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Joint Impact of Early Life Adversity and Comt Val158Met (rs4680) Genotypes on the Adult Cortisol Response to Psychological Stress

Bibliographic Data

ID19307657
AuthorsWilliam R Lovallo (0000-0002-8489-3509, The University of Texas at San Antonio Health Science Center, corresponding author), Mary-Anne Enoch (Norman Regional Hospital), Kristen H Sorocco (0000-0002-8457-9632, Norman Regional Hospital), Andrea S Vincent (0000-0001-9693-5764, Norman Regional Hospital), Ashley Acheson (0000-0002-3843-5726, Norman Regional Hospital), Andrew J Cohoon (Norman Regional Hospital), Colin Hodgkinson (0000-0002-5365-8119, Norman Regional Hospital), Colin A Hodgkinson, David Goldman (0000-0002-1724-5405, Norman Regional Hospital)
Year2017
Volume79
Issue6
Pages631-637
Publication date2017-07-01
Open AccessNo
TypeARTICLE
VenuePsychosomatic Medicine (JOURNAL)
Journal identifiersISSN: 0033-3174 • E-ISSN: 1534-7796
PublisherOvid Technologies (Wolters Kluwer Health) (PUBLISHER)
DOI10.1097/psy.0000000000000481
PMID28452825
OpenAlexW2608252078
LanguageEN
Citations received2
References cited65

OBJECTIVE: Exposure to stress during critical periods of development can diminish stress reactivity by the hypothalamic-pituitary-adrenocortical axis. Genetic characteristics may further modify this effect of early adversity, leading to a gene by environment (G × E) interaction on stress reactivity in adulthood. Val-allele carriers of a common polymorphism of the COMT gene (Val158Met, rs4680) have rapid removal of catecholamines in the prefrontal cortex, limbic system, and reward centers. Carriers of the Val and Met alleles may therefore respond differently to the environment and differ in the long-term impact of exposure to early life adversity (ELA). METHODS: We measured saliva cortisol reactivity to public speaking and mental arithmetic stress in 252 healthy young adults exposed to low, medium, and high levels of ELA and who were genotyped for the Val158Met polymorphism. RESULTS: Cortisol responses showed a G × E interaction (F(4,243) = 2.78, p = .028); simple effects tests showed that Met/Met carriers had progressively smaller cortisol responses with greater levels of ELA. In comparison, Val/Val homozygotes had blunted responses that did not vary with ELA exposure. CONCLUSIONS: Met/Met homozygotes seem sensitive to stressful events in childhood and adolescence, leading to environmental programming of the stress axis. Glucocorticoid responsivity may represent a common pathway revealing targeted genetic vulnerabilities to the long-term effects of early life stress. The results suggest that further G × E studies of ELA are warranted in relation to health behaviors and health outcomes in adulthood

Allele · Biology · Developmental psychology · Gene · Glucocorticoid · Hormone · Hypothalamic–pituitary–adrenal axis · Maternal deprivation · Polymorphism (computer science) · rs4680 · Stressor · Adrenal Hormones and Disorders · Clinical Psychology · Endocrinology · Genetics · Internal Medicine · Medicine · Neurotransmitter Receptor Influence on Behavior · Psychology · Stress Responses and Cortisol

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Citations per year0.5
Citation span2022 - 2025 (4)
Highly citedNo

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