We commend the authors on the substantial body of evidence they present supporting the application of hierarchical response models to our understanding of the facultative adjustment of development and reproduction to the environment. Throughout, they appropriately highlight the value of the energetic model (corresponding to their Tier 1) of life history. Low energetic resource availability (e.g., poverty, malnutrition) consistently delays menarche (Tanner, Reference Tanner1962), and it makes good evolutionary sense in such an environment that resources will be accumulated slowly, growth will be slow, and maturation delayed (Ellison, Reference Ellison1990). Hierarchical response models bring an additional layer to this perspective incorporating the impact of the social environment, associated with local mortality on reproductive development and timing (e.g., Coall & Chisholm, Reference Coall and Chisholm2003; Nettle & Bateson, Reference Nettle and Bateson2015; Walker et al., Reference Walker, Gurven, Hill, Migliano, Chagnon and De Souza2006). Here, the mortality or social perception of that mortality corresponds to Tier 2 in E, R, and K’s model.

Consistent with E, R, and K, Coall and Chisholm’s (Reference Coall and Chisholm2003) model proposed a hierarchical relationship between energy availability and the mortality-related psychosocial resource availability, such that energy availability may moderate the influence of early mortality on reproductive development and timing. Women who lack the energy and nutrients to support pregnancy and lactation do not reproduce – early or late. Hence, the delayed reproduction to accumulate resources. However, women with at least adequate energy and nutrients – who also face sufficient social risk and uncertainty – do reproduce early. Without energy above a certain threshold (Frisch, Reference Frisch1988), it does not matter what else is present in the environment, as it will not influence reproduction. Thus, the metabolic demands of survival and pregnancy and lactation thus take precedence over psychosocial influences related to mortality perception on age at menarche. The metabolic and immune system consequences of good health and nutrition seem to act as bioassays (Ellison, Reference Ellison1990), indicating the probable availability of material resources for gestation and lactation. By analogy, Chisholm (Reference Chisholm1999) referred to the endocrine consequences of the psychosocial stress produced by high local mortality rates as a socioassay. He argued that reproducing as early and often as energetics allow (maximizing current reproduction) may guard against lineage extinction in high-mortality environments. Therefore, within this response hierarchy, age at menarche (fecundity) and ultimately reproduction (fertility) are influenced (within their reaction norm), first by health and nutrition, and then by the psychosocial environment (Coall & Chisholm, Reference Coall and Chisholm2003; Sear, Sheppard, & Coall, Reference Sear, Sheppard and Coall2019; Surbey, Reference Surbey1998).

This hierarchical model makes clear the need to collect empirical evidence across a range of different societies, including those where resources are scarce and those where resources are abundant. E, R, and K suggest that “various researchers have criticized using data from wealthy industrialized countries to test evolutionary hypotheses” [p4]. We read these researchers as criticizing research that has only used data from wealthy industrialized countries to test evolutionary hypotheses. Industrialized countries can provide very useful data for testing evolutionary hypotheses (Stulp, Sear, & Barrett, Reference Stulp, Sear and Barrett2016), but applying conclusions drawn from studying such countries to all of humanity is likely to lead to highly misleading conclusions (Sear et al Reference Sear, Sheppard and Coall2019). A very clear example of this problem is the widespread belief in the human evolutionary behavioral sciences, as described in the E, R, and K’s opening para, that higher extrinsic mortality (EM) risk (inevitably) leads to “faster life history strategies.” The cross-cultural survey of empirical evidence presented by E, R, and K, building on the hierarchical model, is therefore highly valuable, and we hope it will have a lasting positive impact on moving this literature away from this overly simplistic belief.

A crucial element that E, R, and K’s model raises is how the local mortality rate, which reflects the threat to survival in the local environment (risk), could influence development and reproduction (physiology and psychology; Rickard, Frankenhuis, & Nettle, Reference Rickard, Frankenhuis and Nettle2014). Some researchers investigating this question propose that these are two separate pathways through which the environment impacts facultative adjustments of the life cycle to the local environment (Nettle & Bateson, Reference Nettle and Bateson2015). The external mortality pathway provides information to the organism based on the current and, thus, likely future environments. The internal physiological pathway receives its information from the physiology; this is where the environment makes a persistent change to the somatic (body) state of the organism (Nettle & Bateson, Reference Nettle and Bateson2015). These may be usefully thought about as Predictive Adaptive Responses (PARs) where the environmental risk (external PAR; Tier 2) and how the risk is embodied physiologically (internal PAR; Tier 1) may be separate pathways (see Borgstede & Scheunpflug, Reference Borgstede and Scheunpflug2024; Hartman,et al., Reference Hartman, Li, Nettle and Belsky2017). Here, a psychological reaction to the environment influences the allocation of resources between the biological processes of survival, growth, and reproduction. The anthropological, between-individual, literature has supported this position showing that both local mortality rates and body weight predict age at sexual maturity (e.g., Kramer & Greaves, Reference Kramer and Greaves2010; Walker et al., Reference Walker, Gurven, Hill, Migliano, Chagnon and De Souza2006).

As E, R, and K note, exactly how these mechanisms work is not yet clear; this is again where existing hierarchical models can add value. While the biological mechanisms linking resource scarcity to delayed reproduction seem relatively clear-cut and are seen across species, how EM becomes embodied as a reproductive schedule and the interaction between childhood and adult environments (Coall et al., Reference Coall, Tickner, McAllister and Sheppard2016) require considerably more research. There may be plausible physiological pathways, such as “weathering” (Geronimus et al., Reference Geronimus, Hicken, Keene and Bound2006), which may trigger earlier reproduction under conditions of psychosocial stress; other mechanisms are as yet under-explored. The consistent association between EM and fertility (Tier 2) is also reflected in the well-known negative relationship between education and fertility that also holds across and within populations (Colleran & Snopkowski, Reference Colleran and Snopkowski2018). In particular, the role of culture, and cultural transmission, in this process has received very little attention.