Children and adolescents exposed to severe stressors exhibit poorer health across the lifespan. However, decades of research evaluating the Stress-Buffering model suggests that social support can attenuate stressors' negative impacts. Psychoneuroimmunology research in this area has shifted from asking whether support buffers stress to when and why support would succeed (or fail) to confer protection. This article takes a lifecourse perspective and proposes that timing of support may shape support's protective value by defining the type of protection that is provided and its operating mechanisms. Specifically, it considers three temporal scenarios: support that occurs during, after, or before stressor exposure. When support intervenes at the same developmental stage as the stressor (concurrent support), buffering effects occur wherein support prevents the development of intermediary mechanisms that reflect or increase disease risk; when support is present at a developmental stage before stressor exposure (prior support), banking effects occur such that support intervenes indirectly by fortifying the individual with resilience-promoting characteristics that in turn prevents the development of intermediary mechanisms; finally, when support arrives at a developmental stage after stressor exposure (later support), counteracting effects occur such that support offsets the impacts of intermediary mechanisms on diseases. It further posits that a match between timing of support and the linkage of interest (e.g., the stressor-mechanism path vs. the mechanism-disease path) is necessary for successful protection. The present paper discusses these postulations, reviews nascent evidence, and proposes future directions.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490906 | PMC |
http://dx.doi.org/10.1016/j.bbih.2024.100876 | DOI Listing |
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