A review and novel theoretical model of how negative emotions influence inflammation: The critical role of emotion regulation
Psychological distress is an inevitable part of life. Research drawing on theories from clinical psychology, health psychology, and psychoneuroimmunology (PNI) has identified relationships between negative emotions such as anxiety and sadness with inflammation. When not regulated properly, negative...
Guardado en:
| Autor principal: | |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Elsevier
2021
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/a4e7a4ce707c41a0b6ebd94f0fa68c34 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | Psychological distress is an inevitable part of life. Research drawing on theories from clinical psychology, health psychology, and psychoneuroimmunology (PNI) has identified relationships between negative emotions such as anxiety and sadness with inflammation. When not regulated properly, negative emotions can create biological wear and tear on the body that can increase risk for morbidity and mortality. This review discusses previously available research on relationships between negative emotions and emotion regulation with inflammation among both physically healthy adults and those with chronic illnesses. I then present a novel comprehensive biobehavioral model of negative emotionality. This model emphasizes the influence of negative emotions and their contribution to heightened inflammation. Further, I also discuss how emotion regulation (including perseverative processes such as worry and rumination) mediates this association. The relationships between negative emotionality and emotion regulation may be bidirectional, and empirical investigation of this model should specifically seek to disentangle these relationships. The proposed model offers the opportunity to advance PNI research through understanding how emotional factors alter inflammation and contribute to accelerated biological aging and disease risk. |
|---|