Department of Clinical Neuroscience
Undergraduate program in Psychology, 6th semester
Main subject: Psychology
Bachelor’s thesis in psychology (2PS013), 15 ECTS points
Spring semester 2012
Do prenatal androgens affect
criminal behavior?
A Swedish population study of risk for crime in
individuals with disorder of sex development
Agnes Ohlsson Gotby
Supervisor: Professor Paul Lichtenstein, Department of Medical Epidemiology and
Biostatistics
Examiner: Professor Petter Gustavsson, Department of Clinical Neuroscience
2
Department of Clinical Neuroscience
Undergraduate program in Psychology, 6th semester
Main subject: Psychology
Bachelor thesis in psychology (2PS013), 15 ECTS points
Spring semester 2012
Do prenatal androgens affect criminal behavior?
A Swedish population study of risk for crime in individuals with disorders of sex
development
Sammanfattning/abstract
Avvikande könsutveckling omfattar alla medfödda sjukdomstillstånd där
könskromosomer, gonader eller det anatomiska könet är atypiskt. I många fall är
nivåerna av androgener under fosterutvecklingen påverkade. Därför utgör avvikande
könsutveckling en möjlighet att studera prenatala androgeners påverkan på
könsskillnader i beteende. Syftet med denna studie var att undersöka sambandet
mellan prenatala androgener och kriminalitet. Vi förutspådde att ökade nivåer av
androgener skulle leda till fler brott samt att lägre androgennivåer skulle resultera i
färre brott. Studien hade en populationsbaserad matchad kohortdesign. Vi
identifierade alla patienter i Sverige sedan 1964 med någon diagnostiserad avvikande
könsutveckling. Slumpmässigt utvalda kontroller (100:1) ur den totala populationen
matchades utifrån födelseår och kön. Oddskvoter (OR) med 95 % konfidensintervall
togs fram för något brott, våldsbrott och sexualbrott genom en logistisk regression.
Studien visade inte på en ökad risk för brott hos individer diagnostiserade med
sjukdomar förknippade med högre prenatala androgennivåer, och inte heller hittades
en minskad risk för individer med lägre prenatala androgennivåer. Hypoteserna kunde
därför inte bekräftas.
Nyckelord: Avvikande könsutveckling, prenatala androgener, kriminalitet
Disorders of sex development (DSD) encompass any congenital conditions in which
development of chromosomal, gonadal or anatomical sex is atypical. Levels of
androgens during fetal development are often affected. Therefore, DSD constitutes a
possibility to study the influence of prenatal androgen on sex-differentiated behavior.
The aim of this study was to investigate the influence of prenatal androgens on
criminality. We predicted that increased levels of androgens would lead to more crime
and that lower androgen levels would result in less crime. The study had a populationbased matched cohort design. We identified all patients in Sweden since 1964
diagnosed with DSD. Random population controls (100:1) were matched by birth
year and sex. Odds ratios (OR) with 95% confidence intervals for any crime, violent
crime or sex crime were obtained using logistic regression. The study did not identify
an increased risk for crime in individuals diagnosed with disorders associated with
higher prenatal androgens, nor was a decreased risk for individuals with lower
prenatal androgen levels found. The hypotheses could therefore not be confirmed.
Key words: Disorders of sex development, prenatal androgens, criminality
3
Do prenatal androgens affect criminal behavior?
A Swedish population study of risk for crime in individuals with disorders of sex
development
Agnes Ohlsson Gotby
Introduction
Disorders of sex development
Disorders of sex development (DSD) is a diverse group of disorders,
encompassing any congenital conditions in which development of chromosomal,
gonadal or anatomical sex is atypical (Hughes, 2008). Sex development is a dynamic
process that involves interaction of genes, signaling molecules, proteins, paracrine
elements, and endocrine factors. If this process is somehow disturbed it can result in
DSD (Acherman & Hughes, 2011). To understand the causes of DSD, it is necessary
to be familiar with normal sexual development and therefore it will be briefly
described.
Normal sex development
Development of gonadal sex.
Until approximately the 6th week post conception, the gonads of the developing
fetus are bipotential, meaning they can develop to either testis or ovary (Acherman &
Hughes, 2011). Sexual determination can be seen as a balancing act between male and
female promoting signals leading to either a male or a female development (DiNapoli
& Capel, 2008). The presence of a Y chromosome will normally lead to a male
development, and a gene called the sex-determining region of the Y (SRY) has been
proven crucial to this process. In XX mice with a transgenic autosomal copy of the
SRY gene, the bipotential gonads will develop to testis, whereas XY mice lacking
SRY will follow a female development pathway (Acherman & Hughes, 2011;
DiNapoli & Capel, 2008). In the past, ovarian development and differentiation was
viewed as a default process that occurred in the absence of male promoting signals.
This has been proven wrong by studies showing that specific genes are involved in
ovarian development, some of which may actually actively antagonize a male
development path (Acherman & Hughes, 2011).
