31.T. Bouchard and M. McGue, “Genetic and Environmental Influences on Human Psychological Differences,” J Neurobiol 54 (2003): 4.
32.L. E. Duncan and M. C. Keller, “A Critical Review of the First 10 Years of Candidate Gene-by-Environment Interaction Research in Psychiatry,” Am J Psychiatry 168 (2011): 1041; S. Manuck and J. McCaffery, “Gene-Environment Interaction,” Ann Rev of Psych 65 (2014): 41.
33.A. Caspi et al., “Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene,” Sci 297 (2002): 851.
34.A. Caspi et al., “Moderation of Breastfeeding Effects on the IQ by Genetic Variation in Fatty Acid Metabolism,” PNAS 104 (2007): 18860; B. K. Lipska and D. R. Weinberger, “Genetic Variation in Vulnerability to the Behavioral Effects of Neonatal Hippocampal Damage in Rats,” PNAS 92 (1995): 8906.
35.J. Crabbe et al., “Genetics of Mouse Behavior: Interactions with Laboratory Environment,” Sci 284 (1999): 1670.
36.A nice example of a dual environment hit: N. P. Daskalakis et al., “The Three-Hit Concept of Vulnerability and Resilience: Toward Understanding Adaptation to Early-Life Adversity Outcome,” PNE 38 (2013): 1858.
37.E. Turkheimer et al., “Socioeconomic Status Modifies Heritability of IQ in Young Children,” Psych Sci 14 (2003): 623; E. M. Tucker-Drob et al., “Emergence of a Gene x Socioeconomic Status Interaction on Infant Mental Ability Between 10 Months and 2 Years,” Psych Sci 22 (2010): 125; M. Rhemtulla and E. M. Tucker-Drob, “Gene-by-Socioeconomic Status Interaction on School Readiness,” Behav Genetics 42 (2012): 549; D. Reiss et al., “How Genes and the Social Environment Moderate Each Other,” Am J Public Health 103 (2013): S111; S. A. Hart et al., “Expanding the Environment: Gene × School-Level SES Interaction on Reading Comprehension,” J Child Psych and Psychiatry 54 (2013): 1047; J. R. Koopmans et al., “The Influence of Religion on Alcohol Use Initiation: Evidence for Genotype × Environment Interaction,” Behav Genetics 29 (1999): 445.
38.S. Nielsen et al., “Prevalence of Alcohol Problems Among Adult Somatic Inpatients of a Copenhagen Hospital,” Alcohol and Alcoholism 29 (1994): 583; S. Manuck et al., “Aggression and Anger-Related Traits Associated with a Polymorphism of the Tryptophan Hydroxylase Gene,” BP 45 (1999): 603; J. Hennig et al., “Two Types of Aggression Are Differentially Related to Serotonergic Activity and the A779C TPH Polymorphism,” Behav Nsci 119 (2005): 16; A. Strobel et al., “Allelic Variation in 5-HT1A Receptor Expression Is Associated with Anxiety- and Depression-Related Personality Traits,” J Neural Transmission 110 (2003): 1445; R. Parsey et al., “Effects of Sex, Age, and Aggressive Traits in Man on Brain Serotonin 5-HT1A Receptor Binding Potential Measured by PET Using [C-11]WAY-100635,” Brain Res 954 (2002): 173; A. Benko et al., “Significant Association Between the C(-1019)G Functional Polymorphism of the HTR1A Gene and Impulsivity,” Am J Med Genetics, Part B, Neuropsychiatric Genetics 153 (2010): 592, M. Soyka et al., “Association of 5-HT1B Receptor Gene and Antisocial Behavior and Alcoholism,” J Neural Transmission 111 (2004): 101; L. Bevilacqua et al., “A Population-Specific HTR2B Stop Codon Predisposes to Severe Impulsivity,” Nat 468 (2010): 1061; C. A. Ficks and I. D. Waldman, “Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR,” Behav Genetics 44 (2014): 427; I. Craig and K. Halton, “Genetics of Human Aggressive Behavior,” Hum Genetics 126 (2009): 101.
