Molecular Psychiatry (2008) 13, 334–347

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ORIGINAL ARTICLE

Interaction between a functional MAOA locus and

childhood sexual abuse predicts alcoholism and
antisocial personality disorder in adult women
F Ducci1, M-A Enoch1, C Hodgkinson1, K Xu1, M Catena2, RW Robin3 and D Goldman1
1
Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA; 2Department of
Psychiatry, University of Pisa, Pisa, Italy and 3Center for the Prevention and Resolution of Violence, Tucson, AZ, USA

Women who have experienced childhood sexual abuse (CSA) have an increased risk of
alcoholism and antisocial personality disorder (ASPD). Among male subjects, a functional
polymorphism (MAOA-LPR, monoamine oxidase A linked polymorphic region) in the promoter
region of the monoamine oxidase A gene (MAOA) appears to moderate the effect of childhood
maltreatment on antisocial behavior. Our aim was to test whether MAOA-LPR influences the
impact of CSA on alcoholism and ASPD in a sample of 291 women, 50% of whom have
experienced CSA; we also tested whether haplotypes covering the region where both MAOA
and monoamine oxidase B (MAOB) genes are located predict risk of alcoholism and ASPD
better than the MAOA-LPR locus alone. Participants included 168 alcoholics (39 with ASPD
(antisocial alcoholics) and 123 controls (no alcoholics, no ASPD). Antisocial behavior was also
modeled as a continuous trait: ASPD symptoms count. The MAOA-LPR low activity allele was
associated with alcoholism (P = 0.005), particularly antisocial alcoholism (P = 0.00009), only
among sexually abused subjects. Sexually abused women who were homozygous for the low
activity allele had higher rates of alcoholism and ASPD, and more ASPD symptoms, than
abused women homozygous for the high activity allele. Heterozygous women displayed an
intermediate risk pattern. In contrast, there was no relationship between alcoholism/antisocial
behavior and MAOA-LPR genotype among non-abused women. The MAOA-LPR low activity
allele was found on three different haplotypes. The most abundant MAOA haplotype
containing the MAOA-LPR low activity allele was found in excess among alcoholics
(P = 0.008) and antisocial alcoholics (P = 0.001). Finally, a MAOB haplotype, which we termed
haplotype C, was significantly associated with alcoholism (P = 0.006), and to a lesser extent
with antisocial alcoholism (P = 0.03). In conclusions, MAOA seems to moderate the impact of
childhood trauma on adult psychopathology in female subjects in the same way as previously
shown among male subjects. The MAOA-LPR low activity allele appears to confer increased
vulnerability to the adverse psychosocial consequences of CSA. Haplotype-based analysis of
the MAOA gene appeared to strengthen the association, as compared to the MAOA-LPR locus
alone. A MAOB haplotype was associated with alcoholism independently from ASPD.
Molecular Psychiatry (2008) 13, 334–347; doi:10.1038/sj.mp.4002034; published online 26 June 2007
Keywords: alcoholism; antisocial personality disorder; MAOA; MAOA-LPR, MAOB; childhood
sexual abuse; gene by environment interaction

Introduction pression,7–9 suicidal behavior;4,8,10,11 post-traumatic

Thirteen percent of American women report child-
hood sexual abuse (CSA),1 and CSA is a critical
environmental exposure for a variety of psychiatric
diseases. Women exposed to CSA have an increased
risk for different psychopathologies in adulthood
including addictions to alcohol and other drugs;2–6
antisocial personality disorder (ASPD);4,5 major de-
Correspondence: Dr F Ducci, Laboratory of Neurogenetics,
NIAAA, NIH, 5625 Fishers Lane, Room 3S32, MSC 9412,
Rockville, MD 20852, USA.
E-mail: duccif@mail.nih.gov
Received 31 January 2007; revised 19 April 2007; accepted 7 May
2007; published online 26 June 2007
stress disorder4,12,13 and eating disorders.6
The impact of CSA on adult mental health is only
one of the complex set of intercorrelated social,
economic and familial disadvantages and as such the
presence of CSA is an indicator of a wider and larger
dysfunction within families.1,5 In addition, within
particular socio-cultural contexts, such as occurs in
certain American Indian tribes, rates of violence and
cumulative trauma are very high, potentially amplify-
ing within-family effects and contributing to the high
vulnerability to psychiatric disorders found overall in
these communities.14 In the American Indian tribe that
is the object of the present study, lifetime prevalences
of alcohol dependence (AD) and ASPD among women

