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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
PubMed

Insights

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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