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Emotion Regulation as a Pathway Connecting Early Life Adversity and Inflammation in Adulthood: a Conceptual Framework
Ambika Mathur1, Jacinda C Li2, Sarah R Lipitz1
1Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA USA.
Early life adversity (ELA) can lead to chronic inflammation in adulthood. Emotion regulation strategies, like cognitive reappraisal, may promote resilience against inflammation in those with a history of ELA.
Area of Science:
- Psychoneuroimmunology
- Developmental Psychology
- Health Psychology
Background:
- Chronic inflammation is linked to major diseases like cardiovascular disease and cancer.
- Early life adversity (ELA) is a risk factor for adult inflammation, potentially via effects on emotion regulation brain circuits.
- Emotion regulation strategies vary, with some (e.g., expressive suppression) being maladaptive and others (e.g., cognitive reappraisal) adaptive.
Purpose of the Study:
- To propose a conceptual framework linking emotion regulation tendencies to inflammation vulnerability or resilience in adults with ELA.
- To review evidence supporting the framework, focusing on emotion dysregulation and cognitive reappraisal in relation to inflammation.
- To discuss contributing factors, interventions, and future research directions.
Main Methods:
- Conceptual review and synthesis of existing research.
- Examination of evidence linking emotion regulation strategies to inflammation markers.
- Analysis of neurobiological, physiological, psychosocial, and ELA-specific factors.
Main Results:
- Evidence suggests emotion dysregulation is associated with higher inflammation (vulnerability) in adults with ELA.
- Cognitive reappraisal is linked to lower inflammation (resilience) in healthy adults with a history of ELA.
- The framework integrates various factors influencing the ELA-inflammation relationship.
Conclusions:
- Emotion regulation plays a critical role in mediating the long-term inflammatory effects of early life adversity.
- Cognitive reappraisal may represent a protective factor against inflammation for individuals with a history of ELA.
- Further research is needed to elucidate mechanisms and develop targeted interventions.
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