Phenotype sex.
The differentiation of the phenotypic sex is mediated by several steroid and
peptide hormones (e.g., androgens and Anti-Müllerian Hormone, AMH) produced by
the developing gonads. In males, AMH is produced by the Sertoli cells in the testis,
which cause regression of Müllerian structures (e.g., fallopian tubes, uterus and upper
two thirds of the vagina). Fetal Leydig cells develop within testis and secrete
androgens by 8 to 9 weeks post-conception. Testosterone is converted to
dihydrotestosterone (DHT) by 5α-reductase, and its action on the androgen receptor
results in androgenization of the external genitalia. In the male, the urogenital sinus
develops into the prostate and the prostatic urethra, the genital tubercle develops into
the glans penis, the urogenital folds fuse to form the shaft of the penis, and the
urogenital swellings form the scrotum (Acherman & Hughes, 2011).
4
Female sexual differentiation involves less significant changes in the external
genitalia. Without the action of AMH, Müllerian structures persist to form the
fallopian tubes, uterus, and upper portion of the vagina. Degeneration of Wolffian
structures is caused by a lack of local testosterone production. The urogenital sinus
develops into the urethra and lower portion of the vagina, the genital tubercle
develops into the clitoris, the urogenital folds form the labia minora, and the
urogenital swellings form the labia majora (Acherman & Hughes, 2011).
Description of included disorders
DSD can have a wide range of presenting phenotypes depending on the
underlying condition and its severity. Below, diagnose groups according to ICD
included in this article will be described further (see also Table 1).
Congenital adrenal hyperplasia (CAH) involves defects in the synthesis of
steroid hormones in the adrenal cortex, and is the most common cause of female DSD
(Hughes, 2008). In Sweden, one affected child is born in every 9800 (Thilén et al.,
1998). The condition affects both sexes, but only leads to abnormal sex development
in girls. It is most often caused by a defect in the 21-hydroxylotate gene (CYP21),
which results in impaired synthesis of cortisol and aldosterone. Instead an excess of
androgens is produced. This might cause a male development of external genitalia in
girls, making it hard to assign the right sex at birth (Nordenström, Servin, Bohlin,
Larsson, & Wedell, 2002).
‘Other adrenogenital disorders’ is a collection diagnosis for conditions where
androgens are increased without any known cause. If the diagnosis is acquired in
childhood it could represent premature adrenarche, with unspecified influence of
androgens produced by the adrenal glands. In adults, the diagnoses are also likely to
imply increased levels of androgens, with unknown etiology. In most cases,
androgens during fetal development are probably not affected. Some cases may also
have CAH with enzyme deficiency (normally diagnosed with E25.0), where
androgens are elevated in utero (Nordenström, A., Ass. Prof. & Fahlhammar, H., MD
PhD, personal correspondence).
The most common cause of ambiguous genitalia in genetic males is resistance
to the action of androgen (androgen insensitivity syndrome, AIS), which can be either
complete (complete androgen insensitivity, CAIS) or partial (partial androgen
insensitivity, PAIS). CAIS is caused by mutations of the gene for the androgen
receptor (AR). The etiology of PAIS is unknown (Hughes, 2008). Estimates of
prevalence of CAIS range from 1 case in 20,400 to 1 in 99,000 genetic males, the
prevalence of PAIS is unknown (Acherman & Hughes, 2011).
In CAIS, the phenotype is female, in spite of normally formed testis and
testosterone production. This demonstrates the key role of androgens in male sexual
differentiation, and the pathophysiology of AIS is related to the normal mechanism of
actions of androgens. Male sexual differentiation, acquisition of secondary sex
characteristics and the onset of spermatogenesis are all affected if AR is
malfunctioning.
CAIS is often first detected and diagnosed in puberty, when it presents as
absence of menarche. Pubic and axillary hair is also often absent or inconsiderable,
but breast development is normal. The uterus is absent as a result of normal AMH
action.
In PAIS, there is some function of the AR, but not enough for complete
masculinization. The phenotype often includes perineo-scrotal hypospadias,
5
micropenis and a bifid scrotum, but varies according to degree of function of AR.
Patients are most often raised as boys (Acherman & Hughes, 2011).
Hypospadias is the most frequent genital malfunction in male newborns,
approximately affecting three to eight cases per 1000 male births. Hypospadias results
from an abnormal penile and urethral development, with incomplete virilization,
leading to a defect in midline fusion of the male urethra, which results in a misplaced
urethral meatus. Although intensively investigated, the etiology of hypospadias is still
mostly unknown, but both environmental and genetic factors are thought to be
involved (Kalfa, Philibert, & Sultan, 2009). A defect in androgen synthesis is held to
be the underlying factor in 20% of the cases (Rey et al., 2005).
