摘要
Adversity might best be thought of as a violation of the expectable environment. Adversity can take many forms, including exposure to biological and psychosocial hazards, which often coexist as complex exposures. Many forms of early adversity are not time limited, making it difficult to tease apart the cumulative effects of adversity from the effects of early life adversity. Exposure to various forms of adversity early in life is associated with alterations in brain development, which in turn is associated with psychological, behavioral, and physical health consequences. Exposure to adversity during critical periods of development is more likely to lead to permanent rather than transient effects on the brain. Parallel studies across humans and animal models of early adversity will prove essential to understanding how adversity becomes neurobiologically embedded. It is now widely recognized that children exposed to adverse life events in the first years of life are at increased risk for a variety of neural, behavioral, and psychological sequelae. As we discuss in this paper, adverse events represent a violation of the expectable environment. If such violations occur during a critical period of brain development, the detrimental effects of early adversity are likely to be long lasting. Here we discuss the various ways adversity becomes neurobiologically embedded, and how the timing of such adversity plays an important role in determining outcomes. We conclude our paper by offering recommendations for how to elucidate the neural mechanisms responsible for the behavioral sequelae and how best to model the effects of early adversity. It is now widely recognized that children exposed to adverse life events in the first years of life are at increased risk for a variety of neural, behavioral, and psychological sequelae. As we discuss in this paper, adverse events represent a violation of the expectable environment. If such violations occur during a critical period of brain development, the detrimental effects of early adversity are likely to be long lasting. Here we discuss the various ways adversity becomes neurobiologically embedded, and how the timing of such adversity plays an important role in determining outcomes. We conclude our paper by offering recommendations for how to elucidate the neural mechanisms responsible for the behavioral sequelae and how best to model the effects of early adversity. a violation of the expectable environment that takes the form of biological hazards, psychosocial hazards, of complex exposures of both hazard types, with negative effects on development. the mechanisms through which environmental experiences impact neurobiology such that these experiences have enduring consequences on brain structure and function. adverse biological factors in the environment that have negative effects on development, such as insufficient nutrients, environmental toxins, and pathogens that induce chronic infection and inflammation. window of heightened brain plasticity for encoding specific environmental inputs through experience-expectant mechanisms that results in irreversible changes in brain function with permanent effects on behavior, for example, as in filial imprinting. neural plasticity mechanism facilitating learning in response to experiences across the lifespan without developmental constraints, for example, strengthening or weakening neural synapse connections. neural plasticity mechanism facilitating the encoding of specific, expectable environmental stimuli, such as patterned light or auditory tones, during constrained developmental windows; underlies critical and sensitive period phenomena. a conceptual and statistical framework for complex adversity exposures that accounts for how different types of adversity interact and generate synergistic effects on development, for example, implemented with toxin mixtures. adverse cognitive, affective, or social experiences that negatively impact development, such as poverty, inadequate caregiving, and maltreatment. constrained window of time when the environment most impacts brain function via experience-expectant mechanisms; similar to a critical period but with residual plasticity after the period ends such that experiences may continue to affect brain function, for example, as in caregiver attachment formation.