Abstract
Original language | English |
---|---|
Article number | 808 |
Journal | Front. Psychiatry |
Volume | 10 |
DOIs | |
Publication status | Published - 2019 |
Keywords
- childhood trauma
- epigenetic association studies
- mental health
- stress disorders
- the hypothalamic-pituitary-adrenal axis (HPA)
- BDNF gene
- childhood adversity
- CRISPR-CAS9 system
- DNA methylation
- DNA modification
- epigenetics
- FKBP5 gene
- gene
- genetic association
- genetic variability
- HTR gene
- human
- hypothalamus hypophysis adrenal system
- MAOA gene
- nonhuman
- NR3C1 gene
- phenotype
- phenotypic variation
- posttraumatic stress disorder
- Review
- sex difference
- single nucleotide polymorphism
- SLC6A4 gene
- variable number of tandem repeat
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Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma : Frontiers in Psychiatry. / Jiang, S.; Postovit, L.; Cattaneo, A.; Binder, E.B.; Aitchison, K.J.
In: Front. Psychiatry, Vol. 10, 808, 2019.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma
T2 - Frontiers in Psychiatry
AU - Jiang, S.
AU - Postovit, L.
AU - Cattaneo, A.
AU - Binder, E.B.
AU - Aitchison, K.J.
N1 - Export Date: 10 February 2020 Correspondence Address: Aitchison, K.J.; Department of Medical Genetics, University of Alberta, Edmonton, Canada; email: kaitchis@ualberta.ca References: Hornor, G., Childhood trauma exposure and toxic stress: what the pnp needs to know (2015) J Pediatr Health Car, 29 (2); Bucci, M., Marques, S.S., Oh, D., Harris, N.B., Toxic stress in children and adolescents (2016) Adv Pediatr, 63 (1); Koenen, K.C., Ratanatharathorn, A., Ng, L., McLaughlin, K.A., Bromet, E.J., Stein, D.J., Posttraumatic stress disorder in the world mental health Surveys (2017) Psychol Med, 47 (13); Danese, A., Moffitt, T.E., Harrington, H., Milne, B.J., Polanczyk, G., Pariante, C.M., Adverse childhood experiences and adult risk factors for age-related disease: depression, inflammation, and clustering of metabolic risk markers (2009) Arch Pediatr Adolesc Med, 163 (12); Brown, D.W., Anda, R.F., Tiemeier, H., Felitti, V.J., Edwards, V.J., Croft, J.B., Adverse childhood experiences and the risk of premature mortality (2009) Am J Prev Med, 37 (5); 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PY - 2019
Y1 - 2019
N2 - Adverse childhood experiences (ACEs) may be referred to by other terms (e.g., early life adversity or stress and childhood trauma) and have a lifelong impact on mental and physical health. For example, childhood trauma has been associated with posttraumatic stress disorder (PTSD), anxiety, depression, bipolar disorder, diabetes, and cardiovascular disease. The heritability of ACE-related phenotypes such as PTSD, depression, and resilience is low to moderate, and, moreover, is very variable for a given phenotype, which implies that gene by environment interactions (such as through epigenetic modifications) may be involved in the onset of these phenotypes. Currently, there is increasing interest in the investigation of epigenetic contributions to ACE-induced differential health outcomes. Although there are a number of studies in this field, there are still research gaps. In this review, the basic concepts of epigenetic modifications (such as methylation) and the function of the hypothalamic-pituitary-adrenal (HPA) axis in the stress response are outlined. Examples of specific genes undergoing methylation in association with ACE-induced differential health outcomes are provided. Limitations in this field, e.g., uncertain clinical diagnosis, conceptual inconsistencies, and technical drawbacks, are reviewed, with suggestions for advances using new technologies and novel research directions. We thereby provide a platform on which the field of ACE-induced phenotypes in mental health may build. © Copyright © 2019 Jiang, Postovit, Cattaneo, Binder and Aitchison.
AB - Adverse childhood experiences (ACEs) may be referred to by other terms (e.g., early life adversity or stress and childhood trauma) and have a lifelong impact on mental and physical health. For example, childhood trauma has been associated with posttraumatic stress disorder (PTSD), anxiety, depression, bipolar disorder, diabetes, and cardiovascular disease. The heritability of ACE-related phenotypes such as PTSD, depression, and resilience is low to moderate, and, moreover, is very variable for a given phenotype, which implies that gene by environment interactions (such as through epigenetic modifications) may be involved in the onset of these phenotypes. Currently, there is increasing interest in the investigation of epigenetic contributions to ACE-induced differential health outcomes. Although there are a number of studies in this field, there are still research gaps. In this review, the basic concepts of epigenetic modifications (such as methylation) and the function of the hypothalamic-pituitary-adrenal (HPA) axis in the stress response are outlined. Examples of specific genes undergoing methylation in association with ACE-induced differential health outcomes are provided. Limitations in this field, e.g., uncertain clinical diagnosis, conceptual inconsistencies, and technical drawbacks, are reviewed, with suggestions for advances using new technologies and novel research directions. We thereby provide a platform on which the field of ACE-induced phenotypes in mental health may build. © Copyright © 2019 Jiang, Postovit, Cattaneo, Binder and Aitchison.
KW - childhood trauma
KW - epigenetic association studies
KW - mental health
KW - stress disorders
KW - the hypothalamic-pituitary-adrenal axis (HPA)
KW - BDNF gene
KW - childhood adversity
KW - CRISPR-CAS9 system
KW - DNA methylation
KW - DNA modification
KW - epigenetics
KW - FKBP5 gene
KW - gene
KW - genetic association
KW - genetic variability
KW - HTR gene
KW - human
KW - hypothalamus hypophysis adrenal system
KW - MAOA gene
KW - nonhuman
KW - NR3C1 gene
KW - phenotype
KW - phenotypic variation
KW - posttraumatic stress disorder
KW - Review
KW - sex difference
KW - single nucleotide polymorphism
KW - SLC6A4 gene
KW - variable number of tandem repeat
U2 - 10.3389/fpsyt.2019.00808
DO - 10.3389/fpsyt.2019.00808
M3 - Article
VL - 10
JO - Front. Psychiatry
JF - Front. Psychiatry
SN - 1664-0640
M1 - 808
ER -