are very high, 0.50 and 0.13, respectively.15 By
comparison, prevalences of AD and ASPD among
US epidemiological samples of woman were 0.08 and
0.02, respectively.16
In this relatively isolated American Indian commu-
nity,4 approximately half of women were exposed to
sexual abuse during childhood/early adolescence and
CSA was found to predict both the development of
alcoholism (odds ratio (OR): 2.1) and ASPD (OR: 2.9).4
In other words, despite the high prevalences of
Alcoholism and ASPD and community-pervasive risk
exposures, CSA still emerged as a major risk factor.
However, while CSA has profound enduring effects
into adulthood, not all abused children develop
psychosocial problems later in life. Interindividual
differences in stress resiliency are likely to be
partially moderated by genetic differences, a phenom-
enon known as gene by environment interaction.
Recent findings17–21 indicate that the monoamine
oxidase A gene (MAOA) might be among those genes
that moderate individual response to stress.
MAOA is an X-linked gene22 encoding the mito-
chondrial enzyme MAOA (EC 1.4.3.4) that metabo-
lizes monoamines including noradrenaline (NE),
dopamine (DA) and serotonin (5-HT). MAOA knock-
out mice have higher levels of DA, 5-HT and NE,
and manifest increased aggressive behavior.23 In the
humans, a common MAOA polymorphism influences
MAOA transcription.24 This locus, termed MAOA-
linked polymorphic region (MAOA-LPR), is a Variable
Number Tandem Repeat (VNTR) located approxi-
mately 1.2 kb upstream to the MAOA start codon
and within the gene’s transcriptional control re-
gion.24,25 Alleles at this VNTR have different number
of copies of a 30-bp repeated sequence with the three
and four repeats alleles being, by far, the most
common. Alleles with four repeats are transcribed
more efficiently than alleles with three copies of the
repeat and therefore are associated with higher
MAOA activity.24 In a relatively recent study,17 it
has been shown that the effect of adversity on
vulnerability to antisocial behavior is contingent on
MAOA-LPR genotype. In a longitudinal sample of
male subjects, Caspi et al.17 have found that mal-
treated boys with the low activity genotype were more
likely to develop antisocial problems later in life than
boys with the high activity genotype. There was also a
main effect of maltreatment on risk for antisocial
behavior, whereas a main effect of MAOA-LPR
genotype was not detected. These results were later
replicated.18 Overall, these findings indicate that
MAOA-LPR contributes to interindividual differences
in stress resiliency. However, it still remains unclear
whether the MAOA-LPR by environment interactive
effect on antisocial behavior described for male
subjects is applicable to female subjects. The few
studies conducted on women have reported incon-
sistent results.19,26,27 In a sample of 196 Caucasian
women, the low activity allele was associated with
adolescent but not adult antisocial behavior only
among maltreated subjects.27 In a sample of 119
MAOA and childhood sexual abuse
F Ducci et al
335
adolescent female subjects, the high activity genotype
rather than the low activity genotype was associated
with increased risk of criminal behavior in the
presence of psychosocial risk.26 Finally, Huang et
al.19 failed to find any significant interactive effect
between MAOA-LPR and maltreatment in a sample of
377 female subjects.
The main purpose of the present study was to
evaluate whether MAOA-LPR predicts alcoholism
and ASPD contingent on early ( < 16 years) exposure
to sexual abuse in a high-risk community sample of
291 adult American Indian women. A secondary aim
was to test whether haplotypes covering the region of
MAOA and the nearby monoamine oxidase B (MAOB)
genes predict alcoholism and ASPD better than the
MAOA-LPR locus alone. In this regard, it is important
to stress that the MAOA-LPR is located within a
relatively large region of high linkage disequilibrium
(LD);28,29 therefore, other functional polymorphisms
might contribute to its effects on transcription. A
recent study exploring 12 single-nucleotide poly-
morphisms (SNPs) in addition to the MAOA-LPR
suggests that this locus might not account for all the
variation in MAOA transcription due to genetic
factors and that other functional loci might exist.28
Such functional loci might be located at the MAOA
gene as well as MAOB. For this reason, we genotyped
nine additional SNPs encompassing the region of the
two MAO genes and performed haplotype-based
analyses.
Methods
This protocol was approved by the Tribal Council of
this Southwest Tribe, and by the Institutional Review
Board of the National Institute on Alcohol Abuse and
Alcoholism, National Institutes of Health. All subjects
provided informed consent before entering the study
and received $40 as compensation for their time. To
maximize confidentiality, the name and exact loca-
tion of the tribe are not listed.
Participants
Two hundred and ninety-one women (mean age7s.d.:
37.80714.58) were recruited from a Southwest
American Indian tribe. In addition, 210 male subjects
that were recruited were not investigated in the
present report because of the low number of them
who were without alcoholism or ASPD (N = 22) and
because of their lower level of exposure to CSA
(N = 21) as compared to women. Recruitment was
blind to the clinical histories of subjects and their
relatives. This intensively studied sample has been
characterized as representative of the source popula-
tion in a variety of respects including socioeconomic
status, and degree of relatedness. An epidemiologic
study using the CAGE30 has shown that the high
