To what degree does early life development impact the trajectory of late life aging? Plenty of evidence suggests a connection, much of it from epidemiological studies that, unfortunately, given little insight into possible mechanisms. Of other work, applying reliability theory to aging can only fit the observed mortality data if we are born with a non-zero level of damage. Further, early exposure to cytomegalovirus, a persistent infection that is corrosive of immune function over the long term, may explain links between socioeconomic status in childhood and pace of late life aging. These are two of many studies to provide hypotheses and at least some supporting evidence.
A diverse set of mechanisms could transform episodic or recurrent early exposures in utero, perinatally, and during infancy and early childhood into delayed impacts on adult illness, disability, and mortality. The mechanisms are associated with organ-specific embryo and fetal cell growth and differentiation, epigenetic changes, exposure to and contraction of early childhood diseases and sustained inflammation, and experiences with stressful conditions and environments. Furthermore, a large and influential body of empirical research documents the long-lasting impact of early nutritional status on adult health and mortality. Finally, there is widespread empirical evidence demonstrating that more diffuse exposures, such as poverty and severe deprivation in infancy and early childhood, can also have lasting impacts.
The mechanisms identified above are the focus of various strands of theories with unique histories and distinct disciplinary foundations. Different as they may be, however, they share an important trait as all invoke perturbations during critical periods of the development of a phenotype triggered by insults before conception, during embryonic and fetal life, perinatally, and across early stages of physical and cognitive growth. These early insults may then lead to disruptions in processes of organ growth, differentiation and function, immune response, neurological development, metabolic regulation, and even the formation of adult preferences and behaviors. After variable but usually prolonged latency periods, the disruptions could manifest themselves as increased susceptibility to adult chronic illness.
This shared feature emphasized by multiple variants of developmental effects on aging coexists with important differences that segregate them into distinct classes associated with different outcomes. For example, mechanisms that depend on epigenetic changes, such as methylation of CpG islands caused by nutrient deficiencies, disrupt metabolic function, and are associated with child and adult obesity. Others involve organ damage caused by an immune overresponse to bacteria, as in the case of acute rheumatic heart fever that increases the risk of adult heart valve stenosis. And yet others depend on misfiring of the hypothalamic-pituitary-adrenal (HPA) axis, an adaptation among some mammals to chronic stress, as when early abuse triggers adult depression, aggressiveness, and anxiety. The differences between these mechanisms range over a number of domains including nature and timing of insults, critical and sensitive periods, chronic illnesses, critical ages after which the damage is manifested, and interactions between initial insults and individuals' lifetime exposure to different environments.