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Published on: June 19, 2019
The stress-coping (mis)match hypothesis for nature × nurture interactions
1Donders Institute for Brain, Cognition, and Behaviour, Centre for Neuroscience, Department of Cognitive Neuroscience, Radboud University Nijmegen Medical Centre, Geert Grooteplein 21 (route 126), 6525 EZ Nijmegen, The Netherlands. j.homberg@cns.umcn.nl
Nature and nurture shape stress-related disorders. The stress-coping (mis)match (SCM) hypothesis suggests coping responses are adaptive when matching current stress, but maladaptive when mismatched.
Area of Science:
- Psychology
- Neuroscience
- Genetics
Background:
- Stress-related disorders like depression result from complex nature-nurture interactions.
- Current research often assumes genotypic stress-sensitivity and exposure inevitably cause maladaptive coping and disorders.
- However, stress-coping responses can also be adaptive.
Purpose of the Study:
- To elaborate the 'environment' mismatch hypothesis into the stress-coping (mis)match (SCM) hypothesis.
- To explain how nature x age-dependent nurture interactions program stress-coping responses.
- To discuss the adaptive or maladaptive nature of these responses based on environmental conditions.
Main Methods:
- Elaboration of the 'environment' mismatch hypothesis.
- Application of the SCM hypothesis to explain stress-coping (mis)matches.
- Discussion of the serotonin transporter promoter polymorphism as a model for nature x nurture interactions.
Main Results:
- Stress-coping responses are adaptive when they match current environmental stress conditions.
- These responses become maladaptive when they mismatch current stress conditions, potentially leading to agitation.
- The SCM hypothesis provides a framework for understanding these dynamics.
Conclusions:
- The SCM hypothesis offers a new perspective on stress-related disorders, moving beyond simple gene-environment interaction models.
- Understanding the match or mismatch between programmed coping and current stress is crucial.
- The hypothesis has implications for the prefrontal-amygdala circuit and therapeutic interventions for stress-related disorders.
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