Gene-environment interaction and psychiatric disorders: Review and future directions

Seminars in Cell and Developmental Biology

Volumn 77, Issue , 2018, Pages 133-143

  Assary, Elham ^a   Vincent, John Paul ^a   Keers, Robert ^a   Pluess, Michael ^a  

^a QUEEN MARY UNIVERSITY OF LONDON   (United Kingdom)

Author keywords

Diathesis Stress; Differential; Gene Environment interaction; Genetics; Psychiatry; Susceptibility

Indexed keywords

AMINE OXIDASE (FLAVIN CONTAINING); CATECHOL METHYLTRANSFERASE; COMT PROTEIN, HUMAN; DOPAMINE 4 RECEPTOR; DRD4 PROTEIN, HUMAN; MONOAMINE OXIDASE A, HUMAN; SEROTONIN TRANSPORTER; SLC6A4 PROTEIN, HUMAN;

ANTISOCIAL PERSONALITY DISORDER; ATTENTION DEFICIT DISORDER; DEPRESSION; ENVIRONMENT; GENETIC PREDISPOSITION; GENETICS; GENOTYPE ENVIRONMENT INTERACTION; HUMAN; MENTAL DISEASE; MENTAL STRESS; PSYCHOLOGY; SCHIZOPHRENIA;

ANTISOCIAL PERSONALITY DISORDER; ATTENTION DEFICIT DISORDER WITH HYPERACTIVITY; CATECHOL O-METHYLTRANSFERASE; DEPRESSION; ENVIRONMENT; GENE-ENVIRONMENT INTERACTION; GENETIC PREDISPOSITION TO DISEASE; HUMANS; MENTAL DISORDERS; MONOAMINE OXIDASE; RECEPTORS, DOPAMINE D4; SCHIZOPHRENIA; SEROTONIN PLASMA MEMBRANE TRANSPORT PROTEINS; STRESS, PSYCHOLOGICAL;

EID: 85031739644     PISSN: 10849521     EISSN: 10963634     Source Type: Journal    
DOI: 10.1016/j.semcdb.2017.10.016     Document Type: Review

References (155)

