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Gene–environment interactions between HPA-axis genes and stressful life events in depression: a systematic review

Published online by Cambridge University Press:  20 May 2019

Caroline Normann  and
Henriette N. Buttenschøn
Caroline Normann*
Affiliation:
Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Denmark
Henriette N. Buttenschøn
Affiliation:
Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Denmark NIDO | Denmark, Regional Hospital West Jutland, Denmark
*
Author for correspondence: Caroline Normann, Email: carolinensoe@gmail.com
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Abstract

Objective:

Depression is a disorder caused by genetics and environmental factors. The aim of this study was to perform a review investigating the interaction between genetic variations located in genes involved in hypothalamus–pituitary–adrenal axis (HPA-axis) and stressful life events (SLEs) in depression.

Methods:

In this systematic review, we selected articles investigating the interaction between genes involved in the HPA-axis, such as Arginine Vasopressin (AVP), Angiotensin Converting Enzyme (ACE), Corticotrophin Releasing Hormone (CRH), Corticotrophin Releasing Hormone Receptor 1 (CRHR1), Corticotrophin Releasing Hormone Receptor 2 (CRHR2), FK506 binding protein (FKBP5), Nuclear Receptor subfamily 3 group C member 1 (NR3C1), Nuclear Receptor subfamily 3 group C member 2 (NR3C2), and SLE. The literature search was conducted using the Pubmed, Embase, and PsychINFO databases in adherence with the PRISMA guidelines.

Results:

The search yielded 48 potentially relevant studies, of which 40 were excluded following screening. Eight studies were included in the final review. A total of 97 single nucleotide polymorphisms (SNPs) were examined in the eight included studies. The most prevalent gene was FKBP5, and the best studied polymorphism was FKBP5:rs1360780. Two of the five studies reported significant gene–environment (G × E) interactions between rs1360780 and SLE. Overall, four studies reported significant G × E interactions between FKBP5, CRH, or CRHR1 and SLE, respectively. No significant G × E interactions were found for the remaining genes.

Conclusions:

Our results suggest that genetic variation in three genes in the HPA-axis possibly moderate the effects of SLEs in depression.

Keywords

depressiongene–environment interactionpolymorphismsingle nucleotidelife change eventsstresspsychological
Type
Review Article
Information
Acta Neuropsychiatrica , Volume 31 , Issue 4 , August 2019 , pp. 186 - 192
Copyright
© Scandinavian College of Neuropsychopharmacology 2019 

