On 2016 Jul 14, Marcus Munafò commented:

This study provides deeper theoretical insights than might be imagined from a cursory reading. Evolutionary life history theory addresses how organisms, including humans, vary in the allocation of resources to growth, survival and reproduction across the life course. Life history strategies are defined by key decisions that trade off finite resources against competing demands to achieve reproductive goals [1, 2]. Both across and within species, the trade-off between the allocation of resources to growth and to reproductive efforts results in organisms employing varying strategies that can be characterised, loosely, as ‘slow’ or ‘fast’. A ‘slow’ life history strategy is characterized by later maturity and proportionally greater investment of resources in a smaller number of offspring, while a ‘fast’ life history strategy involves more effort directed towards reproduction, such as earlier puberty and sexual activity [2, 3]. Typically, animals pursue a fast life history strategy (‘live fast, die young’) under adverse environmental conditions of high extrinsic mortality. In such conditions, as Day and colleagues suggest, earlier sexual maturation may increase reproductive fitness. However, Day and colleagues also suggest that associations between earlier puberty and a greater propensity for risk-taking behaviours, lower educational attainment, and adverse health outcomes, contradicts this evolutionary perspective. On the contrary, directing effort into risky and aggressive behaviour is best considered as an important part of a fast life history strategy, in which competition for mates is crucial [1]. Viewed in this light, adolescent behaviours of unprotected sex and earlier pregnancy, as well as violence, law breaking, and substance abuse, can be seen as central components or consequences of a fast strategy in which the future is discounted relative to the present [1, 4]. Variation in these physiological and behavioural traits in response to changing environments may reflect a suite of adaptations – psychological and somatic – that increase fitness on average despite poor social and health consequences [5], as resources are diverted from longevity towards short-term reproductive goals under conditions of adversity.

The human life history literature suggests strategies are contingent on variation in the environment rather than variations in genotype. Day and colleagues illustrate the central role genetics can play in testing key hypotheses arising out of life history theory, where reliance on observational data has previously limited causal inference. The key point is that variants identified in GWAS studies may reflect environmental (and hence modifiable) risk factors, as well as direct genetic effects [6]. An ever-increasing range of social and psychological traits relevant to life history theory are proving tractable to GWAS, including, for example, social deprivation [7] and endocrine biomarkers including cortisol [8] and sex steroids [9]. Genetic instruments associated with social outcomes could be used as a proxy for environmental harshness, while instruments for endocrine status may provide causal evidence for status seeking and reproductive behaviours known to occur in other species, but that are not amenable to experimental analysis in humans. The results of emerging GWAS therefore provide us with unprecedented opportunities for testing the predictions of life history theory, with implications for our understanding of the determinants of health and social behaviour. The elegant demonstration by Day and colleagues of causal links between earlier puberty and both key reproductive traits and adverse outcomes provides compelling evidence that evolutionary life history theory can shed light on human reproductive behaviour, health and disease, even in a modern Western environment. Combining causal analysis from genetic epidemiology and theoretical insights from evolutionary models may help to launch a science of evolutionary social epidemiology, combining knowledge of ‘how’ exposures lead to certain outcomes with an understanding of ‘why’ these relationships may exist. Reframing our understanding of the development of significant social and health outcomes in this way may lead to novel insights to inform future interventions.

Rebecca Lawn, Abigail Fraser, Marcus Munafò and Ian Penton-Voak

1. Ellis, B.J. and Bjorklund, D.F. Beyond mental health: an evolutionary analysis of development under risky and supportive environmental conditions: an introduction to the special section. Developmental Psychology, 2012. 48(3): p. 591.
2. Chisholm, J.S., Death, hope and sex: Steps to an evolutionary ecology of mind and morality. 1999, Cambridge: University of Cambridge Press.
3. Ellis, B.J., et al., Fundamental dimensions of environmental risk. Human Nature, 2009. 20: p. 204-268.
4. Simpson, J.A., et al., Evolution, stress, and sensitive periods: the influence of unpredictability in early versus late childhood on sex and risky behavior. Developmental psychology, 2012. 48: p. 674-686.
5. Gluckman, P.D. and Beedle, A.S. Match fitness: development, evolution, and behavior: comment on Frankenhuis and Del Giudice (2012). Developmental Psychology, 2012. 48: p. 643– 646.
6. Gage, S.H., et al., G= E: What GWAS can tell us about the environment. PLoS Genet, 2016. 12: e1005765.
7. Hill, W.D., et al., Molecular genetic contributions to social deprivation and household income in UK Biobank (n= 112,151). bioRxiv, 2016.
8. Bolton, J.L., et al., Genome wide association identifies common variants at the SERPINA6/SERPINA1 locus influencing plasma cortisol and corticosteroid binding globulin. PLoS Genet, 2014. 10: e1004474
9. Vandenput, L. and C. Ohlsson, Genome-wide association studies on serum sex steroid levels. Molecular and cellular endocrinology, 2014. 382: p. 758-766.