prevalence of alcoholism in this data set is reflective
of the population.31 Elder tribal members who were
considered matriarchs or patriarchs and who posses-
sed a good knowledge of family structures provided
Molecular Psychiatry
 MAOA and childhood sexual abuse
F Ducci et al
336
information on large multigenerational genealogies.
Participants were older than 21 years and eligible for
tribal enrollment, having at least one-quarter tribal
heritage.4
Psychiatric assessment
Psychiatric diagnoses were made according to Diag-
nostic and Statistical Manual of Mental Disorders
(DSM)-III-R criteria using the Schedule for Affective
Disorders and Schizophrenia-Lifetime version
(SADS-L) by following operationally defined criteria
and using the instructions of Spitzer et al.32,33 ASPD
was diagnosed according to DSM-III-R. Validity of
standard criteria for psychiatric diagnosis can be
problematic within special cultural groups. There-
fore, provisions were taken to limit diagnostic errors
due to culture-specific phenomena. SADS-L inter-
views were administered to all subjects by a psycho-
logist with extensive experience in tribal customs and
culture (RWR). As the high rate of unemployment in
this population might lead to an overestimation of the
prevalence of ASPD, participants were questioned in
detail about the specific circumstances that may have
contributed to their unemployment status. In addi-
tion, the SADS-L criterion, ‘does not maintain close
social ties’, was added to the DSM-III-R criteria to
compensate for the absence of some ASPD items on
the SADS-L. Diagnoses were made from these data by
two blind raters: a clinical social worker and a clinical
psychologist. The rates of agreement between the two
raters were acceptable; the kappa coefficient for
alcohol abuse diagnosis was 0.72, for AD 0.96 and
for ASPD 0.97. Diagnostic differences between the
two raters were resolved in a consensus conference
that included a senior psychiatrist experienced in
diagnosis in American Indian people. ASPD symp-
toms count was based on SADS-L items.
Among the 291 female participants, 168 had a
lifetime diagnosis of an alcohol use disorder (AUD)
and 86% of these had AD. Thirty-nine participants
had both ASPD and AUD. All subjects with ASPD
were affected by AUD. Controls (N = 123) were non-
ASPD and non-alcoholic. Among male participants,
89% were affected by AUD (187/210) and 39% by
ASPD (82/210). Only 22 male participants were non-
ASPD and non-alcoholic.
To increase our power to detect a gene effect on
antisocial behavior, the latter variable was also
modeled as a continuous trait: ASPD symptoms
count. The mean7s.d. ASPD symptom count for this
sample of women was 4.1874.14. For comparison,
among male participants, the mean7s.d. ASPD
symptom count was 7.6975.04.
Assessment of CSA
Exposure to sexual abuse during childhood was
retrospectively assessed in a subset of 187 women
and 126 men. The data for CSA were mainly collected
during the psychiatric interview sessions and to
lesser extent were based on medical records, which
were available in cases where the victim had received
Molecular Psychiatry
treatment at health service facilities. Therefore,
information on CSA was largely dependent upon
recall of past events and only clearly recalled infor-
mation was collected.
CSA was defined as direct physical sexual contact
with a perpetrator at least 5 years older than the
victim, and in victim’s experiencing such contact
before the age of 16 years. Peer experiences and
sexual abuse not involving direct physical contact
were excluded. As noted, questions about CSA were
asked during SADS-L psychiatric interview sessions.
Subjects had completed approximately 2 h of inter-
viewing before being asked the following seven
questions:
(1) Were you ever sexually abused or molested as a
child before the age of 16 years?
If answered yes to question 1, the subject was then
asked the following questions:
(2) Who first sexually abused or molested you?
(3) At what age did this (first abuse or molestation)
begin?
(4) How often did it (the abuse or molestation) occur?
(5) What did this person do to sexually abuse or
molest you? Describe what she/he did.
(6) Were you sexually abused or molested by an
additional individual?
If answered yes to question 6, the subject was asked
questions 2–6 again.
The semistructured nature of the interview per-
mitted opportunities for further disclosure of events
by subjects including frequency, duration and out-
come of reported abuse. There is evidence that by
using this format, accurate recall and reporting of
childhood experiences is enhanced.34 Standard mea-
sures of child sexual abuse were not used primarily
because they assume a nuclear family structure,
inapplicable to this Indian community and to permit
descriptions of events and experiences, which may
vary from existing models.35
In the current sample, 51% of interviewed women
(N = 95/187) admitted CSA in childhood, as pre-
viously reported.15 For comparison, prevalence of
CSA in men was 16% (21/126).
Genotyping
We genotyped the MAOA-LPR locus and nine addi-
tional SNPs spanning the 230 kb region where both
the MAOA and MAOB genes are located. These two
genes are separated by approximately 20 kb and are
disposed tail-to-tail. Locations of polymorphisms
within the two genes are shown in Figure 1.
MAOA-LPR
The MAOA gene promoter VNTR polymorphism was
amplified from 25 ng genomic DNA using these
primer sequences: forward 50 -CCC AGG CTG CTC
CAG AAA CAT G-30 and reverse 50 -GTT CGG GAC
CTG GGC AGT TGT G-30 . Because of the high GC
content in the VNTR region, amplification was
performed using Invitrogen’s PlatinumTaq and PCRX