1. Collins, P.Y., et al. Grand challenges in global mental health. Nature 475:7354 (2011), 27–30.
2. Organization, W.H, The Global Burden of Disease: 2004 Update, in The Global Burden of Disease: 2004 Update. 2008, World Health Organization.
3. Teicher, M.H., Samson, J.A., Childhood maltreatment and psychopathology: a case for ecophenotypic variants as clinically and neurobiologically distinct subtypes. Am. J. Psychiatry 170:10 (2013), 1114–1153.
4. Battle, C.L., et al. Childhood maltreatment associated with adult personality disorders: findings from the Collaborative Longitudinal Personality Disorders Study. J. Pers. Disord. 18:2 (2004), 193–211.
5. Nanni, V., Uher, R., Danese, A., Childhood maltreatment predicts unfavorable course of illness and treatment outcome in depression: a meta-analysis. Am. J. Psychiatry 169:2 (2012), 141–151.
6. Plomin, R., Owen, M.J., McGuffin, P., The genetic basis of complex human behaviors. Science 264:5166 (1994), 1733–1739.
7. Sullivan, P.F., Neale, M.C., Kendler, K.S., Genetic epidemiology of major depression: review and meta-analysis. Am. J. Psychiatry 157:10 (2000), 1552–1562.
8. Lichtenstein, P., et al. Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a population-based study. Lancet 373:9659 (2009), 234–239.
9. Sullivan, P.F., Kendler, K.S., Neale, M.C., Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Arch. Gen. Psychiatry 60:12 (2003), 1187–1192.
10. McGuffin, P., et al. The heritability of bipolar affective disorder and the genetic relationship to unipolar depression. Arch. Gen. Psychiatry 60:5 (2003), 497–502.
11. Bertelsen, A., Harvald, B., Hauge, M., A Danish twin study of manic-depressive disorders. Br. J. Psychiatry, 130(4), 1977, 330.
12. Smoller, J.W., Finn, C.T., Family, twin, and adoption studies of bipolar disorder. Am. J. Med. Genet. C Semin. Med. Genet. 123c:1 (2003), 48–58.
13. Kendler, K.S., Eaves, L.J., Models for the joint effect of genotype and environment on liability to psychiatric illness. Am. J. Psychiatry, 1986.
14. Kendler, K.S., et al. Stressful life events: genetic liability, and onset of an episode of major depression in women. Am. J. Psychiatry 152:6 (1995), 833–842.
15. Caspi, A., et al. Role of genotype in the cycle of violence in maltreated children. Science 297:5582 (2002), 851–854.
16. Kessler, R.C., et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: results from the national comorbidity survey. Arch. Gen. Psychiatry 51:1 (1994), 8–19.
17. Alemany, S., et al. Childhood abuse: the BDNF-Val66Met polymorphism and adult psychotic-like experiences. Br. J. Psychiatry 199:1 (2011), 38–42.
18. Hosang, G.M., et al. Interaction between stress and the BDNF Val66Met polymorphism in depression: a systematic review and meta-analysis. BMC Med., 2014, 7.
19. Hosang, G.M., et al. Stressful life events and the brain-derived neurotrophic factor gene in bipolar disorder. J. Affect. Disord. 125:1–3 (2010), 345–349.
20. Heils, A., et al. Functional promoter and polyadenylation site mapping of the human serotonin (5-HT) transporter gene. J. Neural Trans. Gen. Sec. JNT 102:3 (1995), 247–254.
21. Lesch, K.-P., et al. Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science, 274(5292), 1996, 1527.
22. Caspi, A., et al. Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science 301:5631 (2003), 386–389.
23. Eley, T.C., et al. Gene-environment interaction analysis of serotonin system markers with adolescent depression. Mol. Psychiatry 9:10 (2004), 908–915.
24. Wilhelm, K., et al. Life events, first depression onset and the serotonin transporter gene. Br. J. Psychiatry 188 (2006), 210–215.
25. Cervilla, J.A., et al. The risk for depression conferred by stressful life events is modified by variation at the serotonin transporter 5HTTLPR genotype: evidence from the Spanish PREDICT-Gene cohort. Mol. Psychiatry 12:8 (2007), 748–755.
26. Gillespie, N.A., et al. The relationship between stressful life events: the serotonin transporter (5-HTTLPR) genotype and major depression. Psychol. Med. 35:01 (2005), 101–111.
27. Surtees, P.G., et al. Social adversity: the serotonin transporter (5-HTTLPR) polymorphism and major depressive disorder. Biol. Psychiatry 59:3 (2006), 224–229.
28. Karg, K., et al. The serotonin transporter promoter variant (5-HTTLPR), stress, and depression meta-analysis revisited: evidence of genetic moderation. Arch. Gen. Psychiatry 68:5 (2011), 444–454.
