Many studies in humans have shown that adverse experience in early life is associated with accelerated reproductive timing, and there is comparative evidence for similar effects in other animals. There are two different classes of adaptive explanation for associations between early-life adversity and accelerated reproduction, both based on the idea of predictive adaptive responses (PARs). According to external PAR hypotheses, early-life adversity provides a 'weather forecast' of the environmental conditions into which the individual will mature, and it is adaptive for the individual to develop an appropriate phenotype for this anticipated environment. In internal PAR hypotheses, early-life adversity has a lasting negative impact on the individual's somatic state, such that her health is likely to fail more rapidly as she gets older, and there is an advantage to adjusting her reproductive schedule accordingly. We use a model of fluctuating environments to derive evolveability conditions for acceleration of reproductive timing in response to early-life adversity in a long-lived organism. For acceleration to evolve via the external PAR process, early-life cues must have a high degree of validity and the level of annual autocorrelation in the individual's environment must be almost perfect. For acceleration to evolve via the internal PAR process requires that early-life experience must determine a significant fraction of the variance in survival prospects in adulthood. The two processes are not mutually exclusive, and mechanisms for calibrating reproductive timing on the basis of early experience could evolve through a combination of the predictive value of early-life adversity for the later environment and its negative impact on somatic state.

Publisher's copyright statement:Additional information: Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-prot purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details. 24Queen's Campus Stockton, University Boulevard, Thornaby, Stockton-on-Tees, TS17 6BH, UK. Children, particularly girls, who experience early familial adversity tend to go 32 on to reach sexual maturity relatively early. This feature of adolescent development is 33 believed to be an evolved strategy that arose because individuals with genes that 34 caused them to mature relatively early under certain conditions left behind more 35 descendants than those who did not. However, although much has been done to 36 uncover the psychological and physiological mechanisms underlying this process, less 37 attention has been paid to the evolutionary reasons behind why it might be 38 advantageous. It has previously been suggested that this strategy evolved because 39 early familial adversity accurately indicated later environmental adversity, under 40 which conditions early reproduction would likely maximize evolutionary fitness. In 41 this paper we contrast this 'external prediction' model with an alternative explanation, 42 which builds upon the existing explanation and is mutually compatible with it, but 43 which is distinct from it. We argue that accelerated development is advantageous 44 because early adversity detrimentally affects the individual's body, increasing later 45 morbidity and mortality; individuals may adapt to this internal setback by accelerating 46 their development. Unlike the external prediction model, this 'internal prediction' 47 relies not upon temporal environmental continuity, but on long-term effects of early 48 circumstances on the body. well-known among these findings, in social contexts where nuclear families 57 predominate, menarche occurs at a younger age among girls with 'absent' fathers (B. 58Jones, Leeton, McLeod, & Wood, 1972;Moffitt, Caspi, Belsky, & Silva, 1992; Tither 59 & Ellis, 2008). Studies that investigate the apparent effects of family circumstances in 60 detail have revealed that early menarche occurs in girls with less affectionate and 61 cohesive parent-child relationships (Chisholm, Quinlivan, Petersen, & Coall, 2005; 62 Graber, Brooks-Gunn, & Warren, 1995;Steinberg, 1988), those who experience 63 greater parent-child conflict (Graber et al., 1995;Kim & Smith, 1998; Mezzich et al., 64 1997), or who are exposed to greater parent-parent conflict (Chisholm et al., 2005; 65 Ellis & Garber, 2000;Ellis, McFadyen-Ketchum, Dodge, Pettit, & Bates, 1999), and 66 those who experi...

Many studies have shown that adverse experience in early life is associated with accelerated reproductive timing in humans. There are two different classes of adaptive explanation for such associations. Both can be seen as predictive adaptive responses (PARs). According to external PAR hypotheses, early-life adversity provides a ‘weather forecast’ of the environmental conditions into which the individual will mature, and it is adaptive for the individual to develop an appropriate phenotype for this anticipated environment. In internal PAR hypotheses, early-life adversity has a lasting negative impact on the individual’s somatic state, such that her health is likely to fail more rapidly as she gets older, and there is an advantage to adjusting her reproductive schedule accordingly. We use a model of fluctuating environments to derive evolveability conditions for acceleration of reproductive timing in response to early-life adversity. For acceleration to evolve via the external PAR process, early-life cues must have a high degree of validity and the level of annual autocorrelation in the individual’s environment must be almost perfect. For acceleration to evolve via the internal PAR process requires that early-life experience must determine a significant fraction of the variance in survival prospects in adulthood. The two processes are not mutually exclusive, and mechanisms for calibrating reproductive timing on the basis of early experience could evolve through a combination of the predictive value of early-life adversity for the later environment and its negative impact on somatic state.

Individuals with insufficient nutrition during development often experience poorer later-life health and evolutionary fitness. The Predictive Adaptive Response (PAR) hypothesis proposes that poor early-life nutrition induces physiological changes that maximize fitness in similar environments in adulthood and that metabolic diseases result when individuals experiencing poor nutrition during development subsequently encounter good nutrition in adulthood. However, although cohort studies have shown that famine exposure in utero reduces health in favorable later-life conditions, no study on humans has demonstrated the predicted fitness benefit under low later-life nutrition, leaving the evolutionary origins of such plasticity unexplored. Taking advantage of a well-documented famine and unique datasets of individual life histories and crop yields from two preindustrial Finnish populations, we provide a test of key predictions of the PAR hypothesis. Known individuals from fifty cohorts were followed from birth until the famine, where we analyzed their survival and reproductive success in relation to the crop yields around birth. We were also able to test whether the long-term effects of early-life nutrition differed between individuals of varying socioeconomic status. We found that, contrary to predictions of the PAR hypothesis, individuals experiencing low early-life crop yields showed lower survival and fertility during the famine than individuals experiencing high early-life crop yields. These effects were more pronounced among young individuals and those of low socioeconomic status. Our results do not support the hypothesis that PARs should have been favored by natural selection and suggest that alternative models may need to be invoked to explain the epidemiology of metabolic diseases.developmental plasticity | silver spoon | human life-history | DoHAD