The role of the monoamine oxidase A gene in moderating the response to adversity and associated antisocial behavior: a review

Figures & data

Figure 1 Flowchart depicting the bibliographic search process.

Table 1 Search syntax to locate articles conducted on human subjects with at least one environmental measure of adversity

PubMed	((((maoa[Title/Abstract]) OR (monoamine oxidase a[Title/Abstract])) AND (antisocial[Title/Abstract] OR agress*[Title/Abstract] OR viol*[Title/Abstract]) AND (advers*[Title/Abstract] OR abus*[Title/Abstract] OR maltreat*[Title/Abstract]))) AND (“2007”[Date – Publication]: “2013”[Date – Publication])
Web of Science	TOPIC: (MAOA OR monoamine oxidase a) AND TOPIC: (antisocial OR agress* OR viol*) AND TOPIC: (advers* OR abus* OR maltreat*). Timespan=2007–2013. Search language=English.

Table 2 Recent studies replicating the relationship between MAOA-uVNTR, adversity, and at least one kind of antisocial outcome in humans

Reference (year)	Sample	Gene(s) studied	Environmental variables	Outcome	Selected results
Nilsson et al^Citation33 (2007)	66 males	MAOA	Family function, maltreatment	Alcohol-related problem behavior	MAOA interacted with family function and maltreatment, such that carriers of the low-activity allele had the greatest alcohol-related problem behavior scores when maltreated or reared in poor-functioning families. The interaction was only marginally significant in a regression model, but was reaffirmed with nonparametric interaction tests.
Reif et al^Citation23 (2007)	184 males referred for forensic assessment	MAOA, 5HHTLPR, DAT	Childhood adversity, history of substance abuse	Violent behavior	Significant main effect of MAOA on violent behavior, short allele carriers being 2.3 times more likely than long allele carriers to engage in violence. Interaction between 5HTTLPR and MAOA, such that MAOA-L subjects with at least one copy of the short 5HTTLPR allele had a 0.78 probability of being classified as violent if reared in an adverse environment.
Sjöberg et al^Citation54 (2007)	119 females	MAOA	Sexual abuse	Stealing, vandalism, violence, total criminality	Sexual abuse and MAOA interacted in predicting total criminality and vandalism, but not violence or stealing. 4R homozygotes displayed the greatest criminality scores.
Vanyukov et al^Citation53 (2007)	148 males	MAOA	Parenting (separately for mothers and fathers)	Disruptive behavior ages 12–18 years (CD, ADHD, substance abuse)	Paternal, but not maternal, care interacted with genotype in predicting ADHD. Relationships between parenting and disruptive behavior disorders were observed in 4-repeat allele carriers but not in participants with the 3-repeat allele for all outcomes. The 4-repeat allele was thus associated with greater disruptive behavior scores as a function of parenting.
Ducci et al^Citation34 (2008)	291 American Indian women	MAOA	Child sexual abuse	Alcoholism, ASPD	Greater presence of the low-activity allele in alcoholics and antisocial alcoholics compared to controls within abused group, but not within nonabused group. Also differences in several MAOA and MAOB SNPs.
Nilsson et al^Citation107 (2008)	119 females	MAOA	Quality of family relations, physical/sexual abuse	Alcohol-related problem behavior	Quality of family relations interacted with MAOA, while the effect of maltreatment varied depending on which groups were compared and was only marginally significant. Homozygous MAOA-L subjects displayed the greater problem scores if family relations were poor.
Hart et al^Citation45 (2009)	865 males	MAOA	Neighborhood child saturation, poverty, urbanicity, racial heterogeneity	Self-reported aggression	MAOA interacted with child saturation (ie, number of children <15 years of age living in a neighborhood) in predicting aggression, but not with other social indexes. MAOA-L subjects had the greater increase in aggression scores.
Kinnally et al^Citation55 (2009)	158 females	MAOA	Parental care and SLEs	Impulsivity, trait aggression, depressive symptoms	Three-way interaction between parental care, SLEs, and MAOA. Favoring rearing practices buffered the detrimental effects of SLEs on impulsivity/aggression in MAOA-L/L subjects, who had similar mean levels as MAOA-L/H carriers and way lower than MAOA-H/H participants. There were no differences in genotype when subjects suffered both poor parental care and a severe stressor.
McDermott et al^Citation67 (2009)	78 males	MAOA	Experimental monetary provocation	Experimental aggression (amount of hot sauce allocated against the provocateur)	MAOA-L subjects displayed more aggression than their counterparts in the high-provocation condition, but not in the low-provocation condition.
