I argue that the two-tier model represents a clear step forward, resolving debates and disentangling complexity in our understanding of human life history strategies. I relate the model to findings from my previous work, as well as to embodied capital and market integration, providing relevant schematics. I then discuss the timing of exposure to mortality cues and the age of the deceased, discussing what the two-tier model does and does not add to these debates.

The relationship between local extrinsic mortality rates and the timing of life-history milestones can be better understood when examined through food environments rather than by population “types,” like small-scale societies or high-income countries. By mapping observed life-history variation onto food environments, which mediate the fundamental relationship between mortality and fertility, the explanatory value of a 2-tiered model becomes less compelling.

Ellis, Reid, and Kramer advance a two-tier model of extrinsic mortality and life history strategies, emphasizing that extrinsic mortality can promote higher reproduction. The article implies this second tier operates via conscious, volitional processes. I present evidence that extrinsic mortality events are not merely environmental cues but also bereavement-inducing events that can define histories principally by disrupting, not facilitating, life strategies.

The two-tiered model proposed by Ellis et al. offers a compelling framework for understanding how extrinsic mortality (EM) sources shape life history strategies, including fertility. This commentary evaluates this model in light of modern fertility trends, identifies gaps in its current formulation, and proposes modifications to enhance its explanatory power in modern contexts.

In this commentary, I highlight the challenge of incorporating the harshness–unpredictability framework into the two-tiered model. While the effects of energetic stress (first tier), which are mostly mediated through biological pathways, can be decomposed into harsh (high mean) and unpredictable (high variance) components, ambient cues to EM (second tier) blur this distinction because they often share the same psychological mediators.

Life history strategies are linked to reproduction. Fast life history strategies place a particular burden on women biologically, socially, and politically. From the point of view of women’s rights and gender equality, slower life history strategies are the more optimal solution. In the article, I show how feminism has an important role to play in slowing down life history strategies.

While I applaud the effort that went into their article, I believe Ellis and colleagues’ two-tiered theory of life history has three problems: (1) relying on a straw man argument; (2) limitations in their data; and (3) alternate theoretical explanations for their correlations. Failure to attend to these issues resulted in a more confident presentation of their conclusions than is warranted.

The two-tiered life history model remains inadequate in addressing how social factors (particularly cultural norms and religious beliefs) interact with biological determinants to shape life history strategies. This limitation significantly constrains the model’s explanatory power when applied to certain historical demographic phenomena. We recommend introducing a third explanatory framework (the cultural-institutional tier) to augment the two-tiered model.

The two-tiered life history (LH) model proposes that different sources of extrinsic mortality (EM) have opposing effects that regulate development toward both slower and faster LH traits. Although the 53 commentators generally endorsed the two-tiered model and empirical conclusions of the target article, the devil is in the details. Some commentators challenged model assumptions (e.g., the mechanistic basis of the two-tiered model; whether the model is genetically confounded; the relative importance of child versus adult mortality). Other commentators proposed extensions/modifications of model concepts and hypotheses (e.g., incorporating density-dependent regulation; use of formal models to generate and test hypotheses; connection to the internal predictive adaptive response [PAR] model). In this reply, we review and address these challenges and proposed extensions/modifications. We hope that this iterative process advances our understanding of the complexity of EM, its opposing tiers, and their dualistic effects–both hierarchical and countervailing–on variation in human life histories.