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To address claims of human exceptionalism, we determine where humans fit within the greater mammalian distribution of reproductive inequality. We show that humans exhibit lower reproductive skew (i.e., inequality in the number of surviving offspring) among males and smaller sex differences in reproductive skew than most other mammals, while nevertheless falling within the mammalian range. Additionally, female reproductive skew is higher in polygynous human populations than in polygynous nonhumans mammals on average. This patterning of skew can be attributed in part to the prevalence of monogamy in humans compared to the predominance of polygyny in nonhuman mammals, to the limited degree of polygyny in the human societies that practice it, and to the importance of unequally held rival resources to women's fitness. The muted reproductive inequality observed in humans appears to be linked to several unusual characteristics of our species-including high levels of cooperation among males, high dependence on unequally held rival resources, complementarities between maternal and paternal investment, as well as social and legal institutions that enforce monogamous norms.

Cleft lip with or without cleft palate (CL +/- P) is of high prevalence in an isolated, inbred indigenous population of the Venezuelan rain forest: 12 contemporary probands are known in a population of 1200. CL +/- P is familial in this population. One kindred contains four affected siblings and a total of eight probands. The mode of transmission of CL +/- P is under investigation through the collection and biological verification of genealogies and through screening for selected sequence-based polymorphisms. Polymerase chain reaction (PCR) assays were successfully applied to recover DNA from blood dried onto filter paper in the field. Eleven samples from probands and their first-degree relatives have been analyzed for DNA sequence-based polymorphisms for TGF-A and HOX7. No significant linkages for either locus were found. Evaluation of the distribution of probands in four genealogies indicates that CL +/- P could be transmitted as an autosomal recessive trait in this population. We believe this is the first report of this mode of transmission for nonsyndromic CL +/- P.