Stress induced proinflammatory adaptations: Plausible mechanisms for the link between stress and cardiovascular disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and theoretical concepts without primary data or systematic review methodology
PubMed 37007994 · doi:10.3389/fphys.2023.1124121
What was done
This was a narrative review synthesizing literature on psychological stress, allostatic load, and the physiological mechanisms linking stress to cardiovascular disease (CVD). The authors examined stress hormone interactions with the immune system, stress-induced proinflammatory cellular pathways, the role of physical activity as a buffer via cross-stressor adaptations across the sympathetic-adreno-medullary (SAM) system and hypothalamic-pituitary-adrenal (HPA) axis, and COVID-19-related stress as an applied model.
What was found
The abstract provides a qualitative conceptual overview and reports no quantitative data, effect sizes, or numerical findings. It states that psychological stress triggers proinflammatory cellular mechanisms that foster low-grade systemic inflammation linked to CVD, and that physical activity reduces stress-induced proinflammation by improving allostatic regulation across the SAM, HPA, and immune systems.
Why it matters
It organizes the mechanistic links connecting chronic psychological stress, systemic inflammation, and cardiovascular risk, while highlighting regular exercise as an intervention capable of inducing neuroendocrine and immune cross-stressor resilience.
Limits
The paper is a non-systematic narrative review providing theoretical and mechanistic synthesis rather than original human data or quantitative meta-analysis. No study selection criteria, risk of bias assessments, sample sizes, or statistical metrics are reported in the abstract.
Cited by
- supports There is a large body of data supporting the fact that chronic stress causes physical harm to the body.