Figure 1 Distribution of 10 genotyped polymorphisms spanning 236 kb of the MAOA/MAOB represented. Exons are
represented in black; the 30 untranslated mRNA regions are in gray.
Enhancer System kits, according to the manufac-
turer’s protocol (Invitrogen, Carlsbad, CA, USA), with
5 mM of each primer and 25 mM deoxynucleoside
triphosphates in a total reaction volume of 15 ml.
Amplifications were performed on a Perkin Elmer
9700 thermocycler (Applied Biosystems, Foster City,
CA, USA) with one cycle at 961C for 10 min followed
by 30 cycles of 941C for 15 s, 601C for 15 s, 721C for
30 s and a final 3 min extension at 721C. The forward
primer was labeled with the fluorescent dye 6-FAM,
and amplicons were visualized on an ABI 3100
capillary sequencer. Allele sizes (allele 3, 263 bp;
allele 3.5, 278 bp; allele 4, 293 bp; allele 5, 323 bp)
were determined using Genotyper 2.5 (Applied
Biosystems).
SNP genotyping
Nine SNPs were genotyped using the Illumina Golden-
Gate assay. In this method, DNA samples (250 ng at
100 ng/ml) are bound to paramagnetic particles and
then assay oligonucleotides are added. Three oligos
are designed for each SNP including two oligos
specific to each allele at the SNP site (allele-specific
oligos, ASO) and a third oligo (locus-specific oligo,
LSO) that hybridizes several bases downstream from
the SNP site. All three oligonucleotides contain a
region of genomic complementarity and universal
PCR primer sites. The LSO also contains a unique
address sequence that targets a particular bead type.
During the hybridization step, the oligonucleotides
hybridize to the genomic DNA bound to paramagnetic
particles. After several wash steps, extension of the
appropriate ASO and ligation of the extended product
to the LSO joins information about the genotype
present at the SNP site to the address sequence at the
LSO. These joined products are then amplified
via PCR. For more detail description of the Golden-
Gate assay, see http://www.illumina.com/products/
prod_snp.ilmn.
Statistical analyses
Genotype/allele frequencies of each marker were
compared between alcoholics and controls (non-
AUD, non-ASPD) using the w2 test. To test whether
the associations between genotype and AUD were
MAOA and childhood sexual abuse
F Ducci et al
337
mainly driven by antisocial alcoholics, the same
analyses were repeated comparing antisocial alco-
holics (AUD þ ASPD) to controls. Mean ASPD symp-
toms count was compared across genotypes using
analysis of variance (ANOVA).
To test for gene  environment interaction, both
allele- and genotype-based analyses were repeated
separately within the sexually abused and non-
sexually abused groups. More formal genes by
environment analyses were conducted using linear
regression when the dependent variable was a
continuous trait (ASPD symptoms count) and logistic
regression when the dependent variable was catego-
rical (AUD; AUD þ ASPD). In both the logistic and
linear regressions, parameters entered in the model
as independent variables were: MAOA, CSA and
MAOA  CSA. Of note, the linear regression was
performed at the genotype level, whereas the logistic
regression was performed at the allelic level due to
the power issue. In fact, allele-based analyses, which
are possible only for categorical traits, have the
advantage of being based on the number of chromo-
somes, which is twice the number of individuals and
have a reduced degree of freedom (1 rather than 2) as
compared to genotype-based analyses. On the other
hand, certain genotypic effects can be missed, and
interpretation of a positive result is more limited.
Hardy Weinberg Equilibrium (HWE) for each locus
and LD between each pair of markers were computed
using Haploview v3.32.36 Diplotypes were assigned
to each individual using PHASE 2.02.37 Haplotypes
were compared between cases and controls using the
w2 test or the Fisher’s exact test when indicated.
Although most of participants included in the
present study belonged to two large multigenerational
pedigrees, the degree of relatedness between any
two individuals in this sample is overall low. The
probability that a chromosome region from any pair of
individuals is shared identical by descent (that is the
kinship coefficient) was calculated for all possible
pairs (related and unrelated) using LOKI v2.4.7
(http://loki.homeunix.net/). The mean kinship coeffi-
cient7s.e. for all pairs of female subjects included in
this study was only 0.004570.0001, which is close to
the average kinship of the source population and is
Molecular Psychiatry
 MAOA and childhood sexual abuse
F Ducci et al
338
less than the second cousin level. Therefore, analyses
assuming independence of individuals were under-
taken and the sample was analyzed using a case/
control approach.
All statistical analyses were conducted using JMP
software v5.1 (SAS Institute, Cary, NC, USA). Criter-
ion for statistical significance was set at 0.05.
Results
Minor allele frequency, position (according to the
NCBI Human Genome Build no. 35.1) and HWE of
each marker are reported in Table 1. At the MAOA-
LPR locus, similarly to what is observed in Caucasian
populations, the three repeats (freq: 0.38) and the four
repeats (freq: 0.62) alleles were, by far, the most
common. The five and 3.5 repeats alleles were found
only in two and one subject, respectively. Since the
functional effect of these rare alleles is controver-
sial,23,24 these individuals were excluded. Genotypes
at all markers were in HWE equilibrium (Table 1).
Main effects of MAOA and MAOB markers
Genotype and allele frequencies at each marker were
compared between controls and alcoholics. To eval-
uate whether significant differences between controls
and alcoholics were mainly driven by antisocial
alcoholics, genotype/allele frequencies were also
compared between controls and alcoholics with
comorbid ASPD (Tables 2 and 3). Several markers
across both MAOA (Table 2) and MAOB (Table 3)
genes showed association with alcoholism.
The three repeat allele of the MAOA-LPR was
significantly more common among antisocial alco-
holics than in controls (d.f. = 1, w2 = 5.2, P = 0.02). Only
a trend toward significance was found when all
alcoholics (antisocial plus non-antisocial alcoholics)
were compared with controls (d.f. = 1, w2 = 3.02,
P = 0.08).
Other markers within both genes displayed sig-
nificant differences between cases and controls both
at the genotypic and allelic levels (Tables 2 and 3).
Table 1 MAF, position and HWE for ten MAOA/MAOB
markers
# Markers Position HWE P-value
1 MAOA-LPR 43249686 0.1914
2 rs1465108 43294463 0.3155
3 rs909525 43309456 0.1551
4 rs979605 43357617 0.5955
5 rs2239448 43358933 1 0.355
6 rs1799836 43384253 1 0.201
7 rs10521432 43389994 0.5225
8 rs12394221 43426203 1 0.077
9 rs5905512 43482648 0.3722
10 rs9887047 43486377 1 0.082
Abbreviations: HWE, Hardy Weinberg Equilibrium; MAF,
minor allele frequency; MAOA, monoamine oxidase A gene;
MAOB, monoamine oxidase B gene.
Molecular Psychiatry
Of note, for MAOA markers, differences in genotype/
allele frequencies between controls and antisocial
alcoholics were stronger than those found comparing
controls with all alcoholics, indicating that signals of
association with alcoholism were mainly driven by
antisocial alcoholics. On the other hand, genotype/
allele frequencies for SNPs located within MAOB
gene were similar between all alcoholics and anti-
social alcoholics, indicating that association between
MAOB markers and alcoholism were independent
from ASPD diagnosis.
Effect of the interaction between MAOA-LPR and CSA
on AUD and antisocial behavior
As shown in Table 4 and Figure 2, sexually abused
women who were homozygous for the low activity
MAOA-LPR allele were more likely to have alcohol-
ism, particularly antisocial alcoholism, compared
with women who were homozygous for the high
activity allele. Heterozygous women displayed an
intermediate risk pattern compared to homozygotes,
consistent with a codominant effect of the MAOA
alleles. In contrast, there was no predictive value of
the MAOA-LPR genotype for antisocial alcoholism in
the women who had not been sexually abused.
Allelic-based analyses (Table 4) were also consistent
with an interaction effect between MAOA-LPR and
CSA. Among sexually abused women, the low
activity allele was more common in alcoholics than
in controls (d.f. = 1; w2 = 7.87; P = 0.005) with differ-
ences being driven by alcoholics who also had ASPD
(d.f. = 1, w2 = 15.42, P = 0.00009). In contrast, no differ-
ences in allele frequencies were found between cases
and controls among non-sexually abused women. In
line with these findings, logistic regression showed
that the interaction effect between CSA and MAOA-
LPR was significant in predicting antisocial alcohol-
ism (logistic regression, MAOA-LPR  CSA: d.f. = 1;
w2 = 7.17; P = 0.007) but not alcoholism in general
(logistic regression, MAOA-LPR  CSA, d.f. = 1;
w2 = 2.77; P = 0.09).
Similar results emerged when antisocial behavior
was modeled as a continuous trait (ASPD symptoms
count) (Figure 3). Linear regression showed a
main effect of sexual abuse on antisocial behavior
(b7s.e.: 2.3170.38; P = 1e-8), whereas a main effect of
MAF MAOA-LPR genotype was not found (MAOA-LPR
(3/3 vs 4/4): b7s.e.: 0.8470.67; P = 0.22; MAOA-LPR
0.384 (3/4 vs 4/4): b7s.e.: 0.1170.46; P = 0.46). The
0.338 interaction effect between MAOA-LPR and CSA
0.349 was significant (CSA  MAOA-LPR (3/3): b7s.e.:
0.312 2.570.68; P = 0.0003; CSA  MAOA-LPR (3/4):
b7s.e.: 1.0870.45; P = 0.02). The whole regression
model explained 22% of the ASPD symptom count
0.096
variance. As shown in Figure 3, within the group of
0.283 sexually abused women, the mean ASPD symptoms
count was the highest among women who were
homozygous for the low activity allele, intermediate
among heterozygous and the lowest among homo-
zygous for the high activity allele (ANOVA: d.f. = 2;
F = 8.0; P = 0.0006). In contrast, MAOA-LPR genotypes
 Table 2 Allelic and genotypic associations of MAOA polymorphisms in 291 American Indian women: controls (C) are compared to all alcoholics (AUD) and to antisocial
alcoholics (ASPD þ AUD)

