Ellis et al. discuss two pathways through which extrinsic mortality may shape life history strategies, particularly those relating to reproduction. First, a direct biological pathway in which energetic constraints slow down sexual reproduction by delaying pubertal maturation and lowering fertility (the energetics hypothesis). Second, an indirect psychosocial pathway in which – once basic energetic conditions have been met – exposure to heightened mortality can accelerate the pace of reproduction and increase the total number of offspring (the developmental hypothesis). They propose a two-tiered model to integrate the two hypotheses into a single framework and demonstrate that these countervailing effects can result in seemingly contradictory life history strategies, such as delayed puberty and higher achieved fertility. The two-tiered model appears to be supported by evidence from various social and historical contexts, including pre- and post-demographic transition societies, as well as studies employing both macro- and micro-level data.

Importantly, this novel framework departs from standard evolutionary accounts by highlighting the role of psychosocial mechanisms in shaping life history outcomes. This insight is particularly relevant for high-resource settings, in which, as the authors astutely remark, energetic constraints have little to no impact even among socially disadvantaged individuals. It also conforms with economist Robert Fogel’s theory of technophysio evolution, which posits that technological advances in food production since the industrial revolution have led to “a form of human evolution that is biological but not genetic, rapid, culturally transmitted, and not necessarily stable” (Fogel & Costa, Reference Fogel and Costa1997, p. 49). In such contexts, psychosocial pathways take precedence over energetic constraints.

One underexplored extension of the two-tiered model is its relevance to socially structured mortality risks. Social stratification produces stark differences in mortality outcomes within populations, even among the most egalitarian welfare states (Mackenbach, Reference Mackenbach2012; Marmot, Reference Marmot2003). Furthermore, mortality inequalities manifest across a wide range of social dimensions, including income, wealth, and occupational class (Torssander & Erikson, Reference Torssander and Erikson2010; van Raalte, Sasson, & Martikainen, Reference van Raalte, Sasson and Martikainen2018). Their relevance for life history strategies rests on three outstanding issues. First, can social inequalities be regarded as sources of extrinsic mortality? Second, what is the specific mechanism through which they lead to systematic differences in life history strategies? Third, are they relevant for other life history outcomes, beyond sexual reproduction?

Extrinsic mortality refers to mortality risks that cannot be attenuated by individual behavior. In spite of tremendous improvements in global health since the industrial revolution, social disparities in health and mortality persist and have even increased in many low-mortality countries (Mackenbach et al., Reference Mackenbach, Kulhánová, Menvielle, Bopp, Borrell, Costa, Deboosere, Esnaola, Kalediene, Kovacs, Leinsalu, Martikainen, Regidor, Rodriguez-Sanz, Strand, Hoffmann, Eikemo, Östergren and Lundberg2015). One of the key sociological insights of our time is that these seemingly disparate phenomena are in fact deeply interrelated (Freese & Lutfey, Reference Freese, Lutfey, Pescosolido, Martin, McLeod and Rogers2011; Link & Phelan, Reference Link and Phelan1995). As our social and technological capacity to control health and disease increases, social conditions become more, not less, important for health and longevity. It is precisely because access to health-preserving technologies, information, and beneficial social ties is contingent upon individuals’ social standing. Debates about the role of social structure versus agency in determining health outcomes notwithstanding, there is ample evidence to suggest that social gradients in mortality cannot be fully mitigated by behavioral change (Cutler & Lleras-Muney, Reference Cutler and Lleras-Muney2010; Nettle, Reference Nettle2010). Thus, from the standpoint of the individual, social inequalities can indeed be regarded as a source of extrinsic mortality.

Moreover, social inequalities in mortality may function as ambient cues for heightened mortality risk through direct observation of death among close social contacts. Demographers have long hypothesized that individuals become aware of their demographic environment, including the risk of mortality, through social learning (Montgomery, Reference Montgomery2000). Much like mortality risk, kinship and other social ties are patterned along class and ethnic divisions (McPherson, Smith-Lovin, & Cook, Reference McPherson, Smith-Lovin and Cook2001). As a result, there are substantial differences between individuals and social groups in their exposure to bereavement across the life course – for example, experiencing the loss of parents during childhood or the cumulative loss of family members by midlife (Donnelly et al., Reference Donnelly, Garcia, Cha, Hummer and Umberson2023; Umberson et al., Reference Umberson, Olson, Crosnoe, Liu, Pudrovska and Donnelly2017). Social disparities in exposure to bereavement may, in turn, impact life history outcomes via the second tier of psychosocial effects.

Lastly, if extrinsic mortality is communicated to the individual via exposure to loss of family members and friends, it may carry implications far beyond decisions relating to reproductive success. Exposure to bereavement shapes how individuals feel, think, and act (Sasson, Reference Sasson2025). It is closely tied to psychological distress and well-being (Auster et al., Reference Auster, Moutier, Lanouette and Zisook2008; Carr, Reference Carr2004; Sasson & Umberson, Reference Sasson and Umberson2014; Stroebe et al., Reference Stroebe, Schut and Stroebe2007), to how long individuals expect to live (Dormont et al., Reference Dormont, Samson, Fleurbaey, Luchini and Schokkaert2018; Hurd & McGarry, Reference Hurd and McGarry2002), and to a variety of resource-allocation decisions throughout the life course. These include investments in human capital, saving and spending behavior, retirement from the labor force, pension and social security claims, and intergenerational transfers (Foltyn & Olsson, Reference Foltyn and Olsson2024; Heimer et al., Reference Heimer, Myrseth and Schoenle2019; Hurd, Smith, & Zissimopoulos, Reference Hurd, Smith and Zissimopoulos2004; Post & Hanewald, Reference Post and Hanewald2013; van Solinge & Henkens, Reference van Solinge and Henkens2010).

In contexts in which exposure to child and young adult mortality is common, for example, as a result of community violence or armed conflict (Aburto et al., Reference Aburto, Di Lego, Riffe, Kashyap, Van Raalte and Torrisi2023; Alburez-Gutierrez, Reference Alburez-Gutierrez2022; Svallfors, Reference Svallfors2024), these effects may manifest relatively early in the life course – including reproductive outcomes. In low-mortality contexts, effects may appear only later in life, though some variation between social groups is expected, depending on the magnitude of social inequalities in mortality. In either case, the second tier of psychosocial effects of extrinsic mortality on life history outcomes warrants further attention.

In sum, the two-tiered model offers a compelling integration of biological and psychosocial pathways through which extrinsic mortality influences life history strategies. This framework not only accounts for paradoxical reproductive patterns but also opens new avenues for understanding how ambient mortality cues shape behavior across the life course. A key implication of this framework relates to the role of social inequalities as ambient cues for heightened mortality, particularly through lifelong exposure to bereavement, and how such inequalities may give rise to different life history strategies and outcomes.