-fecundity signalling accounts; it neither establishes an exclusively sexual-selection origin nor supports the comparative claim that original sexual selection is unlikely. A pluralistic model remains viable, but the order and magnitude of putative causal contributions are presently indeterminate.