MAOA G C AUDa ASPD þ AUD d.f. w2b P-valueb d.f. w2c P-valuec A C AUD ASPD þ AUD d.f. w2b P-valueb d.f. w2c P-valuec
(N = 123) (N = 168) (N = 39) (N = 246) (N = 336) (N = 78)

MAOA-LPR 3/3 0.10 (13) 0.14 (23) 0.23 (9)

3/4 0.47 (56) 0.55 (92) 0.51 (20) 2 3.95 0.13 2 5.50 0.06 3 0.34 0.41 0.49 1 3.02 0.08 1 5.2 0.02
4/4 0.43 (51) 0.31 (52) 0.26 (10)
rs1465108 TT 0.06 (8) 0.12 (20) 0.23 (9)
TC 0.41 (51) 0.53 (88) 0.50 (19) 2 8.72 0.01 2 11.74 0.003 T 0.27 0.38 0.47 1 7.90 0.005 1 10.65 0.001
CC 0.52 (64) 0.35 (59) 0.28 (11)
rs909525 AA 0.51 (61) 0.32 (54) 0.23 (9)
AG 0.43 (51) 0.56 (91) 0.56 (21) 2 10.02 0.007 2 13.40 0.001 A 0.72 0.6 0.5 1 8.51 0.003 1 12.92 0.0003

F Ducci et al
MAOA and childhood sexual abuse
GG 0.07 (8) 0.12 (20) 0.23 (9)
rs979605 AA 0.05 (6) 0.12 (20) 0.21 (8)
AG 0.41 (50) 0.47 (79) 0.49 (19) 2 7.83 0.02 2 12.24 0.002 A 0.25 0.36 0.49 1 7.26 0.007 1 10.42 0.001
GG 0.54 (67) 0.41 (68) 0.31 (12)
rs2239448 AA 0.09 (11) 0.16 (26) 0.23 (9)
AG 0.44 (54) 0.48 (78) 0.49 (19) 2 4.15 0.13 2 7.44 0.02 A 0.31 0.39 0.47 1 4.01 0.05 1 6.94 0.008
GG 0.47 (58) 0.38 (63) 0.28 (11)

Abbreviations: A, allele; ASPD, antisocial personality disorder; AUD, alcohol use disorder; d.f., degree of freedom; G, genotype; MAOA, monoamine oxidase A gene.
Significant P-values are in bold.
a
AUD includes alcoholics with and without ASPD.
b
All alcoholics compared to controls.
c
Antisocial alcoholics compared to controls.
Molecular Psychiatry

339
Molecular Psychiatry

340
Table 3 Allelic and genotypic association of MAOB polymorphisms in 291 American Indian women: controls (C) are compared to both all alcoholics (AUD) and to
antisocial alcoholics (ASPD þ AUD)

MAOA and childhood sexual abuse

MAOB G C AUDa ASPD þ AUD d.f. w2b P-valueb d.f. w2c P-valuec A C AUD ASPD þ AUD d.f. w2b P-valueb d.f. w2c P-valuec
(N = 123) (N = 168) (N = 39) (N = 246) (N = 336) (N = 78)

rs1799836 TT 0.60 (74) 0.68 (112) 0.67 (26)

TC 0.32 (40) 0.32 (53) 0.31 (12) 2 5.76 0.06 2 1.53 0.46 T 0.76 0.82 0.82 1 3.20 0.07 1 1.09 0.29
CC 0.07 (9) 0.02 (3) 0.03 (1)

F Ducci et al
rs10521432 TT 0.00 (0) 0.02 (4) 0.03 (1)
TC 0.11 (14) 0.21 (34) 0.21 (8) 2 9.11 0.01 2 4.98 0.08 T 0.06 0.13 0.13 1 8.13 0.006 1 3.92 0.04
CC 0.89 (109) 0.77 (129) 0.76 (30)
rs12394221 AA 0.92 (113) 0.80 (134) 0.82 (32)
AG 0.08 (10) 0.19 (31) 0.15 (6) 2 9.41 0.01 2 4.60 0.10 A 0.96 0.89 0.89 1 8.74 0.004 1 4.32 0.04
GG 0.00 (0) 0.01 (2) 0.02 (1)
rs5905512 TT 0.52 (64) 0.53 (88) 0.49 (19)
TC 0.38 (47) 0.38 (64) 0.46 (18) 2 0.05 0.97 2 1.26 0.53 T 0.71 0.72 0.72 1 0.04 0.84 1 0.01 0.91
CC 0.10 (12) 0.09 (15) 0.05 (2)
rs9887047 TT 0.90 (111) 0.80 (133) 0.79 (31)
TC 0.10 (12) 0.20 (32) 0.18 (7) 2 7.49 0.02 2 4.78 0.09 T 0.95 0.89 0.88 1 6.49 0.01 1 4.33 0.03
CC 0.00 (0) 0.01 (2) 0.03 (1)

Abbreviations: A, allele; ASPD, antisocial personality disorder; AUD, alcohol use disorder; d.f., degree of freedom; G, genotype; MAOB, monoamine oxidase B gene.
Significant P-values are in bold.
a
AUD includes alcoholics with and without ASPD.
b
All alcoholics were compared to controls.
c
Antisocial alcoholics were compared to controls.
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341
Table 4 Interaction between MAOA-LPR and childhood sexual abuse: genotype and allele frequencies are compared between
cases and controls separately within the groups exposed and non-exposed to sexual abuse during childhood/early adolescence

Sexual abuse G C AUDa ASPD þ AUD d.f. w2b P-value d.f. w2c P-value
(N = 95)

3/3 0.04 (1) 0.18 (12) 0.37 (9) 2 8.72 0.02 2 13.51 0.001
3/4 0.37 (10) 0.53 (36) 0.45 (11)
4/4 0.59 (16) 0.29 (20) 0.17 (4)

A C AUD ASPD þ AUD d.f. w2b P-value d.f. w2c P-value

3 0.22 (12) 0.44 (60) 0.60 (29) 1 7.87 0.005 1 15.42 0.00009
4 0.78 (42) 0.56 (76) 0.40 (19)

No sexual abuse G C AUD ASPD þ AUD d.f. w2b P-value d.f. w2c P-value
(N = 92)

3/3 0.09 (4) 0.04 (2) 0.00 (0) 2 3.97 0.13 2 NA NA

3/4 0.38 (16) 0.58 (29) 0.50 (5)
4/4 0.52 (22) 0.38 (19) 0.50 (5)

A C AUD ASPD þ AUD d.f. w2b P-value d.f. w2c P-value

3 0.29 (24) 0.33 (33) 0.25 (5) 1 0.42 0.51 1 0.10 0.75
4 0.71 (60) 0.67 (67) 0.75 (15)

Abbreviations: A, allele; C, controls; ASPD þ AUD, antisocial alcoholics; AUD, alcohol use disorder; d.f., degree of freedom;
G, genotype; NA, non-applicable.
Significant P-values are in bold.
a
AUD includes alcoholics with and without ASPD.
b
All alcoholics were compared to controls.
c
Antisocial alcoholics were compared to controls.

