Ellis, Reid, and Kramer (ERK) propose a framework applied to human development to investigate how exposures to extrinsic mortality shape life history strategies. Their model is two-tiered as it integrates two hypotheses – the energetics and developmental hypotheses. ERK evaluate their model by reviewing a large empirical record on low- and middle-income countries, providing a solid basis for their conclusions: harsh environmental conditions characterized by high-mortality risk from diverse external sources, in particular energetic stress (the model’s first tier) and ambient cues to extrinsic mortality (the model’s second tier), have countervailing effects on the development of life history strategies, both delaying pubertal maturation and promoting accelerated pace of reproduction and higher offspring number. We shall comment hereafter on three salient contributions of this article.
1. Energetics, the environment, and fertility
The environmental constraints on fertility are well studied in economic demography, particularly the impact of pollution on fertility (Hirazawa, Kamada, & Sato, Reference Hirazawa, Kamada and Sato2019). In this sense, this literature is aligned with environmental science (Skakkebæk et al., Reference Skakkebæk, Lindahl-Jacobsen, Levine, Andersson, Jørgensen, Main, Lidegaard, Priskorn, Holmboe, Bräuner, Almstrup, Franca, Znaor, Kortenkamp, Hart and Juul2022). We find the energetics hypothesis much more stimulating. Surprisingly, the role of energetic constraints in explaining demographic trends has been largely overlooked in economics. While the role of energy is stressed in certain economic history works (see Wrigley (Reference Wrigley2010)) and is even central in econophysics (Georgescu-Roegen, Reference Georgescu-Roegen1986), its role in population dynamics has been seldom examined, not even in the literature on the transition from Malthusian stagnation to economic growth (Galor & Weil, Reference Galor and Weil2000). However, this line of research has become vivid in the last decade with the debate on energy poverty in low- and middle-income countries. Chang et al. (Reference Chang, Dong, He and Zhang2024) showed on Chinese data that the relationship between energy poverty and fertility intentions is far more complex, featuring the intersection of different mechanisms arising from cultural, economic (along the developmental hypothesis), and health channels: the latter two constrain fertility while the former raises it. Henceforth, the relationship between energy poverty and fertility exhibits an inverted U-shape. It would be interesting to reassess ERK’s results, focusing on multidimensional energy poverty indicators. And it is per se complex: just like in ERK, the two tiers interfere.
2. Extrinsic mortality, fertility, and development
ERK’s demonstration is all more convincing as the economic theory has long shown that what the life history theory refers as the developmental hypothesis, especially through mortality fluctuations, is central in shaping not only life history strategies but also sustained economic growth and development (Galor & Weil, Reference Galor and Weil2000; Kalemli-Ozcan, Reference Kalemli-Ozcan2002; Boucekkine, de la Croix, & Licandro, Reference Boucekkine, de la Croix and Licandro2003).
Several competing economic theories have been advanced to explain net fertility dynamics in response to mortality shocks. In considering the disciplinary intersection of ERK and our own, we believe their model (in particular the second tier acting through ambient cues to extrinsic mortality) closely aligns with the economic models assuming that the fertility transition is mostly explained by the reduction in child survival uncertainty (Kalemli-Ozcan, Reference Kalemli-Ozcan2003). They rightly argue that the insurance hypothesis is consistent with the life history model: uncertainty about child survival generates a precautionary demand for children to ensure a sufficiently large family size (Taylor, Newman, & Kelly, Reference Taylor, Newman and Kelly1976). The insurance hypothesis predicts that reductions in child mortality and morbidity will reduce total and net fertility rates (Bousmah, Reference Bousmah2017a, Reference Bousmah2017b). Nevertheless, a fundamental question remains: is the fertility response to uncertainty about child survival significant enough to substantially affect net fertility?
In this respect, theoretical findings of the endogenous fertility literature are mixed. While some models imply that both gross and net fertility are affected by child mortality (Kalemli-Ozcan, Reference Kalemli-Ozcan2003), others exhibit an effect of child mortality on total fertility only (Doepke, Reference Doepke2005; Boucekkine, Desbordes, & Latzer, Reference Boucekkine, Desbordes and Latzer2009), implying that other factors are at play to influence net fertility rates. These factors are manifold – wages (Becker, Reference Becker1981), consumption growth (Becker & Barro, Reference Becker and Barro1988), women’s relative wages (Galor & Weil, Reference Galor and Weil1996), human capital (Becker, Murphy, & Tamura, Reference Becker, Murphy and Tamura1990), technological progress (Galor & Weil, Reference Galor and Weil2000), and/or changes in gender roles (Lagerlöf, Reference Lagerlöf2003b). In this sense, ERK’s view on the interaction between mortality and fertility seems rather partial, especially as a theory of demographic transition.