29. Sharpley, C.F., et al. An update on the interaction between the serotonin transporter promoter variant (5-HTTLPR), stress and depression, plus an exploration of non-confirming findings. Behav. Brain Res. 273 (2014), 89–105.
30. Uher, R., McGuffin, P., The moderation by the serotonin transporter gene of environmental adversity in the etiology of depression: 2009 update. Mol. Psychiatry 15:1 (2010), 18–22.
31. Risch, N., et al. Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis. JAMA 301:23 (2009), 2462–2471.
32. Munafò, M.R., et al. Gene × Environment interactions at the serotonin transporter locus. Biol. Psychiatry 65:3 (2009), 211–219.
33. Culverhouse, R.C., et al. Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression. Mol. Psychiatry, 2017.
34. Moffitt, T.E., Caspi, A., Bias in a protocol for a meta-analysis of 5-HTTLPR, stress, and depression. BMC Psychiatry, 14(1), 2014, 179.
35. Levy, E.R., et al. Localization of human monoamine oxidase-A gene to Xp11. 23-11.4 by in situ hybridization: implications for norrie disease. Genomics 5:2 (1989), 368–370.
36. Shih, J., Chen, K., Ridd, M., Monoamine oxidase: from genes to behavior. Annu. Rev. Neurosci. 22:1 (1999), 197–217.
37. Sabol, S.Z., Hu, S., Hamer, D., A functional polymorphism in the monoamine oxidase A gene promoter. Hum. Genet. 103:3 (1998), 273–279.
38. Deckert, J., et al. Excess of high activity monoamine oxidase A gene promoter alleles in female patients with panic disorder. Hum. Mol. Genet. 8:4 (1999), 621–624.
39. Frazzetto, G.et al., Early trauma and increased risk for physical aggression during adulthood: the moderating role of MAOA genotype. PLoS One, 2(5), 2007, e486.
40. Foley, D.L., et al. Childhood adversity: monoamine oxidase a genotype, and risk for conduct disorder. Arch. Gen. Psychiatry 61:7 (2004), 738–744.
41. Kim-Cohen, J., et al. MAOA, maltreatment, and gene-environment interaction predicting children's mental health: new evidence and a meta-analysis. Mol. Psychiatry 11:10 (2006), 903–913.
42. Haberstick, B.C., et al. Monoamine oxidase A (MAOA) and antisocial behaviors in the presence of childhood and adolescent maltreatment. Am. J. Med. Genet. B Neuropsychiatr. Genet. 135B:1 (2005), 59–64.
43. Taylor, A., Kim-Cohen, J., Meta-analysis of gene-environment interactions in developmental psychopathology. Dev. Psychopathol. 19:4 (2007), 1029–1037.
44. Byrd, A.L., Manuck, S.B., MAOA, childhood maltreatment, and antisocial behavior: meta-analysis of a gene-environment interaction. Biol. Psychiatry 75:1 (2014), 9–17.
45. Grossman, M.H., Emanuel, B.S., Budarf, M.L., Chromosomal mapping of the human catechol-O-methyltransferase gene to 22q11.1 → q11.2. Genomics 12:4 (1992), 822–825.
46. van Os, J., Kenis, G., Rutten, B.P.F., The environment and schizophrenia. Nature 468:7321 (2010), 203–212.
47. Henquet, C., et al. An experimental study of catechol-O-Methyltransferase Val158Met moderation of [Delta]-9-Tetrahydrocannabinol-Induced effects on psychosis and cognition. Neuropsychopharmacology 31:12 (2006), 2748–2757.
48. Caspi, A., et al. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction. Biol. Psychiatry 57:10 (2005), 1117–1127.
49. Collip, D., et al. COMT Val158Met-stress interaction in psychosis: role of background psychosis risk. CNS Neurosci. Ther. 17:6 (2011), 612–619.
50. van Winkel, R., et al. Evidence that the COMT(Val158Met) polymorphism moderates sensitivity to stress in psychosis: an experience-sampling study. Am. J. Med. Genet. B Neuropsychiatr. Genet. 147B:1 (2008), 10–17.
51. Zammit, S., et al. Genotype effects of CHRNA7, CNR1 and COMT in schizophrenia: interactions with tobacco and cannabis use. Br. J. Psychiatry 191:5 (2007), 402–407.
52. Zammit, S., et al. Cannabis: COMT and psychotic experiences. Br. J. Psychiatry 199:5 (2011), 380–385.
53. Kantrowitz, J.T., et al. Adolescent cannabis use: psychosis and catechol-O-methyltransferase genotype in African Americans and Caucasians. Psychiatr. Q. 80:4 (2009), 213–218.
54. Modinos, G., et al. Molecular genetic gene–environment studies using candidate genes in schizophrenia: a systematic review. Schizophr. Res. 150:2 (2013), 356–365.
55. D'Souza, U.M., Craig, I.W., Functional polymorphisms in dopamine and serotonin pathway genes. Hum. Mutat. 27:1 (2006), 1–13.