were not associated with antisocial behavior among
non-sexually abused participants (ANOVA: d.f. = 2;
F = 2.07; P = 0.14). Results were not driven by few
outliers as shown in the Supplementary material in
Figure 5.
MAOL-LPR has been previously reported to in-
crease risk of exposure to maltreatment,19 a pheno-
menon known as gene by environment correlation.17
Gene by environment correlation could lead to a false
significant gene by environment interactions. There-
fore, we compared allele frequencies at the MAO-LPR
between participants exposed and not exposed to
sexual abuse but we did not find a significant
difference (allele based analyses: d.f. = 1; w2 = 2.14,
P = 0.14; genotype based analyses: d.f. = 2, w2 = 3.28;
P = 0.19) indicating that what we observed is mainly a
‘true’ MAOA-LPR by CSA interactive effect. Never-
theless, the direction of the trend is in the same
direction as Huang et al., and could tend to amplify
the effect of MAOA-LPR on antisocial alcoholism.
Haplotype-based analyses
The haplotype-block structure of the region contain-
ing MAOA and MAOB genes is shown in Figures 4a
and b. D0 values tended to be greater within each gene;
therefore, we divided the region into two blocks of
reduced recombination: one including all five MAOA
markers and one block including all MAOB markers
except for SNP rs1799836, which showed very low LD
with almost all other markers. However, some degree
of LD was also detected between MAOA and MAOB
markers. Frequencies of haplotypes encompassing
each gene are shown in Figure 4b. To easily identify
parts shared by different haplotypes, alternative
alleles at each locus are colored in red or black.
Within MAOA gene, we found five different haplo-
types (labeled A–E) with frequencies higher than
0.01. These haplotypes accounted for 99% of all
haplotype diversity in the region. Two haplotypes
(A and B) were by far the most common and dis-
played a yin–yang configuration. The low activity
allele at the MAOA-LPR locus was found on three
different haplotype backgrounds. For MAOB, we
found three haplotypes with frequencies higher than
0.05 that accounted for 98% of all the haplotype
diversity. Since frequencies of rare haplotypes
computed with Phase are imprecise, carriers of rare
haplotypes (freq < 1%) were excluded from the follow-
ing analyses.
MAOA. Within the MAOA gene, haplotype
frequencies differed significantly between all
alcoholics and controls (d.f. = 4; w2 = 11.82; P = 0.02) as
well as between antisocial alcoholics and controls
(d.f. = 4, w2 = 14.37, P = 0.006) (Table 5). Post hoc
analyses comparing each haplotype with all other

Molecular Psychiatry
 MAOA and childhood sexual abuse
F Ducci et al

342

Figure 2 Fractions of participants with alcoholism plus antisocial personality disorder (AUD þ ASPD), alcoholism without
ASPD (AUD no ASPD) and controls (C) are presented for each MAOA-LPR genotype category separately within sexually
molested (N = 95) and non-sexually molested participants (N = 92). 3/3 = homozygous for the low activity allele; 3/4 =
heterozygous; 4/4 = homozygous for the high activity allele.

Figure 3 ASPD symptoms count is compared across the three MAOA-LPR genotypes separately within sexually molested
(N = 95) and non-sexually molested participants (N = 92). 3/3 = homozygous for the low activity allele; 3/4 = heterozygous;
4/4 = homozygous for the high activity allele; b = regression coefficient; CSA = childhood sexual abuse. *** = P < 0.001.

haplotypes combined revealed that significance was B. This haplotype was significantly more common in
mainly driven by the most common MAOAL-PR low alcoholics (d.f. = 1, w2 = 7.05; P = 0.008) compared to
activity allele-containing haplotype, namely haplotype controls. As previously seen for the MAOA-LPR,

Molecular Psychiatry
 MAOA and childhood sexual abuse
F Ducci et al

343

Figure 4 MAOA and MAOB haplotype-block structure (3A) and frequencies of haplotypes within MAOA and MAOB genes
(3B). Hap = haplotype. In (a) numbers indicate pairwise D 0 values, when the number is not indicated D 0 is equal to 1. In (b),
alternative alleles at each locus are depicted in red or black to facilitate comparison between haplotypes.

Table 5 Frequencies of MAOA and MAOB haplotypes are compared between cases and controls

Haplotype C AUDa ASPD þ AUD d.f. w2b P-value w2c P-value d.f. w2b,* P-value w2c,* P-value

MAOA
A 4CAGG 0.61 (149) 0.54 (174) 0.48 (32) 1 2.17 0.14 4.91 0.03 11.82 0.02 14.37 0.006
B 3TGAA 0.25 (62) 0.36 (114) 0.48 (32) 1 7.05 0.008 10.41 0.001
C 3CAGG 0.07 (16) 0.03 (10) 0.01 (1) 1 3.59 0.06 2.75 0.13# 4
D 4CAGA 0.06 (14) 0.03 (11) 0.03 (2) 1 1.67 0.19 1.03 0.53#
E 3TGGG 0.02 (5) 0.03 (11) 0.04 (3) 1 1.03 0.31 0.99 0.38#

MAOB
A CATT 0.73 (173) 0.74 (236) 0.75 (54) 1 0.009 0.92 0.03 0.85 9.49 0.007 5.66 0.06
B CACT 0.22 (51) 0.15 (49) 0.14 (10) 1 3.77 0.05 2.15 0.14 2
C TGCC 0.04 (10) 0.10 (33) 0.11 (8) 1 7.41 0.006 4.65 0.03

Abbreviations: ASPD þ AUD, antisocial alcoholics; AUD, alcohol use disorder; C, controls; d.f., degree of freedom; MAOA,
monoamine oxidase A gene; MAOB, monoamine oxidase B gene; N, number of chromosomes.
Significant P-values are in bold. Carriers of haplotypes with frequencies < 1% are excluded.
a
AUD includes alcoholics with and without ASPD.
b
All alcoholics were compared to controls.
c
Antisocial alcoholics were compared to controls.
*Global P-value.
#
P-value reported were computed using the Fisher’s exact test.

