Future Directions in the Study of Early-Life Stress and Physical and Emotional Health: Implications of the Neuroimmune Network Hypothesis

Abstract

Early-life stress is associated with increased vulnerability to physical and emotional health problems across the lifespan. The recently-developedneuroimmune network hypothesis proposes that one of the underlying mechanisms for these associations is that early-life stress amplifies bidirectional crosstalk between the brain and the immune system, contributing to several mental and physical health conditions that have inflammatory underpinnings, such as depression and coronary heart disease. Neuroimmune crosstalk is thought to not only perpetuate inflammation and neural alterations linked to early-life stress exposure, but may also foster behaviors that can further compromise health, such as smoking, drug abuse and consumption of high-fat diets. The goal of the present review is to briefly summarize the neuroimmune network hypothesis and use it as a starting point for generating new questions about the role of early-life stressin establishing a dysregulated relationship between neural and immune signaling, with consequences for lifespan physical and emotional health. Specifically, we aim to discuss implications and future directions for theory andempirical research on early-life stress, as well as forinterventions that may improve the health and wellbeing of children and adolescents living in adverse conditions.

Puberty and the Evolution of Developmental Science

“…For instance, the association of early harsh conditions with earlier menarche is attenuated by secure attachment in infancy (Sung et al., ). Ongoing inquiry also points beyond stress response systems to neuroimmune interactions that mediate pathways from early adversity to inflammation and health (Hostinar, Nusslock, & Miller, ). A longitudinal study of adolescent Canadian girls, for example, found an association of proinflammatory phenotype with early life adversity but not with current social stress (Ehrlich, Ross, Chen, & Miller, ).…”

Transdiagnostic neural correlates of volitional emotion regulation in anxiety and depression

“…One such example of symptom overlap across those with anxiety and depressive disorders is emotion dysregulation, as evinced by reports of negative biases (Beck & Clark, 1997;Gotlib, Krasnoperova, Yue, & Joormann, 2004) and difficulty in managing negative emotions in ways that are adaptive (Aldao, Nolen-Hoeksema, & Schweizer, 2010;Amstadter, 2008;Fernandez, Jazaieri, & Gross, 2016;Hostinar, Nusslock, & Miller, 2017;Shapero, Abramson, & Alloy, 2016;Tripp, McDevitt-Murphy, Avery, & Bracken, 2015;Tull, Bardeen, DiLillo, Messman-Moore, & Gratz, 2015). A well-studied form of emotion regulation is cognitive reappraisal, an antecedent emotion regulation strategy that occurs prior to or when an emotional experience is unfolding and involves the cognitive transformation (e.g., reinterpretation) of an emotional experience in order to change its emotional meaning (Gross, 1998).…”

Inflammaging 2018: An update and a model

“…In the past twenty years, the concept of inflammaging has shed light on such grey zone of systemic inflammation in aged people, a condition that spans from the healthy aging status to overt inflammatory ARDs/GSs. In turn, inflammaging is accelerated by persis-tent infections (cytomegalovirus) [17], lifestyle habits such as nutrient excess (metaflammation and obesity) [7,18], physical and psychosocial/emotional stressors [19,20] and gut microbiota dysbiosis [10].…”