56. Burmeister, M., McInnis, M.G., Zollner, S., Psychiatric genetics: progress amid controversy. Nat. Rev. Genet. 9:7 (2008), 527–540.
57. Gizer, I.R., Ficks, C., Waldman, I.D., Candidate gene studies of ADHD: a meta-analytic review. Hum. Genet. 126:1 (2009), 51–90.
58. Faraone, S.V., et al. Molecular genetics of attention-deficit/hyperactivity disorder. Biol. Psychiatry 57:11 (2005), 1313–1323.
59. Mannuzza, S., et al. Adult outcome of hyperactive boys. Educational achievement: occupational rank, and psychiatric status. Arch. Gen. Psychiatry 50:7 (1993), 565–576.
60. Neuman, R.J., et al. Prenatal smoking exposure and dopaminergic genotypes interact to cause a severe ADHD subtype. Biol. Psychiatry 61:12 (2007), 1320–1328.
61. Grizenko, N., et al. Maternal stress during pregnancy, ADHD symptomatology in children and genotype: gene-Environment interaction. J. Can. Acad. Child Adolesc. Psychiatry 21:1 (2012), 9–15.
62. Zohsel, K., et al. Mothers' prenatal stress and their children's antisocial outcomes–a moderating role for the dopamine D4 receptor (DRD4) gene. J. Child Psychol. Psychiatry 55:1 (2014), 69–76.
63. Langley, K., et al. Testing for gene × environment interaction effects in attention deficit hyperactivity disorder and associated antisocial behavior. Am. J. Med. Genet. B: Neuropsychiatr. Genet. 147B:1 (2008), 49–53.
64. Monroe, S.M., Simons, A.D., Diathesis-stress theories in the context of life stress research: implications for the depressive disorders. Psychol. Bull. 110:3 (1991), 406–425.
65. Belsky, J., Fearon Bell, R.M.P.B., Parenting, attention and externalizing problems: testing mediation longitudinally, repeatedly and reciprocally. J. Child Psychol. Psychiatry 48:12 (2007), 1233–1242.
66. Ellis, B.J., et al. Differential susceptibility to the environment: an evolutionary–neurodevelopmental theory. Dev. Psychopathol. 23:1 (2011), 7–28.
67. Pluess, M., Belsky, J., Vantage sensitivity: individual differences in response to positive experiences. Psychol. Bull. 139:4 (2013), 901–916.
68. Pluess, M., Vantage sensitivity: environmental sensitivity to positive experiences as a function of genetic differences. J. Pers. 85:1 (2017), 38–50.
69. Ding, Y., et al. Evidence of positive selection acting at the human dopamine DF gene locus. PNAS 99 (2002), 309–314.
70. Belsky, J., Pluess, M., Beyond diathesis stress: differential susceptibility to environmental influences. Psychol. Bull. 135:6 (2009), 885–908.
71. DeWitt, T.J., Sih, A., Wilson, D.S., Costs and limits of phenotypic plasticity. Trends Ecol. Evol. 13:2 (1998), 77–81.
72. Sih, A., Effects of early stress on behavioral syndromes: an integrated adaptive perspective. Neurosci. Biobehav. Rev. 35:7 (2011), 1452–1465.
73. Frankenhuis, W.E., Panchanathan, K., Individual differences in developmental plasticity may result from stochastic sampling. Perspect. Psychol. Sci. 6:4 (2011), 336–347.
74. Kuepper, Y., et al.; 5-HTTLPR S-Allele: A genetic plasticity factor regarding the effects of life events on personality?. Genes Brain Behav., 2012.
75. Pluess, M., et al. 5-HTTLPR moderates effects of life events on neuroticism: differential susceptibility to environmental influences. Prog. Neuropsychopharmacol. Biol. Psychiatry. 34 (2010), 1070–1074.
76. Belsky, J., Pluess, M., Beyond risk, resilience, and dysregulation: phenotypic plasticity and human development. Dev. Psychopathol. 25:4 Pt 2 (2013), 1243–1261.
77. Kochanska, G., et al. Children's genotypes interact with maternal responsive care in predicting children's competence: diathesis-stress or differential susceptibility?. Dev. Psychopathol. 23 (2011), 605–616.
78. Hankin, B.L., et al. Differential susceptibility in youth: evidence that 5-HTTLPR x positive parenting is associated with positive affect ‘for better and worse'. Transl. Psychiatry, 2011, 1.
79. Cicchetti, D., Rogosch, F.A., Thibodeau, E.L., The effects of child maltreatment on early signs of antisocial behavior: genetic moderation by tryptophan hydroxylase, serotonin transporter, and monoamine oxidase A genes. Dev. Psychopathol. 24:3 (2012), 907–928.
80. Van I Jzendoorn, M., Belsky, J., Bakermans-Kranenburg, M., Serotonin transporter genotype 5HTTLPR as a marker of differential susceptibility? A meta-analysis of child and adolescent gene-by-environment studies. Trans. psychiatry, 2(8), 2012, e147.