39.H. Brunner et al., “Abnormal Behavior Associated with a Point Mutation in the Structural Gene for Monoamine Oxidase A,” Sci 262 (1993): 578; H. G. Brunner et al., “X-Linked Borderline Mental Retardation with Prominent Behavioral Disturbance: Phenotype, Genetic Localization, and Evidence for Disturbed Monoamine Metabolism,” Am J Hum Genetics 52 (1993): 1032.
40.O. Cases et al., “Aggressive Behavior and Altered Amounts of Brain Serotonin and Norepinephrine in Mice Lacking MAOA,” Sci 268 (1995): 1763; J. J. Kim et al., “Selective Enhancement of Emotional, but Not Motor, Learning in Monoamine Oxidase A–Deficient Mice,” PNAS 94 (1997): 5929.
41.J. Buckholtz and A. Meyer-Lindenberg, “MAOA and the Neurogenetic Architecture of Human Aggression,” TINS 31 (2008): 120; A. Meyer-Lindenberg et al., “Neural Mechanisms of Genetic Risk for Impulsivity and Violence in Humans,” PNAS 103 (2006): 6269; J. Fan et al., “Mapping the Genetic Variation of Executive Attention onto Brain Activity,” PNAS 100 (2003): 7406; L. Passamonti et al., “Monoamine Oxidase-A Genetic Variations Influence Brain Activity Associated with Inhibitory Control: New Insight into the Neural Correlates of Impulsivity,” BP 59 (2006): 334; N. Eisenberger et al., “Understanding Genetic Risk for Aggression: Clues from the Brain’s Response to Social Exclusion,” BP 61 (2007): 1100.
42.O. Cases et al., “Aggressive Behaviour and Altered Amounts of Brain Serotonin and Norepinephrine in Mice Lacking MAOA,” Sci 268 (1995): 1763; J. S. Fowler et al., “Evidence That Brain MAO A Activity Does Not Correspond to MAO A Genotype in Healthy Male Subjects,” BP 62 (2007): 355.
43.The “warrior gene” in the science literature: C. Holden, “Parsing the Genetics of Behavior,” Sci 322 (2008): 892; D. Eccles et al., “A Unique Demographic History Exists for the MAO-A Gene in Polynesians,” J Hum Genetics 57 (2012): 294; E. Feresin, “Lighter Sentence for Murder with ‘Bad Genes,’” Nat News (30 October, 2009); P. Hunter, “The Psycho Gene,” EMBO Rep 11 (2010): 667.
Criticism of the scientists in the Maori study for overselling the significance of their finding: D. Wensley and M. King, “Scientific Responsibility for the Dissemination and Interpretation of Genetic Research: Lessons from the ‘Warrior Gene’ Controversy,” J Med Ethics 34 (2008): 507; S. Halwani and D. Krupp, “The Genetic Defense: The Impact of Genetics on the Concept of Criminal Responsibility,” Health Law J 12 (2004): 35.
44.A. Caspi et al., “Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene,” Sci 297 (2002): 851.
45.J. Buckholtz and A. Meyer-Lindenberg, “MAOA and the Neurogenetic Architecture of Human Aggression,” TINS 31 (2008): 120.
46.J. Kim-Cohen et al., “MAOA, Maltreatment, and Gene Environment Interaction Predicting Children’s Mental Health: New Evidence and a Meta-analysis,” Mol Psychiatry 11 (2006): 903; A. Byrd and S. Manuck, “MAOA, Childhood Maltreatment and Antisocial Behavior: Meta-analysis of a Gene-Environment Interaction,” BP 75 (2013): 9; G. Frazzetto et al., “Early Trauma and Increased Risk for Physical Aggression During Adulthood: The Moderating Role of MAOA Genotype,” PLoS ONE 2 (2007): e486; C. Widom and L. Brzustowicz, “MAOA and the ‘Cycle of Violence’: Childhood Abuse and Neglect, MAOA Genotype, and Risk for Violent and Antisocial Behavior,” BP 60 (2006): 684; R. McDermott et al., “MAOA and Aggression: A Gene-Environment Interaction in Two Populations,” J Conflict Resolution 1 (2013): 1043; T. Newman et al., “Monoamine Oxidase A Gene Promoter Variation and Rearing Experience Influences Aggressive Behavior in Rhesus Monkeys,” BP 57 (2005): 167; X. Ou et al., “Glucocorticoid and Androgen Activation of Monoamine Oxidase A Is Regulated Differently by R1 and Sp1,” J Biol Chemistry 281 (2006): 21512.