differences in haplotype frequencies were driven by
antisocial alcoholics (d.f. = 1, w2 = 10.41, 0.001).
Since MAOA haplotype B displayed a main effect
on alcoholism, which was stronger than that observed
for the MAOA-LPR locus alone (Table 2), we
performed interaction analysis between this haplo-
type and CSA.
MAOA haplotype B and CSA significantly inter-
acted with sexual abuse (logistic regression: depen-
dent variable = AUD: haplotype B  CSA: d.f. = 1;
w2 = 4.47; P = 0.03; dependent variable = ASPD þ AUD:
d.f. = 1; w2 = 4.04; P = 0.04). Similarly to what we
observed with the MAOA-LPR alone (Table 6), there
was a significant difference in haplotype B between
cases and controls only within women who were
exposed to CSA, and but not among non-abused
women.
MAOB. Within the MAOB gene, haplotype
frequencies were significantly different between
alcoholics and controls (AUD d.f. = 2; w2 = 9.49;
P = 0.007) but only a trend was found when
antisocial alcoholics were compared to controls
(d.f. = 2; w2 = 5.66; P = 0.06) (Table 5). Differences
were mainly driven by haplotype C, which was
more common among alcoholics than controls

Molecular Psychiatry
 MAOA and childhood sexual abuse
F Ducci et al
344
Table 6 Interaction between MAOA haplotype B (3TGAA) and childhood sexual abuse: haplotype frequencies are compared
between cases and controls separately within groups of participants exposed and non-exposed to sexual abuse during childhood
and early adolescence
MAOA haplotype B
Sex abused C 0.17 (9)
AUDc 0.41 (52)
AUD þ ASPD 0.54 (25)
No sex abused C 0.19 (17)
AUDc 0.20 (19)
AUD þ ASPD 0.19 (3)
Abbreviations: ASPD þ AUD, antisocial alcoholics; AUD, alcohol use disorder; C, controls; d.f. = degree of freedom; MAOA,
monoamine oxidase A gene.
Significant P-values are in bold. Carriers of haplotypes with frequencies < 1% are excluded.
a
All alcoholics were compared to controls.
b
Antisocial alcoholics were compared to controls.
c
AUD includes alcoholics with and without ASPD.
(AUD: d.f. = 1, w2 = 7.41; P = 0.006). In contrast to what
was observed for MAOA, the frequency of MAOB
haplotype C was almost the same in all alcoholics and
in antisocial alcoholics.
The interaction analysis between MAOB haplotype
C and CSA did not reveal significant G  E (logistic
regression, dependent variable = AUD: haplotype
C  CSA: d.f. = 1; w2 = 2.11; P = 0.14; dependent
variable = AUD þ ASPD: haplotype C  CSA: d.f. = 1;
w2 = 0.30; P = 0.58).
Discussion
It is well known that women exposed to CSA have an
increased risk of developing a broad range of psycho-
pathologies, including ones that are sometimes re-
garded as ‘atypical’ for this sex, such as ASPD.
However, not all women exposed to CSA develop
adverse psychosocial consequences. Interindividual
variation in stress resiliency is at least partially
mediated by genetic factors and recent findings have
indicated that a functional locus within the MAOA
gene (MAOA-LPR) moderates responses to childhood
maltreatment.17–20 However, no previous study has
focused specifically on CSA and only a few studies so
far have explored the interaction between MAOA and
child victimization in female cohorts.19,26,27
The main purpose of the present study was to test
whether MAOA-LPR interacts with exposure to sexual
abuse in a community sample of American Indian
women with an extremely high rates of CSA.4 CSA in
this community should be seen as an index of a more
complex matrix of adverse conditions from which the
abused women suffered and as part of broader
familial and social dysfunction.4 Consistent with
previous findings derived from male samples,17–20
our results support the involvement of MAOA gene in
moderating individual sensitivity to childhood trau-
ma. Sexually abused women who were homozygous
for the low activity MAOA-LPR allele had higher rates
of alcoholism, particularly antisocial alcoholism, and
Molecular Psychiatry
No haplotype B d.f. w2a P-value d.f. w2b P-value
0.83 (45) 10.57 0.002 16.12 0.00001
0.59 (76) 1 1
0.46 (21)
0.81 (73) 0.05 0.87 0.05 0.82
0.80 (75) 1 1
0.79 (11)
more symptoms of antisocial behavior, as compared
with women who were homozygous for the high
activity allele. Heterozygous women displayed an
intermediate risk pattern. In contrast, there was no
relationship between alcoholism/antisocial behavior
and MAOA-LPR genotype in women who had not
been sexually abused. This result is consistent with
the gene by environment interaction model and might
indicate that carriers of the low activity allele who
have been exposed to sexual abuse are at higher risk
of developing alcoholism with antisocial features,
whereas individual with the high activity genotype
are protected from developing antisocial behavior
after exposure to CSA.
The effects of CSA on adult antisocial personality
disturbances were very strong (Figure 3). Early life
traumatic events occurring during a period of neuronal
plasticity have been shown in both humans and
animal models to determine long-lasting neuroendo-
crine changes that induce hypersensitivity of the
hypothalamic–pituitary–adrenal (HPA) axis to new
stressors.38–40 In humans, CSA appears to cause
persistent hyperreactivity of both the HPA axis and
autonomic system.38 Furthermore, adverse experiences
early in life cause structural changes in the brain.40
Rats exposed to maternal deprivation have long-lasting
suppression of adult neurogenesis in the hippocam-
pus, a brain region that is involved in the processing of
emotional experience.40 The effect of MAOA on the
hippocampus may underlie the interaction between
MAOA and childhood trauma. Carriers of the low
activity variant of MAOA-LPR display hyperactivation
of the hippocampus and amygdala during the retrieval
of negatively valenced emotional material.41 Therefore,
the heightened sensitivity to adverse experiences of
carriers of the low activity MAOA genotype might be
due to their impaired ability to extinct adverse
memories and conditioned fears.
The functional effects of MAOA-LPR are more
difficult to predict in female subjects than in male
subjects. As this gene is located on the X chromo-

