What Doesn't Kill You Makes You Stronger? Examining Relationships Between Early-Life Stress, Later-Life Inflammation...

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.