Long postmenopausal lifespans distinguish humans from all other primates. This pattern may have evolved with mother-child food sharing, a practice that allowed aging females to enhance their daughters' fertility, thereby increasing selection against senescence. Combined with Charnov's dimensionless assembly rules for mammalian life histories, this hypothesis also accounts for our late maturity, small size at weaning, and high fertility. It has implications for past human habitat choice and social organization and for ideas about the importance of extended learning and paternal provisioning in human evolution.

Extended provisioning of offspring and long postmenopausal life spans are characteristic of all modem humans but no other pri mates. These traits may have evolved in tandem. Analysis of rela tionships between women's time allocation and children's nutri tional welfare among the Hadza of northern Tanzania yields results consistent with this proposition. Implications for current thought about the evolution of hominid food sharing, life his tory, and social organization are discussed. k r i s t e n h a w k e s is Professor of Anthropology at the University of Utah (Salt Lake City, Utah 84112, U.S.A.). She earned a B.S. from Iowa State University (1968) and a Master's (1970) and Ph.D. (1976) from the University of Washington and has done ex tended fieldwork with the Binumarien of the eastern highlands of Papua New Guinea, the Ache of eastern Paraguay, and the Hadza of northern Tanzania. Her recent publications include "Why Hunter-Gatherers Work: An Ancient Version of the Prob lem of Public Goods" (c u r r e n t a n t h r o p o l o g y 34:341-61), "For aging Differences between Men and Women: Behavioral Ecology of the Sexual Division of Labor," in Power, Sex, and Tradition, edited by S. Shennan and J. Steele (London: Routledge, 1996), and (with J. F. O'Connell and L. Rogers) "The Behavioral Ecology of Modern Hunter-Gatherers and Human Evolution" [Trends in Ecology and Evolution 12:29-32). j a m e s f. o ' c o n n e l l is Professor of Anthropology at the Univer sity of Utah. Bom in 1943, he was educated at the University of 1. This work was supported by the National Science Foundation, the Swan Fund, B. Bancroft, the University of Utah, and the Uni versity of California at Los Angeles. We thank Utafiti (Tanzanian National Research Council) for permission to pursue fieldwork, C. Kamazora for guidance, D. Bygott and J. Hanby for continued vital assistance, and the Hadza themselves for tolerance, advice, and support. K. Heath, J. Coltrain, K. Lupo, L. Travis, and B. Clark con tributed many hours to coding field notes; T. Schurtz provided pa tient data management; D. Huth gave us statistical advice. U. Hanly prepared the figure and provided important editorial assis tance. R. Bliege Bird, K. Hill, E. Cashdan, and A. Rogers offered in structive criticism of an earlier draft. California, Berkeley (Ph.D., 1971). He has been a research fellow in prehistory at the Research School of Pacific Studies, Austra lian National University. His research interests are prehistoric and modem hunter-gatherers and evolutionary ecology, and his publications include "Ethnoarchaeology Needs a General Theory of Behavior" (Journal of Archaeological Research 3:205-55) and (with F. J. Allen) the edited volume Transitions: Pleistocene to Holocene in Australia and Papua New Guinea (Antiquity 269). N i c h o l a s g. b l u r t o n j o n e s is Professor in the Departments of Anthropology, Education, and Psychiatry at the University of California, Los Angeles. He received his D.Phil. in zoology from Oxford University in 1964, and his research interest...

SummaryHuman monogenic pain syndromes have provided important insights into the molecular mechanisms that underlie normal and pathological pain states. We describe an autosomal-dominant familial episodic pain syndrome characterized by episodes of debilitating upper body pain, triggered by fasting and physical stress. Linkage and haplotype analysis mapped this phenotype to a 25 cM region on chromosome 8q12–8q13. Candidate gene sequencing identified a point mutation (N855S) in the S4 transmembrane segment of TRPA1, a key sensor for environmental irritants. The mutant channel showed a normal pharmacological profile but altered biophysical properties, with a 5-fold increase in inward current on activation at normal resting potentials. Quantitative sensory testing demonstrated normal baseline sensory thresholds but an enhanced secondary hyperalgesia to punctate stimuli on treatment with mustard oil. TRPA1 antagonists inhibit the mutant channel, promising a useful therapy for this disorder. Our findings provide evidence that variation in the TRPA1 gene can alter pain perception in humans.Video Abstract

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