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References

Aborelius, L, Owens, MJ, Ploysky, PM and Nemeroff, CB (1999) The role of corticotropin-releasing factor in depression and anxiety disorders. Journal of Endocrinology 160(1), 1–12.CrossRefGoogle Scholar
Aguilera, G, Alexander, K, Luo, X and Akbasak, BS (1995) The renin angiotensin system and the stress response. Annals of the New York Academy of Sciences 29(771), 173–186.CrossRefGoogle Scholar
Armando, I, Volpi, S, Aguilera, G and Saavedra, JM (2007) Angiotensin II AT1 receptor blockade prevents the hypothalamic corticotropin-releasing factor response to isolation stress. Brain Research 92(9), 1142.Google Scholar
Assary, E, Vincent, JP, Keers, R and Pluess, M (2017) Gene-environment interaction and psychiatric disorders: review and future directions. Seminars in Cell and Developmental Biology 10(16), 1084–9521.Google Scholar
Beck, AT, , W.C., et al. Beck Depression Inventory. [cited 2018 February 8th] Available at https://www.bmc.org/sites/default/files/For_Medical_Professionals/Pediatric_Resources/Pediatrics__MA_Center_for_Sudden_Infant_Death_Syndrome__SIDS_/Beck-Depression-Inventory-BDI.pdfGoogle Scholar
Bigdeli, TB, Ripke, S, Peterson, RE, Trzaskowski, M, Bakanu, SA, Abdellaoui, A, et al. (2017) Genetic effects influencing risk for major depressive disorder in China and Europe. Translational Psychiatry 7(3), 1074.CrossRefGoogle ScholarPubMed
Binder, EB (2009) The role of FKBP5, a co-chaperone of the glucocorticoid receptor in the pathogenesis and therapy of affective and anxiety disorders. Psychoneuroendocrinology 34(1), 186–195.CrossRefGoogle ScholarPubMed
Bremmer, MA, Deeg, DJ, Beekman, AT, Pennix, BW, Lips, P and Hoogendijk, WJ (2007) Major depression in late life is associated with both hypo- and hypercortisolemia. Biological Psychiatry 62(5), 479–486.CrossRefGoogle ScholarPubMed
Briley, DA, Livengood, J and Derringer, J (2018) Behaviour genetic frameworks of causal reasoning for personality psychology. The European Journal of Personality 32(3), 202–220.CrossRefGoogle Scholar
Briley, DA, Livengood, J, Derringer, J, Tucker-Drob, EM, Fraley, RC and Roberts, BW (2019) Interpreting behavior genetic models: seven developmental processes to understand. Behavior Genetics 49(2): 196–210.CrossRefGoogle Scholar
Buttenschøn, HN, Krogh, J, Nielsen, MN, Kaerlev, L, Nordentoft, M and Mors, O (2017) Association analyses of depression and genes in the hypothalamus–pituitary–adrenal axis. Acta Neuropsychiatrica 29(1), 59–64.CrossRefGoogle ScholarPubMed
Coleman, J and Eley, TC (2018) Genome-wide gene-environment analyses of depression and reported lifetime traumatic experiences in UK Biobank. [cited 2018 Feb. 9th] Available at https://www.biorxiv.org/search/%252BGenome-wide%252Bgene-environment%252Banalyses%252Bof%252Bdepression%252Band%252Breported%252Blifetime%252Btraumatic%252Bexperiences%252Bin%252BUK%252BBiobankGoogle Scholar
Dempster, EL, Burcesu, I, Wigg, K, Kiss, E, Baji, I, Gadoros, J, et al. (2009) Further genetic evidence implicates the vasopressin system in childhood-onset mood disorders. The European Journal of Neuroscience 30(8), 1615–1619.CrossRefGoogle ScholarPubMed
Depression – Fact Sheet (2017) Available at http://www.who.int/mediacentre/factsheets/fs369/en/Google Scholar
Dunn, EC, Wiste, A, Radmanesh, F, Aimli, L, Gogarten, S, Sofer, T, et al. (2016) Genome-Wide Association Study (GWAS) and Genome-Wide Environment Interaction Study (GWEIS) of depressive symptoms in African American and Hispanic/Latina Women. Depression and Anxiety 33(4), 265–280.CrossRefGoogle ScholarPubMed
First Michael, B, Williams Janet, BW, Robert, L, Gibbon, M and Williams, J (1995) Structured Clinical Interview for DSM-IV (SCID-I) (User’s Guide and Interview) Research Version. New York Psychiatric Institute.CrossRefGoogle Scholar