Prom-Wormley et al^Citation56 (2009)	721 females	MAOA	Childhood adversity (not abuse), parental ASPD	Conduct disorder	MAOA had a direct effect and an interactive effect with childhood adversity on CD. MAOA-L/L females had a greater proportion of CD in medium levels of exposure to adversity than did carriers of other genotypes, but were protected against CD at the highest adversity levels.
Weder et al^Citation101 (2009)	114 male children (73 maltreated, 41 controls)	MAOA	Childhood adversity	Aggression, rule-breaking, inattention	The interaction between MAOA and trauma exposure predicted inattention but not rule-breaking or aggression, and differences in aggression between genotype groups only existed at moderate levels of trauma. The MAOA-L variant was related to greater inattention scores at low to moderate levels of trauma, but high-activity allele carriers scored higher when exposed to extreme adversity.
Beach et al^Citation108 (2010)	538	MAOA	Childhood maltreatment	Depressive symptoms and ASPD	G wp × E effects of MAOA and maltreatment on both outcomes. MAOA-L was the risk allele for ASPD in women and MAOA-H for depressive symptoms in both sexes. The MAOA × maltreatment interaction in male ASPD was nonsignificant.
Derringer et al^Citation109 (2010)	841 twins	MAOA	Childhood harsh discipline and sexual assault	Substance abuse, lifetime ASPD, childhood CD	Genotype interacted with sexual assault in predicting ASB and CD, but only a small proportion of participants (3%) had suffered this stressor. Low-activity carriers displayed the greater scores in ASB and CD. Harsh discipline increased alcohol and tobacco abuse, ASPD and CD, but did not interact with genotype.
Edwards et al^Citation110 (2010)	186 males	MAOA	Childhood physical discipline	Delinquency, aggression, child externalizing problems	Significant G × E interaction for delinquency with multiple and maternal reports, but not with teacher or self reports. Higher antisocial scores for MAOA-L participants.
Enoch et al^Citation36 (2010)	6,129 Children 4 to 7 years old	MAOA	SLE and family adversity	Behavioral disinhibition	Females carrying low-activity alleles were more susceptible than their counterparts to SLEs for hyperactivity at 4 years and 7 years of age. SLEs at 1.5 to 2.5 years had a greater effect for MAOA-L boys at age 7.
Tikkanen et al^Citation66 (2011)	174 male alcoholic offenders	MAOA	Childhood physical abuse	Violent behavior	Interaction between MAOA genotype and heavy drinking, and between MAOA and childhood abuse, in predicting violent recidivism. Abuse and alcohol consumption heightened risk for violent behavior in high-activity allele carriers, but not in MAOA-L subjects.
Wakschlag et al^Citation13 (2010)	176	MAOA	Prenatal exposure to cigarettes, harsh parenting, maternal antisocial behavior, paternal antisocial behavior	CD, hostile attribution bias (judging nonangry faces as angry)	MAOA interacted with prenatal exposure to cigarettes in predicting CD. CD symptoms were higher at greater prenatal smoking exposure in female carriers of the high- activity allele, whereas, for males, the low-activity allele was the risk variant. For hostile attribution bias, a milder MAOA × prenatal smoking exposure was found on females, with the high-activity allele associated with greater angry-face identification.
Aslund et al^Citation37 (2011)	1,825	MAOA	Childhood maltreatment	Delinquency, vandalism, stealing, violence	Main and interactive G × E effect on global delinquency index. MAOA-L maltreated boys and MAOA-H/H maltreated girls exhibited the highest delinquency rates.
Beaver et al^Citation5 (2011)	493	MAOA	Compound measure of protective (eg, social support, religiosity) and risk (eg, neighborhood disadvantage, maternal negativity) factors	Incarceration, anger, hostility	Significant G × E interaction between MAOA and risk-protective factors for anger and hostility in males. Almost significant G × E interaction for incarceration. The MAOA-L. allele was associated with higher anger and hostility in unfavorable environments, and with lower scores in favoring environments, when compared with MAOA-H.
Fergusson et al^Citation38 (2011)	398 males	MAOA	Childhood abuse (sexual and physical)	Property and violent offending, convictions, conduct problems, hostility	Significant G × E interactions for most outcomes, especially for self-reported property offending, but not for convictions. When taken separately, sexual abuse had a more significant effect on all outcomes than physical abuse. MAOA-L participants had markedly higher ASB scores than MAOA-H carriers if exposed to early abuse.