81. Baumann, C., et al. The interaction of early life experiences with COMT val158met affects anxiety sensitivity. Genes Brain Behav. 12:8 (2013), 821–829.
82. Berry, D., et al. Gene-environment interaction between dopamine receptor D4 7-repeat polymorphism and early maternal sensitivity predicts inattention trajectories across middle childhood. Dev. Psychopathol. 25:2 (2013), 291–306.
83. Belsky, J., Pluess, M., Genetic moderation of early child-Care effects on social functioning across childhood: a developmental analysis. Child Dev. 84:4 (2013), 1209–1225.
84. Knafo, A., Israel, S., Ebstein, R.P., Heritability of children's prosocial behavior and differential susceptibility to parenting by variation in the dopamine receptor D4 gene. Dev. Psychopathol. 23:1 (2011), 53–67.
85. Bakermans-Kranenburg, M.J., et al. Experimental evidence for differential susceptibility: dopamine D4 receptor polymorphism (DRD4 VNTR) moderates intervention effects on toddlers' externalizing behavior in a randomized controlled trial. Dev. Psychol. 44:1 (2008), 293–300.
86. Park, A., et al. Interaction between the DRD4 VNTR polymorphism and proximal and distal environments in alcohol dependence during emerging and young adulthood. J. Abnorm. Psychol. 120:3 (2011), 585–595.
87. Bakermans-Kranenburg, M.J., van IJzendoorn, M.H., Differential susceptibility to rearing environment depending on dopamine-related genes: new evidence and a meta-analysis. Dev. Psychopathol. 23:1 (2011), 39–52.
88. Pluess, M., Individual differences in environmental sensitivity. Child Dev. Perspec. 9:3 (2015), 138–143.
89. Belsky, J., et al. Vulnerability genes or plasticity genes?. Mol. Psychiatry 14 (2009), 746–754.
90. Bosker, F.J., et al. Poor replication of candidate genes for major depressive disorder using genome-wide association data. Mol. Psychiatry 16:5 (2011), 516–532.
91. Collins, A.L., et al. Hypothesis-driven candidate genes for schizophrenia compared to genome-wide association results. Psychol. Med. 42:3 (2012), 607–616.
92. Donnelly, P., Progress and challenges in genome-wide association studies in humans. Nature 456:7223 (2008), 728–731.
93. McClelland, G.H., Judd, C.M., Statistical difficulties of detecting interactions and moderator effects. Psychol. Bull. 114:2 (1993), 376–390.
94. Duncan, L.E., Keller, M.C., A critical review of the first 10 years of candidate gene-by-Environment interaction research in psychiatry. Am. J. Psychiatry 168:10 (2011), 1041–1059.
95. Munafo, M.R., Flint, J., Replication and heterogeneity in gene x environment interaction studies. Int. J. Neuropsychopharmacol. 12:6 (2009), 727–739.
96. Pluess, M., Belsky, J., Conceptual issues in psychiatric gene-environment interaction research. Am. J. Psychiatry 169:2 (2012), 222–232.
97. Kwon, J.M., Goate, A.M., The candidate gene approach. Alcohol. Res. Health 24:3 (2000), 164–168.
98. Pe'er, I., et al. Estimation of the multiple testing burden for genomewide association studies of nearly all common variants. Genet. Epidemiol. 32:4 (2008), 381–385.
99. Purcell, S.M., et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature 460:7256 (2009), 748–752.
100. Shi, J., et al. Common variants on chromosome 6p22: 1 are associated with schizophrenia. Nature 460:7256 (2009), 753–757.
101. Schizophrenia Psychiatric Genome-Wide Association Study Consortium C, Genome-wide association study identifies five new schizophrenia loci. Nat. Genet. 43:10 (2011), 969–976.
102. Ripke, S., et al. Genome-wide association analysis identifies 13 new risk loci for schizophrenia. Nat. Genet. 45:10 (2013), 1150–1159.
103. Anderson‐Schmidt, H., et al. Selected rapporteur summaries from the XX world congress of psychiatric genetics: hamburg, Germany, october 14–18, 2012. Am. J. Med. Genet. B: Neuropsychiatr. Genet. 162:2 (2013), 96–121.
104. Schizophrenia Working Group of the Psychiatric Genomics, C., Biological insights from 108 schizophrenia-associated genetic loci. Nature 511:7510 (2014), 421–427.
105. Uher, R., Gene?environment interactions in severe mental illness. Front. Psychiatry, 2014, 48.
106. Aschard, H., et al. Challenges and opportunities in genome-wide environmental interaction (GWEI) studies. Hum. Genet. 131:10 (2012), 1591–1613.
