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FKBP5 and resistant attachment predict cortisol reactivity in infants: gene-environment interaction
Maartje P C M Luijk1, Fleur P Velders, Anne Tharner
1Centre for Child and Family Studies, Leiden University, The Netherlands.
Psychoneuroendocrinology
|June 16, 2010
Summary
Infant attachment quality and FKBP5 gene variants interact to affect stress responses. Insecure-resistant attachment combined with specific FKBP5 gene variations increases cortisol reactivity, highlighting gene-environment interactions in early development.
Area of Science:
- Developmental Psychology
- Behavioral Genetics
- Neuroendocrinology
Background:
- Parent-infant attachment quality significantly impacts infant physiological stress regulation.
- The hypothalamic-pituitary-adrenal (HPA) axis, a key stress regulatory system, is influenced by genetic factors.
- Specific single nucleotide polymorphisms (SNPs) in HPA-axis related genes are potential candidates for influencing stress reactivity.
Purpose of the Study:
- To investigate the relationship between the quality of parent-infant attachment and HPA-axis related SNPs on cortisol reactivity during the Strange Situation Procedure (SSP).
- To examine gene-environment interactions, specifically between attachment security and HPA-axis genetic variations, in predicting infant stress responses.
Main Methods:
- Assessed parent-infant attachment quality using the Strange Situation Procedure (SSP).
- Genotyped infants for HPA-axis related SNPs, including BclI, TthIIII, GR-9β, N363S, ER22/23EK, and FKBP5 (rs1360780).
- Measured salivary cortisol reactivity in response to the stressful SSP in a large, population-based sample.
Main Results:
- The FKBP5 rs1360780 SNP, but not GR haplotype, was significantly associated with cortisol reactivity.
- A significant interaction effect was observed between insecure-resistant attachment and the FKBP5 rs1360780 SNP.
- Infants with one or two T-alleles of FKBP5 rs1360780 and insecure-resistant attachment exhibited a 'double-risk' for heightened cortisol reactivity.
Conclusions:
- Parent-infant attachment quality and genetic predispositions interact to shape infant stress regulation.
- Insecure-resistant attachment combined with specific FKBP5 genetic variants confers heightened vulnerability to stress.
- Findings underscore the importance of gene-environment interactions in understanding individual differences in HPA-axis function and stress-related outcomes.
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