Gillespie, CF, Phifer, J, Bradley, B and Ressler, KJ (2009) Risk and resilience: genetic and environmental influences on development of the stress response. Depression and Anxiety 26(11), 984–992.CrossRefGoogle Scholar
Hamilton, M (1967) Development of a rating scale for primary depressive illness. The British Journal of Clinical Psychology 6(4), 278–296.CrossRefGoogle ScholarPubMed
Hardeveld, F, Spijker, J, Peyrot, WJ, De Graaf, R, Hendriks, SM, Nolen, WA, et al. (2015) Glucocorticoid and mineralocorticoid receptor polymorphisms and recurrence of major depressive disorder. Journal of Neuroendocrinology 55, 154–163.CrossRefGoogle ScholarPubMed
Harkness, KL, Bruce, AE and Lumley, MN (2006) The role of childhood abuse and neglect in the sensitization to stressful life events in adolescent depression. Journal of Abnormal Child Psychology 115(4), 730–741.CrossRefGoogle ScholarPubMed
Heim, C and Nemeroff, C (2001) The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies. Biological Psychiatry 49(12), 1023–1039.CrossRefGoogle ScholarPubMed
Heim, C, Newport, D, Mletzko, T, Miller, AH and Nemeroff, CB (2008) The link between childhood trauma and depression: insights from HPA axis studies in humans. Psychoneuroendocrinology 33(6), 693–710.CrossRefGoogle ScholarPubMed
Heim, C, Plotsky, PM and Nemeroff, CB (2004) Importance of studying the contributions of early adverse experience to neurobiological findings in depression. Neuropsychopharmacology 29(4), 641–648.CrossRefGoogle ScholarPubMed
Ikeda, M, Shimasaki, A, Takahashi, A, Kondo, K, Saito, T, Kawase, K, et al. (2016) Genome-wide environment interaction between depressive state and stressful life events. The Journal of Clinical Psychiatry 77(1), 29–30.CrossRefGoogle ScholarPubMed
Ioannidis, JPA, Ntzani, EF, Trikalinos, TA and Contopulos-Ioadinnis, DG (2001) Replication validity of genetic association studies. Nature 29(4), 306–309.Google ScholarPubMed
Isaksson, J, Comasco, E, Åslund, C, Rehn, M, Tuvblad, C, Andershed, H, et al. (2016) Associations between the FKBP5 haplotype, exposure to violence and anxiety in females. Psychoneuroendocrinology 72(206), 196–204.CrossRefGoogle ScholarPubMed
Keller, MC (2013) Gene environment interaction studies have not properly controlled for potential confounders: the problem and the (simple) solution. Biological Psychiatry 75, 18–24.CrossRefGoogle Scholar
Lavebratt, C, Aberg, E, Sjöholm, LK and Forsell, Y (2010) Variations in FKBP5 and BDNF genes are suggestively associated with depression in a Swedish population-based cohort. The Journal of Affective Disorders 125(1–3), 249–255.CrossRefGoogle Scholar
Liu, Z, Liu, W, Yao, L, Yang, C, Xiao, L, Wan, Q, et al. (2013) Negative life events and corticotropin-releasing-hormone receptor1 gene in recurrent major depressive disorder. Scientific Reports 3, 1548.CrossRefGoogle ScholarPubMed
Loannidis, JPA (2005) Why most published research findings are false. Plos Medicine 2(8), 0696–0701.Google Scholar
Matosin, N, Halldorsdottir, T and Binder, EB (2018). Understanding the molecular mechanisms underpinning gene by environment interactions in psychiatric disorders: the FKBP5 model. Biological Psychiatry 83(10), 821–830.CrossRefGoogle ScholarPubMed
Mazurka, R, Wynne-Edwards, EK and Harkness, KL (2015) Stressful life events prior to depression onset and the cortisol response to stress in youth with first onset versus recurrent depression. Journal of Abnormal Child Psychology 44(6), 1173–1184.CrossRefGoogle Scholar
Meaney, S, Weaver, IC, et al. (2005) Preclinical studies also suggest that early-life stress affects HPA axis function in adulthood. The Journal of Affective Disorders 225, 422–428.Google Scholar
Monroe, M (1991) Diathesis-stress theories in the context of life stress research: implications for the depressive disorders. Psychological Bulletin 110(3), 406–425.CrossRefGoogle ScholarPubMed