107. Otowa, T., et al. The first pilot genome-Wide gene-Environment study of depression in the japanese population. PLoS One, 2016, e0160823.
108. Dunn, E.C., et al. GENOME‐WIDE association study (gwas) and GENOME‐WIDE by environment interaction study (gweis) of depressive symptoms in african american and hispanic/latina women. Depress. Anxiety 33:4 (2016), 265–280.
109. Ikeda, M., et al. Genome-wide environment interaction between depressive state and stressful life events. J. Clin. Psychiatry, 77(1), 2016, e29.
110. Almli, L.M., et al. Correcting systematic inflation in genetic association tests that consider interaction effects: application to a genome-wide association study of posttraumatic stress disorder. JAMA Psychiatry 71:12 (2014), 1392–1399.
111. Kraft, P., et al. Exploiting gene-environment interaction to detect genetic associations. Hum. Hered. 63:2 (2007), 111–119.
112. Dudbridge, F., Power and predictive accuracy of polygenic risk scores. PLoS Genet., 9(3), 2013, e1003348.
113. Peyrot, W.J., et al. Effect of polygenic risk scores on depression in childhood trauma. Br. J. Psychiatry 205:2 (2014), 113–119.
114. Mullins, N., et al. Polygenic interactions with environmental adversity in the aetiology of major depressive disorder. Psychol. Med. 46:04 (2016), 759–770.
115. Musliner, K.L., et al. Polygenic risk, stressful life events and depressive symptoms in older adults: a polygenic score analysis. Psychol. Med. 45:08 (2015), 1709–1720.
116. Domingue, B.W., et al. Genetic heterogeneity in depressive symptoms following the death of a spouse: polygenic score analysis of the US Health and Retirement Study. Am. J. Psychiatry, 2017, 16111209 (p. appi. ajp. 2017).
117. Sen, S., et al. A prospective cohort study investigating factors associated with depression during medical internship. Arch. Gen. Psychiatry 67:6 (2010), 557–565.
118. Trotta, A., et al. Interplay between schizophrenia polygenic risk score and childhood adversity in first-Presentation psychotic disorder: a pilot study. PLoS One, 11(9), 2016, e0163319.
119. French, L., et al. Early cannabis use: polygenic risk score for schizophrenia and brain maturation in adolescence. JAMA psychiatry 72:10 (2015), 1002–1011.
120. Menne-Lothmann, C., et al. Genetic and environmental causes of individual differences in daily life positive affect and reward experience and its overlap with stress-sensitivity. Behav. Genet. 42:5 (2012), 778–786.
121. Wichers, M., et al. The dynamic interplay between negative and positive emotions in daily life predicts response to treatment in depression: a momentary assessment study. Br. J. Clin. Psychol. 51:2 (2012), 206–222.
122. Wichers, M., et al. Evidence that moment-to-moment variation in positive emotions buffer genetic risk for depression: a momentary assessment twin study. Acta Psychiatr. Scand. 115:6 (2007), 451–457.
123. van Winkel, M., et al. Impact of variation in the BDNF gene on social stress sensitivity and the buffering impact of positive emotions: replication and extension of a gene–environment interaction. Eur. Neuropsychopharmacol. 24:6 (2014), 930–938.
124. Plomin, R., Haworth, C.M., Davis, O.S., Common disorders are quantitative traits. Nat. Rev. Genet. 10:12 (2009), 872–878.
125. Mortensen, P.B., et al. Effects of family history and place and season of birth on the risk of schizophrenia. New Engl. J. Med. 340:8 (1999), 603–608.
126. McGrath, J.J., et al. Neonatal vitamin D status and risk of schizophrenia: a population-based case-control study. Arch. Gen. Psychiatry 67:9 (2010), 889–894.
127. Varese, F., et al. Childhood adversities increase the risk of psychosis: a meta-analysis of patient-control, prospective-and cross-sectional cohort studies. Schizophr. Bull., 2012, sbs050.
128. Muntaner, C., et al. Socioeconomic position and major mental disorders. Epidemiol. Rev. 26:1 (2004), 53–62.
129. Stilo, S.A., et al. Social disadvantage: cause or consequence of impending psychosis?. Schizophr. Bull. 39:6 (2013), 1288–1295.
130. Brown, G.W., et al. Functional polymorphism in the brain-derived neurotrophic factor gene interacts with stressful life events but not childhood maltreatment in the etiology of depression. Depress. Anxiety 31:4 (2014), 326–334.
131. Fearon, P., et al. Incidence of schizophrenia and other psychoses in ethnic minority groups: results from the MRC AESOP Study. Psychol. Med. 36:11 (2006), 1541–1550.