Lee et al^Citation51 (2011)	672 males	MAOA	Deviant peer affiliation	Overt and covert ASB	Interaction between deviant peer affiliation and MAOA for overt but not for covert ASB. The high-activity allele was associated with greater problematic alcohol consumption and overt ASB scores.
Nilsson et al^Citation35 (2011)	1,586	MAOA	Quality of family relations, sexual abuse	Alcohol use disorder	MAOA genotype interacted with sexual abuse in predicting alcohol use disorder (controlling for socioeconomic factors), but not with family relations. MAOA-L males had the highest mean levels of alcohol abuse, whereas MAOA-HIH was the risk allele for females.
Pardini et al^Citation57 (2011)	197 males (war veterans)	MAOA	Brain injury (prefrontal versus non-prefrontal versus controls)	Trait aggression	Genotype × group interaction, such that, among non-prefrontal-lesion patients, high activity carriers had greater aggression scores than low activity carriers, with the opposite trend in healthy controls and no differences in genotype in prefrontal-lesion subjects. Positive correlations between aggression, early traumatic experiences, and posttraumatic stress disorder symptoms within healthy and non-prefrontal-lesion participants, but not in prefrontal-damaged subjects.
Cicchetti et al^Citation41 (2012)	672 low income children (10–12 years of age)	MAOA, TPH1, 5HTTLPR	Childhood maltreatment	ASB	Maltreated MAOA-L children had higher lifetime ASB scores, as well as during the past 6 months. These G × E interactions were found only for self-reported ASB, but not for peer or adult ratings.
Fergusson et al^Citation42 (2012)	399 males	MAOA	Maternal prenatal smoking, IQ at age 8–9 years, childhood maltreatment, family material deprivation	Property and violent offending, convictions	G × E interactions for self-reported violent offending and self-reported property offending, but not as strong for convictions. MAOA-L carriers displayed greater antisocial scores than MAOA-H subjects if exposed to early adversity, with childhood maltreatment outscoring other risk factors.
McGrath etal^Citation111 (2012)	192 females (oversampled for prenatal smoking)	MAOA	Childhood maltreatment	Conduct problems	Maltreatment had a stronger effect on conduct problems for carriers of the high-activity allele than for the low-activity variant, but conduct problems were more related to other antisocial dimensions (eg, impulsiveness, interpersonal aggression) in the latter group.
Nikulina et al^Citation52 (2012)	575	MAOA	Physical abuse, sexual abuse, neglect, multiple maltreatment	Dysthymia, major depressive disorder, alcohol abuse	The low-activity allele protected females from the effects of physical abuse on dysthymia. The 3,3 or 3 allele form protected Whites against dysthymia, major depressive disorder, and alcohol abuse symptomatology if sexually abused, while the 4,4 or 4 allele genotype protected non-Whites.
Simons et al^Citation43 (2012)	224	MAOA, 5HTTLPR, DRD4	Hostile/demoralizing rearing environment (including harsh parenting)	Delinquency, aggression, and adoption of the “street code”	Interaction between cumulative plasticity alleles (ie, number of “risk” alleles) and hostile environment on adoption of the street code and aggression. Mediation analyses revealed that the best-fitting model was one in which the G × E predicted aggression through adoption of the street code. Number of plasticity alleles (including the MAOA-L variant) predicted antisocial scores as a function of environmental adversity - lowest ASB in favoring environments, highest in detrimental ones.
Gallardo-Pujol et al^Citation70 (2013)	57 males	MAOA	Experimental social exclusion	Experimental aggression (point subtraction aggression paradigm)	Significant G × E (MAOA × social exclusion) effect. Excluded MAOA-L participants scored more than twice on experimental aggression than their MAOA-H counterparts.
Hill et al^Citation44 (2013)	209 infants (5 weeks postpartum)	MAOA	Maternal stress, marital satisfaction, anxiety, depression, neighborhood deprivation	Irritability (count of fuss-cry maneuvers in a standardized assessment)	Prenatal life events predicted irritability more strongly in MAOA-L than in MAOA-H children. MAOA-L infants displayed more fuss-cry behaviors than MAOA-H carriers if raised in deprived neighborhoods, whereas no differences existed in the rest.
Kuepper et al^Citation68 (2013)	239	MAOA	Experimental provocation	Experimental aggression (a variant of Taylor aggression paradigm)	Low-activity allele carriers delivered more intense noise blasts in response to high provocation, both in usual trials and after receiving a very strong, proactive blast. No sex differences were observed.

