An interaction between a neuropeptide Y gene polymorphism and early adversity modulates endocrine stress responses.
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An interaction between a neuropeptide Y gene polymorphism and early adversity modulates endocrine stress responses. / Witt, Stephanie H; Buchmann, Arlette F; Blomeyer, Dorothea; Nieratschker, Vanessa; Treutlein, Jens; Esser, Günter; Schmidt, Martin H; Bidlingmaier, Martin; Wiedemann, Klaus; Rietschel, Marcella; Laucht, Manfred; Wüst, Stefan; Zimmermann, Ulrich S.
In: PSYCHONEUROENDOCRINO, Vol. 36, No. 7, 7, 2011, p. 1010-1020.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - An interaction between a neuropeptide Y gene polymorphism and early adversity modulates endocrine stress responses.
AU - Witt, Stephanie H
AU - Buchmann, Arlette F
AU - Blomeyer, Dorothea
AU - Nieratschker, Vanessa
AU - Treutlein, Jens
AU - Esser, Günter
AU - Schmidt, Martin H
AU - Bidlingmaier, Martin
AU - Wiedemann, Klaus
AU - Rietschel, Marcella
AU - Laucht, Manfred
AU - Wüst, Stefan
AU - Zimmermann, Ulrich S
PY - 2011
Y1 - 2011
N2 - Interindividual variability in the regulation of the human stress system accounts for a part of the individual's liability to stress-related diseases. These differences are influenced by environmental and genetic factors. Early childhood adversity is a well-studied environmental factor affecting an individual's stress response which has been shown to be modulated by gene-environment interaction (GxE). Neuropeptide Y (NPY) plays a role in stress regulation and genetic variation in NPY may influence stress responses. In this study, we analyzed the association of a common variant in the NPY gene promoter, rs16147, with cortisol and ACTH responses to acute psychosocial stress in young adults from the Mannheim Study of Children at Risk (MARS), an ongoing epidemiological cohort study following the outcome of early adversity from birth into adulthood. We found evidence of a GxE interaction between rs16147 and early adversity significantly affecting HPA axis responses to acute psychosocial stress. These findings suggest that the neurobiological mechanisms linking early adverse experience and later neuroendocrine stress regulation are modulated by a gene variant whose functional relevance is documented by increasing convergent evidence from in vitro, animal and human studies.
AB - Interindividual variability in the regulation of the human stress system accounts for a part of the individual's liability to stress-related diseases. These differences are influenced by environmental and genetic factors. Early childhood adversity is a well-studied environmental factor affecting an individual's stress response which has been shown to be modulated by gene-environment interaction (GxE). Neuropeptide Y (NPY) plays a role in stress regulation and genetic variation in NPY may influence stress responses. In this study, we analyzed the association of a common variant in the NPY gene promoter, rs16147, with cortisol and ACTH responses to acute psychosocial stress in young adults from the Mannheim Study of Children at Risk (MARS), an ongoing epidemiological cohort study following the outcome of early adversity from birth into adulthood. We found evidence of a GxE interaction between rs16147 and early adversity significantly affecting HPA axis responses to acute psychosocial stress. These findings suggest that the neurobiological mechanisms linking early adverse experience and later neuroendocrine stress regulation are modulated by a gene variant whose functional relevance is documented by increasing convergent evidence from in vitro, animal and human studies.
KW - Adult
KW - Humans
KW - Adolescent
KW - Young Adult
KW - Cohort Studies
KW - Child
KW - Longitudinal Studies
KW - Child, Preschool
KW - Infant
KW - Life Change Events
KW - Social Environment
KW - Endocrine System/metabolism/physiology
KW - Gene-Environment Interaction
KW - Hypothalamo-Hypophyseal System/metabolism/physiology
KW - Neuropeptide Y/genetics/physiology
KW - Pituitary-Adrenal System/metabolism/physiology
KW - Polymorphism, Genetic/physiology
KW - Stress, Psychological/genetics/physiopathology/psychology
KW - Adult
KW - Humans
KW - Adolescent
KW - Young Adult
KW - Cohort Studies
KW - Child
KW - Longitudinal Studies
KW - Child, Preschool
KW - Infant
KW - Life Change Events
KW - Social Environment
KW - Endocrine System/metabolism/physiology
KW - Gene-Environment Interaction
KW - Hypothalamo-Hypophyseal System/metabolism/physiology
KW - Neuropeptide Y/genetics/physiology
KW - Pituitary-Adrenal System/metabolism/physiology
KW - Polymorphism, Genetic/physiology
KW - Stress, Psychological/genetics/physiopathology/psychology
M3 - SCORING: Journal article
VL - 36
SP - 1010
EP - 1020
JO - PSYCHONEUROENDOCRINO
JF - PSYCHONEUROENDOCRINO
SN - 0306-4530
IS - 7
M1 - 7
ER -
