Year: 2019
Type: article
Abstract: The significant contribution of stress to the development of disease is unequivocal. Often labeled as the silent or proxy killer, chronic stress is a major underlying origin of the top leading causes of death, globally. 1 The magnitude and ways that stress affects individuals and populations is far reaching with impacts that can be seen as early as during the embryonic stage spanning into adulthood. 2 Despite the concerted effort from cross-disciplinary research to understand the stress-related underpinnings of disease, explanatory mechanisms to inform individualized intervention targets remain an enigma. While it is clear a link between a wide range of psychological to objective biological measures of stress and chronic disease exists, the mechanistic explanation of how stress over time leads to end-organ damage is unclear. This stems from several roadblocks rooted in: (1) ambiguous definitions of stress; (2) the inability to adequately measure stress in its naturally occurring state; (3) the inability to discern measures of the stress response given the extreme heterogeneity by inter and intraindividual characteristics; and (4) lack of knowledge on the interplay between subjective and objective measures of stress. Further, the emphasis on aggregate versus individual level information, and binning of symptoms into rigid diagnostic categories has undoubtedly hampered progress in understanding individual trajectories towards end-organ damage.
Source: npj Digital Medicine
Authors: Sarah M. Goodday, Stephen Friend
Institution: University of Oxford
Language: English
Subfield: Behavioral Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,680
OpenAlex ID: W2966772620