It is refreshing to see more nuanced approaches to how life-history models can be applied to humans. Ellis, Reid, and Kramer compose an intricate 2-tier model to better understand the global variation we see in sexual maturation and reproductive timings and how they are linked to extrinsic mortality rates. It might also be helpful to think about this in relation to food environments rather than by “types” of society (small-scale, industrialised, etc.), which assumes that mortality rates and food security are constant within each context. In small-scale societies, local extrinsic mortality rates change over time, and food security changes with the season or due to natural fluctuations. In industrialised countries, mortality rates and food availability vary by socioeconomic strata. Focusing on changing food environments produces a simpler explanation for thinking about how local mortality rates affect puberty, growth, and fertility.

In wealthy countries, children who live in poverty often inhabit obesogenic environments with an overabundance of highly calorific, ultra-processed foods that are low on nutritional value (Cetateanu & Jones, Reference Cetateanu and Jones2014; Giskes et al., Reference Giskes, van Lenthe, Avendano-Pabon and Brug2011; Lee et al., Reference Lee, Cardel, Donahoo, Feingold, Ahmed, Anawalt, Blackman, Boyce, Chrousos, Corpas, de Herder, Dhatariya, Dungan, Hofland, Kalra, Kaltsas, Kapoor, Koch, Kopp, Korbonits, Kovacs, Kuohung and Wilson2000; Ulijaszek, Reference Ulijaszek2024). This promotes the production of adipose tissue and early pubertal maturity, especially for girls (Sheppard et al., Reference Sheppard, Garcia and Sear2015). In contrast, girls in wealthier neighbourhoods eat more nutrient-rich high-fibre diets, which promote skeletal growth and later pubertal maturity, as characterised by the growth-reproduction life-history trade-off. In small-scale societies that inhabit environments that are closer to what we imagine our evolutionary past to have been like, food would be of relatively higher nutritional value but less abundant than what we see in contemporary high-income countries. Access to nutritious food is expected to promote skeletal growth and slower pubertal development, but at the same time, those groups who struggle to get enough food at all will slow bone growth and pubertal development due to the adaptive strategy to simply stay alive, i.e. the trade-off between survival and growth/maintenance. This is why, overall, age at puberty is later, on average, in resource-stressed settings compared to in high-income countries, but the variation observed within each setting can be explained by differential types of nutrition (Sheppard & Van Winkle, Reference Sheppard and Van Winkle2020; Stearns & Rodrigues, Reference Stearns and Rodrigues2020). “Energetics” is therefore too simple a term; what matters is the type of energy – simply calorific or high nutritional quality – leading to either adiposity or skeletal growth. Table 1 summarises this argument.

Table 1.

Expected responses to mortality in different food environments

Among disadvantaged populations in wealthy countries, the life-history prediction is that higher extrinsic mortality rates, characteristic of deprived neighbourhoods, promote faster sexual maturity and higher fertility, with the mechanism being access to high-calorie, low-nutrition food. In high-income countries, there is a suite of related risks that come with poverty; father absence, higher crime rates, substance abuse, etc. (Pepper & Nettle, Reference Pepper and Nettle2014, Reference Pepper and Nettle2017; Sheppard et al., Reference Sheppard, Pearce and Sear2016) that all contribute to increased perceived extrinsic mortality risk, which is associated with early sexual maturation and higher birth rates. These stressors are embodied via various hormonal reactions such as elevated cortisol and reduced androgens, which affect the rate of development (albeit differently for boys and girls) (Sheppard et al., Reference Sheppard, Garcia and Sear2015). The point is that this is allowed to happen because the food is there, if it weren’t – if these neighbourhoods were food barren like in some very harsh ancestral conditions – puberty would be later in favour of survival.

Thinking about our evolutionary past, when subjected to high rates of ambient extrinsic mortality, we would still expect to see faster maturation and more births (not necessarily surviving), but only if there is enough food to do so; if there is insufficient food, it is better to prioritise survival. If mortality is high and food is plentiful, then everything speeds up to offset the risk of dying (Chisholm, Reference Chisholm1993; Stearns et al., Reference Stearns, Ackermann, Doebeli and Kaiser2000). When mortality is low and food is scarce, things slow down, and when mortality is low and food is plentiful, then things are neither fast nor slow because trade-offs are strongest when conditions are harsh.

While the 2-tiered model offers a valuable synthesis of how mortality and energetics influence development and fertility, its core insights may appear more novel than they are. Researchers working in this space generally recognise that energetics and mortality exposure are context-dependent and interact in complex ways. What this model does well is highlight the need to disentangle different pathways, but it may also overcomplicate what can be more parsimoniously understood by situating mortality cues within their nutritional setting rather than by population type.