Wigley B R, Stillman E C, Craig-Atkins E
School of Biosciences, University of Sheffield, Sheffield, UK.
School of Mathematical and Physical Sciences, University of Sheffield, Sheffield, UK.
Am J Biol Anthropol. 2025 Feb;186(2):e70005. doi: 10.1002/ajpa.70005.
This paper explores conflicting perspectives on the adaptive significance of phenotypic plasticity during fetal and early postnatal development and the impact that stressors experienced during this critical early-life period have on later-life morbidity and mortality risk.
The sample (n = 216) comprised archeologically-recovered human skeletons. A geometric morphometric (GM) method was employed to evaluate first permanent molar (M1) fluctuating asymmetry (FA) and provide a proxy for early-life stress. Shifts in later-life physiology were inferred through two inflammatory lesions: periosteal new bone formation (PNBF) and periodontal disease (PD). To explore mortality risk, age-at-death was estimated through dental development for skeletally immature individuals (n = 104) and through senescent skeletal changes for mature skeletons (n = 112).
Significant differences were found in M1 FA between groups, with the immature cohort associated with elevated FA. Within-group analysis revealed age-at-death in the immature group had a significant positive relationship with M1 FA and PD presence. In the mature group, alongside sex and the co-occurrence of PD and PNBF, FA was a significant predictor of a shorter life. Higher FA was also associated with active and bilaterally expressed PNBF.
It is theorized that early-life stress, if survived, programmed a hyperinflammatory response to environmentally-mediated physiological perturbations which increased the chances of survival during subsequent development but also elevated later-life mortality risk. Findings demonstrate a complicated relationship between developmental stress and physiological shifts that helps to illustrate the adaptive significance of early-life programming and support the Thrifty Phenotype hypothesis.
本文探讨了关于胎儿期和出生后早期发育过程中表型可塑性的适应性意义的相互冲突的观点，以及在这一关键的生命早期阶段所经历的应激源对后期发病和死亡风险的影响。
样本（n = 216）包括从考古发掘中获得的人类骨骼。采用几何形态测量（GM）方法评估第一恒磨牙（M1）的波动不对称性（FA），并作为生命早期应激的指标。通过两种炎症性病变推断后期生理变化：骨膜新生骨形成（PNBF）和牙周病（PD）。为了探究死亡风险，对于骨骼未成熟个体（n = 104），通过牙齿发育估计死亡年龄；对于成熟骨骼（n = 112），通过衰老骨骼变化估计死亡年龄。
各群体之间在M1 FA上存在显著差异，未成熟队列的FA较高。组内分析显示，未成熟组的死亡年龄与M1 FA和PD的存在呈显著正相关。在成熟组中，除了性别以及PD和PNBF的共同出现外，FA是寿命较短的显著预测因素。较高的FA还与活跃的双侧表达的PNBF相关。
理论认为，生命早期应激若能存活下来，会对环境介导的生理扰动产生过度炎症反应，这增加了后续发育过程中的生存机会，但也提高了后期的死亡风险。研究结果表明发育应激与生理变化之间存在复杂的关系，这有助于阐明生命早期编程的适应性意义，并支持节俭表型假说。