Replication: D. L. Foley et al., “Childhood Adversity, Monoamine Oxidase A Genotype, and Risk for Conduct Disorder,” AGP 61 (2004): 738; D. M. Fergusson et al., “MAOA, Abuse Exposure and Antisocial Behaviour: 30-Year Longitudinal Study,” Brit J Psychiatry 198 (2011): 457.
Weaker effect in girls: E. C. Prom-Wormley et al., “Monoamine Oxidase A and Childhood Adversity as Risk Factors for Conduct Disorder in Females,” Psych Med 39 (2009): 579.
Replicates for whites but not blacks: C. S. Widom and L. M. Brzustowicz, “MAOA and the ‘Cycle of Violence’: Childhood Abuse and Neglect, MAOA Genotype, and Risk for Violent and Antisocial Behavior,” BP 60 (2006): 684.
Failure of replication: D. Huizinga et al., “Childhood Maltreatment, Subsequent Antisocial Behavior, and the Role of Monoamine Oxidase A Genotype,” BP 60 (2006): 677; S. Young et al., “Interaction Between MAO-A Genotype and Maltre
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47.R. Sjoberg et al., “A Non-additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior,” Neuropsychopharmacology 33 (2008): 425; R. McDermott et al., “Monoamine Oxidase A Gene (MAOA) Predicts Behavioral Aggression Following Provocation,” PNAS 106 (2009): 2118; D. Gallardo-Pujol et al., “MAOA Genotype, Social Exclusion and Aggression: An Experimental Test of a Gene-Environment Interaction,” Genes, Brain and Behav 12 (2013): 140; A. Reif et al., “Nature and Nurture Predispose to Violent Behavior: Serotonergic Genes and Adverse Childhood Environment,” Neuropsychopharmacology 32 (2007): 2375.
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49.M. Bakermans-Kranenburg and M. van Ijzendoorn, “Differential Susceptibility to Rearing Environment Depending on Dopamine-Related Genes: New Evidence and a Meta-analysis,” Development Psychopathology 23 (2011): 39; J. Sasaki et al., “Religion Priming Differentially Increases Prosocial Behavior Among Variants of the Dopamine D4 Receptor (DRD4) Gene,” SCAN 8 (2013): 209; M. Sweitzer et al., “Polymorphic Variation in the Dopamine D4 Receptor Predicts Delay Discounting as a Function of Childhood Socioeconomic Status: Evidence for Differential Susceptibility,” SCAN 8 (2013): 499.
50.F. Chang et al., “The World-wide Distribution of Allele Frequencies at the Human Dopamine D4 Receptor Locus,” Hum Genetics 98 (1996): 91; C. Chen et al., “Population Migration and the Variation of Dopamine D4 Receptor (DRD4) Allele Frequencies Around the Globe,” EHB 20 (1999): 309.
51.M. Reuter and J. Hennig, “Association of the Functional Catechol-O-Methyltransferase VAL158MET Polymorphism with the Personality Trait of Extraversion,” Neuroreport 16 (2005): 1135; T. Lancaster et al., “COMT val158met Predicts Reward Responsiveness in Humans,” Genes, Brain and Behav 11 (2012): 986; A. Caspi et al., “A Replicated Molecular-Genetic Basis for Subtyping Antisocial Behavior in ADHD,” AGP 65 (2007): 203; N. Perroud et al., “COMT but Not Serotonin-Related Genes Modulates the Influence of Childhood Abuse on Anger Traits,” Genes, Brain and Behav 9 (2010): 193.
COMT variants also associated with cognitive end points: F. Papaleo et al., “Genetic Dissection of the Role of Catechol-O-Methyltransferase in Cognition and Stress Reactivity in Mice,” J Nsci 28 (2008): 8709; F. Papaleo et al., “Effects of Sex and COMT Genotype on Environmentally Modulated Cognitive Control in Mice,” PNAS 109 (2012): 20160; F. Papaleo et al., “Epistatic Interaction of COMT and DTNBP1 Modulates Prefrontal Function in Mice and in Humans,” Mol Psychiatry 19 (2013): 311.
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