Otowa, T, Kawamura, Y, Tsutsumi, A, Kawakami, N, Kan, C, Shimada, T, et al. (2016) The first pilot genome-wide gene-environment study of depression in the Japanese population. PloS One 11(8), e0160823.CrossRefGoogle ScholarPubMed
Pariante, CM and Lightman, S (2008) The HPA axis in major depression: classical theories and new developments. Cell Press 31(9), 464–468.Google ScholarPubMed
Pérez-Pérez, B, Cristóbal-Narváez, P, Sheinbaum, T, Kwapil, TR, Ballespí, S, Peña, E, et al. (2018) Interaction between FKBP5 variability and recent life events in the anxiety spectrum: evidence for the differential susceptibility model. PLoS One 13(2): e0193044.CrossRefGoogle ScholarPubMed
Peyrot, WJ, Milaneschi, YA, Abdellaoui, A, Sullivan, PF, Hottenga, JJ, Boomsma, DI, et al. (2014) Effect of polygenic risk scores on depression in childhood trauma. The British Journal of Psychiatry 205(2), 113–119.CrossRefGoogle ScholarPubMed
Reed, V, Franz, G, Pfister, H, Steiger, A, Sonntag, H, Trenkwalder, C, et al. (1998) To what degree does the Composite International Diagnostic Interview (CIDI) correctly identify DSM-IV disorders? Testing validity issues in a clinical sample. The International Journal of Methods in Psychiatric Research 7(3), 142–155.CrossRefGoogle Scholar
Rogers, J, Raveendran, M, Fawcett, GL, Fox, AS, Shelton, SE, Oler, JA, et al. (2013) CRHR1 genotypes, neural circuits and the diathesis for anxiety and depression. Molecular Psychiatry 18(6), 700–707.CrossRefGoogle ScholarPubMed
Sanchez, MM(2006) The impact of early adverse care on HPA axis development: nonhuman primate models. Hormones and Behavior 50(4), 623–631.CrossRefGoogle ScholarPubMed
Shimasaki, A, Kondo, K, Saito, T, Esaki, K, Otsuka, Y, Mano, K, et al. (2014) A genetic variant in 12q13, a possible risk factor for bipolar disorder, is associated with depressive state, accounting for stressful life events. PLoS One 9(12), e115135.CrossRefGoogle ScholarPubMed
Sullivan, PF, Neale, MC and Kendler, KS (2000) Genetic epidemiology of major depression: review and meta-analysis. The American Journal of Psychiatry 157(10), 1552–1562.CrossRefGoogle Scholar
Tabor, HK, Risch, NJ and Myers, RM (2002) Candidate-gene approaches for studying complex genetic traits: practical considerations. Nature Reviews Genetics 3(5), 391–397.CrossRefGoogle ScholarPubMed
Uher, R (2014) Gene–environment interactions in common mental disorders: an update and strategy for a genome-wide search. Social Psychiatry and Psychiatric Epidemiology 49(1), 3–14.CrossRefGoogle ScholarPubMed
Ulrike, E (2013) Enduring psychobiological effects of childhood adversity. Psychoneuroendocrinology 38(9), 1850–1857.Google Scholar
Van Bodegom, M, Homberg, JR and Henckens, MJAG (2017) Modulation of the hypothalamic-pituitary-adrenal axis by early life stress exposure. Frontiers in Cellular Neuroscience 19(11), 87.Google Scholar
Videbech, P and Rosenberg, R (2013) Klinisk Neuropsykiatri, Chapter 6. Vol. 2nd Edn. Denmark: FADLs forlag. p. 90.Google Scholar
Welch, V, Petticrew, M and Tugwell, P (2012) PRISMA-equity 2012 extension: reporting guidelines for systematic reviews with a focus on health equity. PLoS Medicine 9(10), e1001333.CrossRefGoogle ScholarPubMed
Wing, JK, Sartorius, N and Üstün, TB (1998) World Health Organization: Diagnosis and Clinical Measurement in Psychiatry. A Reference Manual for SCAN. England: Cambridge University Press, p. 148.CrossRefGoogle Scholar
World Health Organization (2017) Depression and Other Common Mental Disorders: Global Health Estimates. Geneva: World Health Organization. Available at http://www.who.int/iris/handle/10665/254610Google Scholar
Zimmermann, P, Bruckl, T., Nocon, A, Pfister, H, Binder, EB, Uhr, M, et al. (2011) Interaction of FKBP5 gene variants and adverse life events in predicting depression onset: results from a 10-year prospective community study. The American Journal of Psychiatry 168(10), 1107–1116.CrossRefGoogle ScholarPubMed