some, male subjects are hemizygotes, whereas female
subjects have two copies of the gene. Further, among
female subjects, one copy of each gene located on
the X chromosome is usually inactivated through a
mechanism, which can be either random or selective.
To date, studies exploring the inactivation status of
MAOA gene on the X chromosome have reported
conflicting findings.42,43 Our results showed that
heterozygous individuals displayed a risk, which
was intermediate between the homozygote, echoing
the neuroimaging findings of Meyer-Lindenberg
et al.41 Meyer-Lindenberg et al. found that the
genotype conferring low MAOA activity predicted
amygdala hypereactivity during emotional arousal in
both male subjects and female subjects. Similarly to
our finding, the functional response of heterozygous
women carrying both high- and low-expressing allele
was intermediate between homozygous female sub-
jects.41 This finding is consistent with a codominant
effect of the alleles not only on neurobiology but on
complex behavior and might be seen as supportive of
a recent study showing that MAOA is among those
genes that escape X inactivation.43 Alternatively, in
brain, the clonality of MAOA allele inactivation is
such that mosaicism of allele expression of the
heterozygotes is relatively fine-grained and the neu-
robehavioral phenotypes of heterozygotes are there-
fore intermediate.
MAOA-LPR is located in a relatively large region of
reduced recombination. Therefore, other functional
loci might partially or totally account for MAOA-LPR
functional effect. In line with this idea, two recent
studies evaluating mRNA expression of MAOA in
human brain28,44 and MAOA activity44 suggest that not
all the variance in MAOA activity/transcription due
to genetic factors is explained by MAOA-LPR and
other functional loci may play a role. For this reason,
we genotyped nine additional SNPs encompassing
the region where both MAOA and MAOB genes are
located. Within this 200 kb region, we identify two
blocks of high LD, which approximately correspond
to the two MAO genes, although some degree of LD
was also found between MAOA and MAOB markers.
Consistent with previous studies, haplotype diversity
within both regions was low on an overall basis.29
In the MAOA gene, the low activity MAOA-LPR
allele was found in three different haplotypes one of
which (haplotype B) was, by far, the most common.
This haplotype displayed a stronger main effect on
alcoholism and ASPD than MAOA-LPR alone. In
contrast, other haplotypes containing the low activity
allele did not show any significant associations with
either alcoholism or ASPD. As previously seen for
MAOA-LPR, the effect of haplotype B on alcoholism
and ASPD was seen only among sexually abused
subjects. Further, other polymorphisms within
MAOA displayed a main effect on alcoholism, which
was more significant than that of the MAOA-LPR.
This finding might indicate that additional functional
loci within MAOA indeed exist. However, this result
should be interpreted cautiously keeping in mind that
MAOA and childhood sexual abuse
F Ducci et al
345
our sample size is small. This result at the haplotype
level would need to be replicated in a larger sample,
or a second functional locus identified, before a clear
conclusion is drawn.
Haplotype-based analysis revealed an association
between MAOB and alcoholism. A MAOB haplotype
(termed haplotype C) was found in excess among
alcoholics as compared to controls. In contrast to
what we observed for MAOA, frequency of this MAOB
haplotype was almost the same in all alcoholics and
antisocial alcoholics, indicating that the association
seen between MAOB and alcoholism in this popula-
tion is independent from the ASPD diagnosis. MAOB
is located in the same chromosome region as the
MAOA gene (Xp11.23–Xp11.4) and the two genes are
separated by only 20 kb. These two genes have a high
degree of sequence identity and most certainly have
a common ancestry.45 As does the MAOA enzyme,
MAOB also degrades monoamines, but with a
different substrate preference: MAOB has higher
affinity for DA,46,47 phenylethylamine48,49 and benzy-
lamine,50 whereas MAOA displays higher affinity for
NA and 5-HT. Further, both enzymes are expressed in
the central nervous system (CNS) but with different
distributions: MAOB is preferentially expressed on
serotonergic51 and histaminergic52 neurons, while
MAOA is mainly expressed in noradrenergic neu-
rons.51,53 Both genes are expressed in glia.52 Since
MAOB is a regulator of monoamine tone and is
expressed in the brain, it is a logical candidate for
susceptibility to neuropsychiatric diseases. Never-
theless, the role of MAOB in vulnerability to psychia-
tric disorders has been less investigated as compared
to MAOA. In contrast, there is an extensive literature
relating low MAOB enzyme activity in platelets to
behavior, including alcoholism, recurrent criminality
and antisocial violent behavior.54,55 However, platelet
MAOB enzyme activity is also perturbed by environ-
mental factors, including smoking, limiting the inter-
pretability of those studies. Positive associations
between MAOB polymorphisms have been reported
with mood disorders56 and platelet MAO activity.57
To our knowledge, this is the first study reporting an
association between genetic variation at MAOB and
alcoholism.
Interestingly, MAOA but not MAOB displayed a
significant interaction with CSA. This result might be
due to the differences in the level of expression of
MAOA and MAOB in the brain during different ages.
In fetal brain, MAOA activity appears earlier than
MAOB and reaches a peak in the newborn period.
MAOB activity progressively increases with age and
peaks in late adulthood.58 The MAOA/MAOB activity
ratio is higher in fetal (2.43) and neonatal brain (2.39)
and decreases in adulthood (0.61).59 Therefore,
MAOA might be more important than MAOB in
moderating the effect of traumatic events that occurs
during the developmental period.
This study has strengths as well as important
limitations. Strengths include the use of a female
sample, which is particularly suitable to explore the
Molecular Psychiatry
 MAOA and childhood sexual abuse
F Ducci et al
346
effect of sexual abuse given the higher prevalence of
CSA in female subjects as compared to male subjects;
the use of a specific type of childhood trauma such as
CSA rather than a more heterogeneous category of
adversities; the use of a relatively isolated population,
which is likely to be genetically and environmentally
more homogenous; assessment of sexual abuse con-
ducted through a face-to-face interview rather than a
self-completed questionnaire and yielding high rates
of reporting; the combination a function-based genetic
association approach with haplotype-based analysis
potentially accessing the effects of unknown func-
tional loci. Finally, the high rates of sexual abuse in
this high-risk population make it particularly suitable
for the study of gene by stress interaction. The main
limitations of the study include the relatively small
sample size; and the arguably necessary retrospective
rather than prospective assessment of CSA.
In conclusion, our results support the role of the
MAOA gene in moderating the impact of childhood
trauma on adult psychopathology in female subjects,
as previously had been shown among male subjects,
with a stepwise, allele dosage effect in these women.
Both homozygotes for the low activity allele and
heterozygous carriers appear to be more vulnerable to
adverse psychosocial consequences of CSA as com-
pared to homozygotes for the high activity allele.
Haplotype-based analysis of the MAOA gene ap-
peared to strengthen the association, as compared to
the MAOA-LPR locus alone. Finally, a haplotype of
the MAOB gene was associated with alcoholism
independently from ASPD diagnosis, and this effect
appears to be at least partially independent of MAOA.
This is the first time that an association between
genetic variation within MAOB and alcoholism has
been reported, suggesting that closer examination of
MAOB would be worthwhile, including attempts to
replicate in other data sets.
Acknowledgments
This research was supported by the Intramural
Research Program of the National Institute on Alcohol
Abuse and Alcoholism, NIH, and in part by the Office
of Research on Minority Health.
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