Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms
By Gregory E. Miller, E. Chen, K. J. Parker. Psychological bulletin, 2011
1,722 citations recorded by the source corpus.
Among people exposed to major psychological stressors in early life, there are elevated rates of morbidity and mortality from chronic diseases of aging. The most compelling data come from studies of children raised in poverty or maltreated by their parents, who show heightened vulnerability to vascular disease, autoimmune disorders, and premature mortality. These findings raise challenging theoretical questions. How does childhood stress get under the skin, at the molecular level, to affect risk for later diseases? And how does it incubate there, giving rise to diseases several decades later? Here we present a Biological Embedding Model, which attempts to address these questions by synthesizing knowledge across several behavioral and biomedical literatures. This model maintains that childhood stress gets “programmed” into macrophages through epigenetic markings, post-translational modifications, and tissue remodeling. As a consequence these cells are endowed with pro-inflammatory tendencies, manifest in exaggerated cytokine responses to challenge and decreased sensitivity to inhibitory hormonal signals. The model goes on to propose that over the lifecourse, these pro-inflammatory tendencies are exacerbated by behavioral proclivities and hormonal dysregulation, themselves the products of exposure to early stress. Behaviorally, the model posits that childhood stress gives rise to excessive threat vigilance, mistrust of others, poor social relationships, impaired self-regulation, and unhealthy lifestyle choices. Hormonally, early stress confers altered patterns of endocrine and autonomic discharge. This milieu amplifies the pro-inflammatory environment already instantiated by macrophages. Acting in concert with other exposures and genetic liabilities, the resulting inflammation drives forward pathogenic mechanisms that ultimately foster chronic disease.
Subfields: Behavioral Neuroscience, Biological Psychiatry, Pediatrics, Perinatology and Child Health
View Paper: https://www.semanticscholar.org/paper/a7e59e2d6515473839e1a124674dee448b8c4623
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Behavioral Neuroscience
- George M. Slavich
- Gregory E. Miller
- G. W. Evans
- Robin Nusslock
- W. Mendes
- E. Epel
- Michael R. Irwin
- Keith Bredemeier
In Biological Psychiatry
In Pediatrics, Perinatology and Child Health
Citations in the corpus
- Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters. (2018, neutral): “…been thought to reflect “glucocorticoid resistance,” a particular kind of dysregulation whereby immune cells (e.g., macrophages) become insensitive to the GR-mediated inhibitory effects of cortisol after prolonged overexposure (Kuhlman et al., 2017; Miller et al., 2002, 2011; Cohen et al., 2012).”
- Early-Life Adversity and Physical and Emotional Health across the Lifespan: A Neuro-Immune Network Hypothesis (2015, background): “When confronted with ambiguous stimuli, whose threat value is uncertain, low-SES youth exhibit larger cardiovascular responses than higher SES youth (22).”
- Out of Control (2015, neutral): “Conflictive, lowquality relationships (Miller et al., 2011) and harsh, inconsistent parenting (Lengua et al.”
- More than a feeling: A unified view of stress measurement for population science (2018, background): “…such as chronic inflammation in adulthood (Slopen et al., 2010; Surtees et al., 2003; Danese et al., 2007) and telomere shortening (Hanssen et al., 2017; Ridout et al., 2017), cognitive and affective processes (Pechtel and Pizzagalli, 2011), and behavioral proclivities (Miller et al., 2011).”