Notes: Studies included here were published in 2007 or later, when the last meta-analysis on the topic was published by Taylor and Kim-Cohen³¹ (2007), except if not listed in such article. Articles are presented chronologically; the order is alphabetical for papers published in the same year. Samples include participants of both sexes unless otherwise specified. Antisocial outcomes include problematic alcohol consumption.

Abbreviations: 5HTTLPR, serotonin transporter linked polymorphic region; ADHD, attention-deficit hyperactivity disorder; ASB, antisocial behavior; ASPD, antisocial personality disorder; CD, conduct disorder; CSF, cerebrospinal fluid; DAT, dopamine transporter; G × E, gene-environment interaction; MAOA, monoamine oxidase A; MAOA-H, monoamine oxidase A high-activity allele; MAOA-L, monoamine oxidase A low-activity allele; MAOB, monoamine oxidase B; ODD oppositional defiant disorder; SLEs, stressful life events; SNP, single nucleotide polymorphism; TPH1, tryptophan hydroxylase 1; uVNTR, upstream variable number of tandem repeats.

Table 3 Recent studies failing to confirm the relationship between MAOA-uVNTR, adversity, and at least one kind of antisocial outcome in humans

Reference (year)	Sample	Gene(s) studied	Environmental variables	Outcome	Selected results
Prichard et al^Citation49 (2008)	1,002 males	MAOA	General childhood adversity (including abuse)	Indicators of ASB	MAOA × adversity interaction only when comparing participants who suffered <2 adversity exposures with those who experienced 2–5 exposures. Carriers of the high activity allele showed the highest ASB scores.
Van der Vegt et al^Citation50 (2009)	239 adopted boys	MAOA	Childhood maltreatment	Externalizing behavior (including aggressive and delinquent behavior)	The interaction between MAOA and maltreatment almost reached significance for delinquency, but not for aggression or the overarching externalizing scale. Main effect for MAOA in all measures, so that carriers of the high-activity allele obtained higher scores than MAOA-L participants.
Williams et al^Citation112 (2009)	210	MAOA	Early life stress	Electroencephalographic activity in a face-processing task	No interaction between number of early stressful events and genotype in any brain region. Interaction between genotype and sex in the processing of emotional-valenced faces. MAOA-L males had clearly reduced responses in several parietal, frontal, and occipital brain areas when presented with angry faces, whereas for females, genotype differences existed only in the superior occipital gyrus, and with an opposite pattern.
Verhoeven et al^Citation46 (2012)	432	MAOA	Childhood adversity	Anger, depression sensitivity	MAOA had a dose-dependent effect on the aggression reactivity facet of depression sensitivity in women, such that MAOA-H/H females scored higher than MAOA-H/L ones, who, in turn, had greater scores than MAOA-L/L. No genotype effects were found on trait or state anger. Childhood adversity did not interact with MAOA genotype for any antisocial outcome.
Haberstick et al^Citation48 (2014)	4,316 males	MAOA	Childhood maltreatment	Adolescent conduct problems, adult antisocial behavior, convictions for violent crimes, disposition toward violence	Significant though mild main effect of MAOA gene on convictions for the whole sample, and on disposition toward violence in White males. Neither main nor interactive effects in any other score. The absence of G × E effects was not due to lack of statistical power.
Sadeh et al^Citation47 (2013)	237 males	MAOA, 5HTTLPR	Childhood maltreatment	Psychopathy	Significant although small difference between MAOA-L and MAOA-H subjects in the impulsive– antisocial psychopathy dimension, higher for low-activity carriers. No interaction of the MAOA gene with childhood maltreatment. MAOA × 5HTTLPR interaction was not tested, but 5HTTLPR showed effects on the affective and interpersonal psychopathy dimensions.

Notes: Studies included here were published in 2007 or later, when the last meta-analysis on the topic was published by Taylor and Kim-Cohen³² (2007), except if not listed in such article. Articles are presented chronologically; the order is alphabetical for papers published the same year. Samples include participants of both sexes unless otherwise specified.

Abbreviations: 5HTTLPR, serotonin transporter linked polymorphic region; ASB, antisocial behavior; G × E, gene–environment interaction; MAOA, monoamine oxidase A; MAOA-H, monoamine oxidase A high-activity allele; MAOA-L, monoamine oxidase A low-activity allele; uVNTR, upstream variable number of tandem repeats.

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