On 2016 Jul 14, Marcus Munafò commented:

This study provides deeper theoretical insights than might be imagined from a cursory reading. Evolutionary life history theory addresses how organisms, including humans, vary in the allocation of resources to growth, survival and reproduction across the life course. Life history strategies are defined by key decisions that trade off finite resources against competing demands to achieve reproductive goals [1, 2]. Both across and within species, the trade-off between the allocation of resources to growth and to reproductive efforts results in organisms employing varying strategies that can be characterised, loosely, as ‘slow’ or ‘fast’. A ‘slow’ life history strategy is characterized by later maturity and proportionally greater investment of resources in a smaller number of offspring, while a ‘fast’ life history strategy involves more effort directed towards reproduction, such as earlier puberty and sexual activity [2, 3]. Typically, animals pursue a fast life history strategy (‘live fast, die young’) under adverse environmental conditions of high extrinsic mortality. In such conditions, as Day and colleagues suggest, earlier sexual maturation may increase reproductive fitness. However, Day and colleagues also suggest that associations between earlier puberty and a greater propensity for risk-taking behaviours, lower educational attainment, and adverse health outcomes, contradicts this evolutionary perspective. On the contrary, directing effort into risky and aggressive behaviour is best considered as an important part of a fast life history strategy, in which competition for mates is crucial [1]. Viewed in this light, adolescent behaviours of unprotected sex and earlier pregnancy, as well as violence, law breaking, and substance abuse, can be seen as central components or consequences of a fast strategy in which the future is discounted relative to the present [1, 4]. Variation in these physiological and behavioural traits in response to changing environments may reflect a suite of adaptations – psychological and somatic – that increase fitness on average despite poor social and health consequences [5], as resources are diverted from longevity towards short-term reproductive goals under conditions of adversity.

The human life history literature suggests strategies are contingent on variation in the environment rather than variations in genotype. Day and colleagues illustrate the central role genetics can play in testing key hypotheses arising out of life history theory, where reliance on observational data has previously limited causal inference. The key point is that variants identified in GWAS studies may reflect environmental (and hence modifiable) risk factors, as well as direct genetic effects [6]. An ever-increasing range of social and psychological traits relevant to life history theory are proving tractable to GWAS, including, for example, social deprivation [7] and endocrine biomarkers including cortisol [8] and sex steroids [9]. Genetic instruments associated with social outcomes could be used as a proxy for environmental harshness, while instruments for endocrine status may provide causal evidence for status seeking and reproductive behaviours known to occur in other species, but that are not amenable to experimental analysis in humans. The results of emerging GWAS therefore provide us with unprecedented opportunities for testing the predictions of life history theory, with implications for our understanding of the determinants of health and social behaviour. The elegant demonstration by Day and colleagues of causal links between earlier puberty and both key reproductive traits and adverse outcomes provides compelling evidence that evolutionary life history theory can shed light on human reproductive behaviour, health and disease, even in a modern Western environment. Combining causal analysis from genetic epidemiology and theoretical insights from evolutionary models may help to launch a science of evolutionary social epidemiology, combining knowledge of ‘how’ exposures lead to certain outcomes with an understanding of ‘why’ these relationships may exist. Reframing our understanding of the development of significant social and health outcomes in this way may lead to novel insights to inform future interventions.

Rebecca Lawn, Abigail Fraser, Marcus Munafò and Ian Penton-Voak

1. Ellis, B.J. and Bjorklund, D.F. Beyond mental health: an evolutionary analysis of development under risky and supportive environmental conditions: an introduction to the special section. Developmental Psychology, 2012. 48(3): p. 591.
2. Chisholm, J.S., Death, hope and sex: Steps to an evolutionary ecology of mind and morality. 1999, Cambridge: University of Cambridge Press.
3. Ellis, B.J., et al., Fundamental dimensions of environmental risk. Human Nature, 2009. 20: p. 204-268.
4. Simpson, J.A., et al., Evolution, stress, and sensitive periods: the influence of unpredictability in early versus late childhood on sex and risky behavior. Developmental psychology, 2012. 48: p. 674-686.
5. Gluckman, P.D. and Beedle, A.S. Match fitness: development, evolution, and behavior: comment on Frankenhuis and Del Giudice (2012). Developmental Psychology, 2012. 48: p. 643– 646.
6. Gage, S.H., et al., G= E: What GWAS can tell us about the environment. PLoS Genet, 2016. 12: e1005765.
7. Hill, W.D., et al., Molecular genetic contributions to social deprivation and household income in UK Biobank (n= 112,151). bioRxiv, 2016.
8. Bolton, J.L., et al., Genome wide association identifies common variants at the SERPINA6/SERPINA1 locus influencing plasma cortisol and corticosteroid binding globulin. PLoS Genet, 2014. 10: e1004474
9. Vandenput, L. and C. Ohlsson, Genome-wide association studies on serum sex steroid levels. Molecular and cellular endocrinology, 2014. 382: p. 758-766.