3. A potential endogeneity problem… not so easy to solve
ERK consider that mortality-fertility relationships are unaffected by economic development or stage in the demographic transition, arguing that some empirical findings on the mortality-fertility link are robust to controlling for indicators of economic development (in between-country studies) or socioeconomic variables between respondents (in within-country studies). However, simply controlling for socioeconomic variables is not sufficient to test whether the association between mortality and fertility is confounded by economic development, as documented above on a sample of endogenous fertility models and inherent mortality-fertility indirect interaction schemes.
Indeed, the endogenous fertility literature refutes, to a certain extent, ERK’s claim about the exogeneity of economic development in the mortality-fertility link. Although mortality decline is central to initiating fertility decline, mortality fluctuations alone are not sufficient to trigger a fertility transition. The quantity-quality tradeoff, also mentioned by EKR, is a key mechanism inherent in endogenous fertility models (Becker & Barro, Reference Becker and Barro1988; Barro & Becker, Reference Barro and Becker1989) to depict the full transition dynamics. Accordingly, a decrease in child mortality lowers the cost of rearing surviving children in the initial generation, such that the demand for survivors increases, leading birth rates to rise in the first place. As the rate of decline in child mortality slows once it approaches zero, fertility rates fall in later generations, and parents decide to invest more in educating each child. Education is a key variable in driving the future responses to the next mortality shocks, further lowering the effective magnitude of future mortality shocks (see Lagerlöf (Reference Lagerlöf2003a) on Sweden). Even though mortality is extrinsic, its effective magnitude is endogenous, at least to a certain extent.
While we agree about the necessity of a two-tiered approach, we believe that the effects of ambient cues to extrinsic mortality on life history strategies may not be considered independent of changes in economic development and their driving forces. Intersecting life history theory and economic models of fertility choice might be a promising avenue of research.
Ellis, Reid, and Kramer (ERK) propose a framework applied to human development to investigate how exposures to extrinsic mortality shape life history strategies. Their model is two-tiered as it integrates two hypotheses – the energetics and developmental hypotheses. ERK evaluate their model by reviewing a large empirical record on low- and middle-income countries, providing a solid basis for their conclusions: harsh environmental conditions characterized by high-mortality risk from diverse external sources, in particular energetic stress (the model’s first tier) and ambient cues to extrinsic mortality (the model’s second tier), have countervailing effects on the development of life history strategies, both delaying pubertal maturation and promoting accelerated pace of reproduction and higher offspring number. We shall comment hereafter on three salient contributions of this article.
1. Energetics, the environment, and fertility
The environmental constraints on fertility are well studied in economic demography, particularly the impact of pollution on fertility (Hirazawa, Kamada, & Sato, Reference Hirazawa, Kamada and Sato2019). In this sense, this literature is aligned with environmental science (Skakkebæk et al., Reference Skakkebæk, Lindahl-Jacobsen, Levine, Andersson, Jørgensen, Main, Lidegaard, Priskorn, Holmboe, Bräuner, Almstrup, Franca, Znaor, Kortenkamp, Hart and Juul2022). We find the energetics hypothesis much more stimulating. Surprisingly, the role of energetic constraints in explaining demographic trends has been largely overlooked in economics. While the role of energy is stressed in certain economic history works (see Wrigley (Reference Wrigley2010)) and is even central in econophysics (Georgescu-Roegen, Reference Georgescu-Roegen1986), its role in population dynamics has been seldom examined, not even in the literature on the transition from Malthusian stagnation to economic growth (Galor & Weil, Reference Galor and Weil2000). However, this line of research has become vivid in the last decade with the debate on energy poverty in low- and middle-income countries. Chang et al. (Reference Chang, Dong, He and Zhang2024) showed on Chinese data that the relationship between energy poverty and fertility intentions is far more complex, featuring the intersection of different mechanisms arising from cultural, economic (along the developmental hypothesis), and health channels: the latter two constrain fertility while the former raises it. Henceforth, the relationship between energy poverty and fertility exhibits an inverted U-shape. It would be interesting to reassess ERK’s results, focusing on multidimensional energy poverty indicators. And it is per se complex: just like in ERK, the two tiers interfere.
