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Two tiers, not one: Different sources of extrinsic mortality have opposing effects on life history traits

Published online by Cambridge University Press:  10 April 2024

Bruce J. Ellis*
Affiliation:
Departments of Psychology and Anthropology, University of Utah, Salt Lake City, UT, USA bruce.ellis@psych.utah.edu; psych.utah.edu/people/faculty/ellis-bruce.php
Brie M. Reid
Affiliation:
Department of Psychology, Department of Public Health & Health Sciences, Institute for Cognitive and Brain Health, Northeastern University, Boston, MA, USA brie_reid@brown.edu; briemreid.com
Karen L. Kramer
Affiliation:
Department of Anthropology, University of Utah, Salt Lake City, UT, USA karen.kramer@anthro.utah.edu; profiles.faculty.utah.edu/u0839608
*
Corresponding author: Bruce J. Ellis; Email: bruce.ellis@psych.utah.edu

Abstract

Guided by concepts from life history (LH) theory, a large human research literature has tested the hypothesis that exposures to extrinsic mortality (EM) promote the development of faster LH strategies (e.g., earlier/faster reproduction, higher offspring number). A competing model proposes that, because EM in the past was intimately linked to energetic constraints, such exposures specifically led to the development of slower LH strategies. We empirically address this debate by examining (1) LH variation among small-scale societies under different environmental conditions; (2) country-, regional-, and community-level correlations between ecological conditions, mortality, maturational timing, and fertility; (3) individual-level correlations between this same set of factors; and (4) natural experiments leveraging the impact of externally caused changes in mortality on LH traits. Partially supporting each model, we found that harsh conditions encompassing energetic stress and ambient cues to EM (external cues received through sensory systems) have countervailing effects on the development of LH strategies, both delaying pubertal maturation and promoting an accelerated pace of reproduction and higher offspring number. We conclude that, although energetics are fundamental to many developmental processes, providing a first tier of environmental influence, this first tier alone cannot explain these countervailing effects. An important second tier of environmental influence is afforded by ambient cues to EM. We advance a two-tiered model that delineates this second tier and its central role in regulating the development of LH strategies. Consideration of the first and second tier together is necessary to account for the observed countervailing shifts toward both slower and faster LH traits.

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© The Author(s), 2025. Published by Cambridge University Press

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