Developmental plasticity is the process by which later life traits are shaped by the early life environment. Specifically, it refers to the process according to which a single genotype (i.e., genetic makeup of an organism) leads to distinct and lasting phenotypes (i.e., outward biological and psychological manifestations) under alterations of environmental interactions.
Developmental plasticity is a concept grounded in the broad field of biology. Its roots trace to the classic “nature versus nurture” debate introduced in the nineteenth century in scientific discourse, that is, the question of the origins of individual differences as a result of environmental versus genetic influences. Developmental plasticity emphasizes the individual’s adaptation to external changes as a result of the combined effect of both genetic and environmental influences, as opposed to solely one or the other.
Multiple explanations regarding the evolutionary nature of developmental plasticity have been suggested. According to the “developmental constraints” model, plasticity uses environmental cues to improve the organism fitness to the environment and maximize chances of survival in early life. However, this adaptation may, in turn, compromise later adult fitness. A classic example of such process is the “thrifty phenotype hypothesis” according to which poor early nutrition triggers a “nutritional thrift” in the form of changes to the endocrine system that aim at preserving the supply of glucose to the developing brain. However, this results in impaired pancreatic function, which in turn predisposes to pathological conditions in adulthood such as metabolic disorders (Monaghan 2007). In contrast, according to “forecasting” models of developmental plasticity, informational cues about the early state of the environment - including during intrauterine life - are used by the developing organism to prepare for the adult environment (e.g., enhancing or depressing traits accordingly), which assumes an accurate long-term forecasting for best outcomes to occur (e.g., Gluckman and Hanson 2004). Applied to the example of poor early nutrition, the organism could prepare for such a lasting condition in adult life, for example, by improving insulin resistance (Wells and Johnstone 2017). Alternative lines of explanations have emphasized the buffering role of maternal and matrilineal phenotypes (rather than the direct effect of the environment) in the adaptation of the offspring fitness to either the early (e.g., Wells and Johnstone 2017) or forecasted adult environment (e.g., Naumova et al. 2016).
Understanding the epigenetic mechanisms underlying developmental plasticity is important to identify sources of interindividual variations with respect to phenotypes of interest. This has important implications in a preventive perspective (e.g., understanding the biological dynamics that mediate the interaction between genotype and environment leading to maladaptive outcomes). Among various such epigenetic alterations, DNA-methylation is a biological process that serves as a developmental plasticity mechanism that has received considerable attention. It refers to an epigenetic biochemical modification that controls molecular mechanisms of cell programming, in particular chromatin structure and gene expression (e.g., repress gene transcription). Growing evidence shows how the environment can significantly alter DNA-methylation patterns (e.g., Smearman et al. 2016). In particular, research suggests that the relationship between adult development and early adverse circumstances including trauma and abusive/neglectful rearing environments are mediated by epigenetic markers such as DNA-methylation in genetic processes involved in key human functions, including stress response and immune systems, or genes involved in oxytocin pathways (for a review see Bick et al. 2012).
Evidence supports the existence of genetic susceptibility risks in maladaptive personality traits such as primary psychopathy and callous-unemotional characteristics, as well as on significant clinical conditions including anxiety and eating disorders (e.g., Dadds et al. 2014; Ziegler et al. 2015). Studies have uncovered the epigenetic modifications of key biological factors associated with such conditions and often emphasized the critical role of genes altering oxytocin pathways in socio-emotional human behavior. For example, methylation of the oxytocin receptor gene and oxytocin blood levels has demonstrated associations with alterations in the socio-cognitive system of empathy (Dadds et al. 2014) and on the neuroendocrinological network phenotypes of social anxiety (Ziegler et al. 2015). However, individual differences exist. The term plasticity itself suggests adaptation to variations of the external conditions, large variability in developmental trajectories, and interindividual differences with respect to essential components of behavior and experience such as personality traits (Stamps 2016). There are also individual differences in the outcomes of this adaptation. For example, Person x Environment models propose that adaptive and maladaptive outcomes, including personality traits, can be triggered by the same factors based on differential susceptibility to favorable and unfavorable environments (e.g., Belsky and Pluess 2013). Specific external conditions (e.g., childhood adversity) do not necessarily lead to the same outcomes depending on one’s susceptibility to environmental influences, and reciprocally, a given genetic risk might be either intensified or repressed in a given environmental context.
The concept of developmental plasticity is inherently related to individual differences in both adaptive and maladaptive psychological outcomes. Shedding light on the mechanisms of developmental plasticity may clarify fundamental scientific questions on the origins of disorders, such as personality maladjustment. To date, capturing developmental plasticity of complex traits is challenging as studies are often underpowered, include many confounds (e.g., separating out adult environments and health habits), and often rely on retrospective self-reporting. Ongoing prospective, longitudinal studies of human cohorts with repeated biological sampling will prove invaluable to shed light on this phenomenon.
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