2. Extrinsic mortality, fertility, and development
ERK’s demonstration is all more convincing as the economic theory has long shown that what the life history theory refers as the developmental hypothesis, especially through mortality fluctuations, is central in shaping not only life history strategies but also sustained economic growth and development (Galor & Weil, Reference Galor and Weil2000; Kalemli-Ozcan, Reference Kalemli-Ozcan2002; Boucekkine, de la Croix, & Licandro, Reference Boucekkine, de la Croix and Licandro2003).
Several competing economic theories have been advanced to explain net fertility dynamics in response to mortality shocks. In considering the disciplinary intersection of ERK and our own, we believe their model (in particular the second tier acting through ambient cues to extrinsic mortality) closely aligns with the economic models assuming that the fertility transition is mostly explained by the reduction in child survival uncertainty (Kalemli-Ozcan, Reference Kalemli-Ozcan2003). They rightly argue that the insurance hypothesis is consistent with the life history model: uncertainty about child survival generates a precautionary demand for children to ensure a sufficiently large family size (Taylor, Newman, & Kelly, Reference Taylor, Newman and Kelly1976). The insurance hypothesis predicts that reductions in child mortality and morbidity will reduce total and net fertility rates (Bousmah, Reference Bousmah2017a, Reference Bousmah2017b). Nevertheless, a fundamental question remains: is the fertility response to uncertainty about child survival significant enough to substantially affect net fertility?
In this respect, theoretical findings of the endogenous fertility literature are mixed. While some models imply that both gross and net fertility are affected by child mortality (Kalemli-Ozcan, Reference Kalemli-Ozcan2003), others exhibit an effect of child mortality on total fertility only (Doepke, Reference Doepke2005; Boucekkine, Desbordes, & Latzer, Reference Boucekkine, Desbordes and Latzer2009), implying that other factors are at play to influence net fertility rates. These factors are manifold – wages (Becker, Reference Becker1981), consumption growth (Becker & Barro, Reference Becker and Barro1988), women’s relative wages (Galor & Weil, Reference Galor and Weil1996), human capital (Becker, Murphy, & Tamura, Reference Becker, Murphy and Tamura1990), technological progress (Galor & Weil, Reference Galor and Weil2000), and/or changes in gender roles (Lagerlöf, Reference Lagerlöf2003b). In this sense, ERK’s view on the interaction between mortality and fertility seems rather partial, especially as a theory of demographic transition.
3. A potential endogeneity problem… not so easy to solve
ERK consider that mortality-fertility relationships are unaffected by economic development or stage in the demographic transition, arguing that some empirical findings on the mortality-fertility link are robust to controlling for indicators of economic development (in between-country studies) or socioeconomic variables between respondents (in within-country studies). However, simply controlling for socioeconomic variables is not sufficient to test whether the association between mortality and fertility is confounded by economic development, as documented above on a sample of endogenous fertility models and inherent mortality-fertility indirect interaction schemes.
Indeed, the endogenous fertility literature refutes, to a certain extent, ERK’s claim about the exogeneity of economic development in the mortality-fertility link. Although mortality decline is central to initiating fertility decline, mortality fluctuations alone are not sufficient to trigger a fertility transition. The quantity-quality tradeoff, also mentioned by EKR, is a key mechanism inherent in endogenous fertility models (Becker & Barro, Reference Becker and Barro1988; Barro & Becker, Reference Barro and Becker1989) to depict the full transition dynamics. Accordingly, a decrease in child mortality lowers the cost of rearing surviving children in the initial generation, such that the demand for survivors increases, leading birth rates to rise in the first place. As the rate of decline in child mortality slows once it approaches zero, fertility rates fall in later generations, and parents decide to invest more in educating each child. Education is a key variable in driving the future responses to the next mortality shocks, further lowering the effective magnitude of future mortality shocks (see Lagerlöf (Reference Lagerlöf2003a) on Sweden). Even though mortality is extrinsic, its effective magnitude is endogenous, at least to a certain extent.
While we agree about the necessity of a two-tiered approach, we believe that the effects of ambient cues to extrinsic mortality on life history strategies may not be considered independent of changes in economic development and their driving forces. Intersecting life history theory and economic models of fertility choice might be a promising avenue of research.
Acknowledgments
Raouf Boucekkine and Ullrika Sahlin acknowledge the support of the Institute of Advanced Study, Durham University, where they were fellows in 2025.
Financial support
This research received no specific grant from any funding agency, commercial, or not-for-profit sectors.
Competing interests
The authors declare none.