Interactive Effects of Corticotropin Releasing Hormone Receptor 1, Serotonin Transporter Linked Polymorphic Region, and Child Maltreatment on Diurnal Cortisol Regulation and Internalizing Symptomatology  

Oleh:

Oshri, Assaf ; Cicchetti, Dante ; Rogosch, Fred A.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Development and Psychopathology vol. 23 no. 4 (Nov. 2011), page 1125-1138.
Topik: Allostatic Load; Diurnal Cortisol Regulation; Depressive Symptoms; Maltreatment; Symptoms
Fulltext: Interactive effects of corticotropin releasing hormone receptor 1, serotonin transporter linked polymorphic region, and child maltreatment.pdf (282.84KB)

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Perpustakaan Pusat (Semanggi) Nomor Panggil: DD21.21 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Within an allostatic load framework, the effect of Gene × Environment (G × E) interactions on diurnal cortisol regulation and internalizing symptomatology were investigated. Variation in the corticotropin releasing hormone receptor 1 (CRHR1) TAT haplotype and serotonin transporter linked polymorphic region (5-HTTLPR) was determined in a sample of maltreated (n = 238, 21.4% with early physical and sexual abuse) and nonmaltreated (n = 255) children (M age = 10.08) participating in a summer research camp. Internalizing and depressive symptoms were assessed by other and self-report. G × E effects for CRHR1 and maltreatment and early abuse on diurnal cortisol regulation were observed; CRHR1 variation was related to cortisol dysregulation only among maltreated children. Early abuse and high internalizing symptoms also interacted to predict atypical diurnal cortisol regulation. The interaction of CRHR1, 5-HTTLPR, and child maltreatment (G × G × E) identified a subgroup of maltreated children with high internalizing symptoms who shared the same combination of the two genes. The findings support an allostatic load perspective on the effects of the chronic stress associated with child maltreatment on cortisol regulation and internalizing symptomatology as moderated by genetic variation.

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