Vulnerability to depression: what is the role of stress genes in gene × environment interaction?
Open accessAbstract
Vulnerability to depression has been linked to the interaction of genetic predisposition with stressful life events. This review considers the associations between serotonergic and hypothalamic–pituitary–adrenal (HPA) systems. We follow the standpoint of a previous Editorial Review (Bhagwagar & Cowen, Psychological Medicine 2008, 38, 307–313) and consider another possible mechanism of vulnerability to depressive disorder, that is we suggest that the gene×environment interaction involves complex participation of serotonergic genes modulating response to stress through the HPA system.
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One proposed mechanism of early life stress interactions with serotonergic genes such as 5-HTTLPR involves modulation of stress responses through HPA axis activity.
“One proposed mechanism of ELS interactions with serotonergic genes such as 5-HTTLPR involves modulation of stress responses through HPA axis activity (El Hage et al. 2009).”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as El Hage et al. 2009
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Kendler, K. S., Thornton, L. M., & Gardner, C. O. (2001) · American Journal of Psychiatry · doi:10.1176/appi.ajp.158.4.582 · Cited by 480 · see citing works
Morning cortisol as a risk factor for subsequent major depressive disorder in adult women
Harris, T. O., Borsanyi, S., Messari, S., Stanford, K., Cleary, S. E., Shiers, H. M., Brown, G. W., & Herbert, J. (2000) · British Journal of Psychiatry · doi:10.1192/bjp.177.6.505 · Cited by 220 · see citing works
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- Canli T, Qiu M, Omura K, Congdon E, Haas BW, Amin Z (2006). Neural correlates of epigenesis. Proceedings of the National Academy of Sciences of the United States of America 103 , 16033-16038.
- DeRijk RH, Wust S, Meijer OC, Zennaro MC, Federenko IS, Hellhammer DH, Giacchetti G, Vreugdenhil E, Zitman FG, de Kloet ER (2006). A common polymorphism in the mineralocorticoid receptor modulates stress responsiveness. Journal of Clinical Endocrinology and Metabolism 91 , 5083-5089.
- Levinson DF (2006). The genetics of depression: a review. Biological Psychiatry 60 , 84-92.
- Mannie ZN, Harmer CJ, Cowen PJ (2007). Increased waking salivary cortisol levels in young people at familial risk of depression. American Journal of Psychiatry 164 , 617-621.
- Pariante CM (2006). The glucocorticoid receptor: part of the solution or part of the problem? Journal of Psychopharmacology 20 , 79-84.
- Stutzmann GE, LeDoux JE (1999). GABAergic antagonists block the inhibitory effects of serotonin in the lateral amygdala: a mechanism for modulation of sensory inputs related to fear conditioning. Journal of Neuroscience 19 , RC8.
- Tjurmina OA, Armando I, Saavedra JM, Li Q, Murphy DL (2004). Life-long serotonin reuptake deficiency results in complex alterations in adrenomedullary responses to stress. Annals of the New York Academy of Sciences 1018 , 99-104.
- Uher R, McGuffin P (2007). The moderation by the serotonin transporter gene of environmental adversity in the aetiology of mental illness: review and methodological analysis. Molecular Psychiatry 13 , 131-146.
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Stress, serotonin, and hippocampal neurogenesis in relation to depression and antidepressant effects
Mahar, I., Bambico, F. R., Mechawar, N., & Nobrega, J. N. (2014) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2013.11.009 · Cited by 694 · see citing works
Gene–environment interactions: early life stress and risk for depressive and anxiety disorders
Nugent, N. R., Tyrka, A. R., Carpenter, L. L., & Price, L. H. (2011) · Psychopharmacology · doi:10.1007/s00213-010-2151-x · Cited by 269 · see citing works
“Moreover, there is strong evidence from human and animal studies that the stress response is modulated in part by serotonergic neurotransmission (for reviews, see El Hage et al. 2009; Holmes 2008).”
BackgroundMechanisms of antidepressant resistance
El-Hage, W., Leman, S., Camus, V., & Belzung, C. (2013) · Frontiers in Pharmacology · doi:10.3389/fphar.2013.00146 · Cited by 111 · see citing works
Self-citationShao, J., Wei, Y., & Wei, X. (2022) · Food Research International · doi:10.1016/j.foodres.2022.111540 · Cited by 58 · see citing works
Yrondi, A., Aouizerate, B., Bennabi, D., Richieri, R., D'Amato, T., Bellivier, F., Bougerol, T., Horn, M., Camus, V., Courtet, P., et al. (2020) · Depression and Anxiety · doi:10.1002/da.22997 · Cited by 37 · see citing works
Self-citation
- Authors
- El Hage, W., Powell, J. F., & Surguladze, S. A.
- Affiliations
- King's College London (GB)
- ORCID
- Powell, J. F.
- Venue
- Psychological Medicine
- Publisher
- Cambridge University Press (CUP)
- Published
- 2009-02-12
- Volume
- 39
- Issue
- 9
- Pages
- 1407-1411
- ISSN
- 0033-2917 (ISSN-L)
- 1469-8978
- OpenAlex
- W2116991563
- Cited by
- 59
- References
- 2
- Citations by year
- 2023: 1 · 2022: 2 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 2 · 2015: 5 · 2014: 5 · 2013: 9 · 2012: 11
- FWCI
- 3.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Psychological Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Servier
- H. Lundbeck A/S
- Cilag
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- depression vulnerability, gene-environment interaction, stress response genes, serotonergic genes, hypothalamic-pituitary-adrenal axis, stress response, genetic susceptibility, life events, depressive disorders
- MeSH terms
- Alleles, Amygdala, Arousal, Major Depressive Disorder, Epistasis, Genetic, Gene Expression Regulation, Gyrus Cinguli, Humans, Hypothalamo-Hypophyseal System, Life Change Events, Phenotype, Pituitary-Adrenal System, Polymorphism, Genetic, Receptors, Glucocorticoid, Social Environment, Receptors, Mineralocorticoid, Genetic Predisposition to Disease, Serotonin Plasma Membrane Transport Proteins
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