132. Moore, T.H., et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet 370:9584 (2007), 319–328.
133. Lindert, J., et al. Sexual and physical abuse in childhood is associated with depression and anxiety over the life course: systematic review and meta-analysis. Int. J. Public Health 59:2 (2014), 359–372.
134. Paananen, R., et al. Social determinants of mental health: a Finnish nationwide follow-up study on mental disorders. J. Epidemiol. Commun. Health 67:12 (2013), 1025–1031.
135. Brown, G.H., TO, Social Origins of Depression: A Study of Psychiatric Disorder in Women. 1978, Tavistock, London.
136. Dunner, D.L., Patrick Fieve, V.R.R., Life events at the onset of bipolar affective illness. Am. J. Psychiatry, 1979.
137. Cross-Disorder Group of the Psychiatric Genomics C, Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs. Nat. Genet. 45:9 (2013), 984–994.
138. Cross-Disorder Group of the Psychiatric Genomics C, Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet 381:9875 (2013), 1371–1379.
139. MacMillan, Harriet L., et al. Childhood abuse and lifetime psychopathology in a community sample. Am. J. Psychiatry 158:11 (2001), 1878–1883.
140. Garno, J.L., et al. Impact of childhood abuse on the clinical course of bipolar disorder. Br. J. Psychiatry, 186(2), 2005, 121.
141. Cross-Disorder Group of the Psychiatric Genomics Consortium, Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet 381:9875 (2013), 1371–1379.
142. Conway, C.C., Slavich, G.M., Hammen, C., Daily stress reactivity and serotonin transporter gene (5-HTTLPR) variation: internalizing responses to everyday stress as a possible transdiagnostic phenotype. Biol. Mood Anxiety Disord., 4(1), 2014, 2.
143. Ofrat, S., Krueger, R.F., How research on the meta-structure of psychopathology aids in understanding biological correlates of mood and anxiety disorders. Biol. Mood Anxiety Disord., 2(1), 2012, 13.
144. Miller, G.A., Rockstroh, B., Endophenotypes in psychopathology research: where do we stand?. Annu. Rev. Clin. Psychol. 9 (2013), 177–213.
145. Aguilera, M., et al. Early adversity and 5-HTT/BDNF genes: new evidence of gene–environment interactions on depressive symptoms in a general population. Psychol. Med. 39:09 (2009), 1425–1432.
146. Gillespie, C.F., et al. Risk and resilience: genetic and environmental influences on development of the stress response. Depress. Anxiety 26:11 (2009), 984–992.
147. Keers, R., Pluess, M., Childhood quality influences genetic sensitivity to environmental influences across adulthood: a life-Course gene-Environment interaction study. Dev. Psychopathol., 2017 (submitted).
148. Starr, L.R., et al. Sensitizing effect of early adversity on depressive reactions to later proximal stress: moderation by polymorphisms in serotonin transporter and corticotropin releasing hormone receptor genes in a 20-year longitudinal study. Dev. Psychopathol. 26:4pt2 (2014), 1241–1254.
149. Kooperberg, C., Leblanc, M., Increasing the power of identifying gene x gene interactions in genome-wide association studies. Genet. Epidemiol. 32:3 (2008), 255–263.
150. van IJzendoorn, M.H., et al. Gene-by-environment experiments: a new approach to finding the missing heritability. Nature Reviews. Genetics, 881, 2011 (author reply 881).
151. Bakermans-Kranenburg, M.J., van IJzendoorn, M.H., The hidden efficacy of interventions: gene × environment experiments from a differential susceptibility perspective. Annu. Rev. Psychol. 66 (2015), 381–409.
152. van Ijzendoorn, M.H., Bakermans-Kranenburg, M.J., Genetic differential susceptibility on trial: meta-analytic support from randomized controlled experiments. Dev. Psychopathol. 27:01 (2015), 151–162.
153. Fox, E., et al. The serotonin transporter gene alters sensitivity to attention bias modification: evidence for a plasticity gene. Biol. Psychiatry 70:11 (2011), 1049–1054.
154. Keers, R., et al. A genome-Wide test of the differential susceptibility hypothesis reveals a genetic predictor of differential response to psychological treatments for child anxiety disorders. Psychother. Psychosom. 85:3 (2016), 146–158.
155. Visscher, P.M., Posthuma, D., Statistical power to detect genetic Loci affecting environmental sensitivity. Behav. Genet. 40:5 (2010), 728–733.