Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators.
Level 5 - mechanism / opinion, no new human data
Narrative review and conceptual framework paper with no primary data
PubMed 18282566 · doi:10.1016/j.ejphar.2007.11.071
What was done
This narrative review synthesized the neurobiological mechanisms of acute versus chronic stress. It evaluated how stress mediators—including glucocorticoids, excitatory amino acids, brain-derived neurotrophic factor (BDNF), polysialated neural cell adhesion molecule (PSA-NCAM), and tissue plasminogen activator (tPA)—drive neural remodeling in the hippocampus, prefrontal cortex, and amygdala, and assessed how these changes connect to allostatic overload, psychiatric illness, and behavioral interventions.
What was found
The abstract reports no numerical data. It notes that acute stress drives adaptive survival responses across neural, cardiovascular, autonomic, immune, and metabolic systems, whereas chronic stress dysregulates these systems. Stress-induced morphological and chemical changes in the hippocampus, prefrontal cortex, and amygdala are described as largely reversible after weeks of stress, though whether months or years of stress cause irreversible changes remains unestablished.
Why it matters
The paper outlines the conceptual model of allostatic overload, framing stress-related brain remodeling as a target for lifestyle interventions like physical activity and social support alongside pharmacotherapy.
Limits
The abstract describes a narrative review with no primary empirical data, sample sizes, or systematic review methodology. Long-term irreversibility of human brain changes from multi-year stress remains unknown based on the provided text.
Cited by
- supports There is a large body of data supporting the fact that chronic stress causes physical harm to the body.