‘Other abnormalities of penis’ includes diagnosis of other congenital
malfunctions of penis than hypospadias, as concealed penis and micropenis. These
diagnoses describe phenotypes that can have different etiology, and can be part of the
clinical picture of more severe disorders, also including e.g., mental retardation, but
also act as an isolated phenomenon. In its isolated form, it has been associated with
low birth weight (Acherman & Hughes, 2011).
‘Hermaphroditism’ is a diagnosis with several possible etiologies. In zoology it
denotes an individual having both male and female gonads, which is common in
many groups of invertebrates (Nationalencyklopedin, 2012). In humans, the presence
of both testis and ovary tissue (ovotesticular DSD, earlier called true
hermaphroditism) is a very rare condition (Kim et al., 2002), reported in
approximately 500 individuals worldwide (Acherman & Hughes, 2011). More
common are various types of mosaic 45,X/46,XY karyotype, sometimes referred to as
mixed gonadal dysgenesis, where the individual has streak gonads (most often testis)
with cells of the other sex’ gonads (most often ovaries). The clinical phenotype
associated with a 45,X/46,XY mosaicism is highly variable, and the true prevalence
of this condition is unknown (Acherman & Hughes, 2011).
Probably, most patients diagnosed with hermaphroditism in this population have
some other DSD diagnose, and hermaphroditism is set as an early diagnose before a
more profound investigation of why the child is presenting with an ambiguous sex has
been performed (Nordenström, A., Ass. Prof., personal correspondence).
Klinefelter’s syndrome (KS), where males have an extra X chromosome
(47XXY), is the most common male sex chromosome aneuploidy and affects 167 per
100 000 men (Stochholm, Bojesen, Jensen, Juul, & Gravholt, 2012). The condition
can be a background factor to hypogonadism. It is caused by meiotic nondisjunction
of the sex chromosomes during gametogenesis, and is associated with lower fertility
and learning difficulties. In many cases, the disease is diagnosed in adolescence or
adulthood, but in as many as approximately 75% of the cases, KS remains
undiagnosed (Acherman & Hughes, 2011).
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Table 1. Included disorders.
Condition
Congenital adrenal
hyperplasia
Prenatal
Abbrevation androgens
CAH
Other adrenogenital
disorders
Cause
Karotype
Prevalence
Phenotype per 100,000
Increased
Defect in the
synthesis of
steroid
hormones
46XX or
46XY
Female or
male
10,2
Not affected
Not affected
or increased
Unknown
46XX or
46XY
Female or
male
Unknown
Not affected
Defect
androgen
receptor
46XY
CAIS
CAIS:1.01female, PAIS 4.90, PAIS:
male
unknown
Undecended
testis
Male, severe
300-800 per
cases may be
100,000
raised as
genetic males
females
Testis
Androgen
insensitivity
syndrome
AIS,
Cannot act
complete:
on target
CAIS, partial:
tissue
PAIS
Hypospadias
Decreased
Abnormal
penile
developement
46XY
Other
malformations of
penis
Decreased
Variable
etiology
46XY
Male
Hermaphroditism
Increased in
women,
decreased in
men
Variable
etiology
45X/46XY
and variants,
46XX/46XY
chimerism
Decreased
Meotic
nondisjunction
of the sex
chromosomes
47 XXY
Klinefelter's
syndrome
KS
Gonad
Varying for
different
diagnosis
Testis
Male or
female
Unknown
Testis, ovary,
dysgenetic
gonads, or
ovotestis
Male
167 per
100,000 men
Hyalinized
testis
Androgen-exposure, aggression and crime
Aggressive behavior is sexually dimorphic, and on average, men exhibit more
aggression than do women (Archer, 2006). One possible explanation to this sexdimorphic trait can be differences in levels of androgens. Studies have shown a
connection between aggression and testosterone levels (Finkelstein et al., 1997;
Kouri, Lukas, Pope, & Oliva, 1995; van Bokhoven et al., 2006), even if results are
somewhat mixed (Archer, 2004). It is hypothesized that prenatal androgens can have
a structural impact on the developing brain and influence sex difference in aggression.
In primates, it has been shown that exposure to prenatal androgens can increase
aggression (Eaton, Goy, & Phoenix, 1973). Studies have shown that CAH girls have a
more male pattern of behavior, i.e., exhibit more rough and tumble play, have more
boy-like toy preference (Nordenström et al., 2002; Servin, Nordenström, Larsson, &
Bohlin, 2003) and higher self-rated aggression (Berenbaum & Resnick, 1997). A
comparison of same-sexed twin and opposite-sexed twin girls (where opposite-sex
twin girls are expected to be exposed to elevated levels of testosterone in uterus) also
indicates an influence of prenatal androgens on aggression (Cohen-Bendahan,
Buitelaar, van Goozen, Orlebeke, & Cohen-Kettenis, 2005).
It is also clear that males commit more crimes than women do (Andersson,
Levander, Svensson, & Levander, 2012). Social factors certainly have a great impact,
but there may also be underlying biological causes. One study showed a connection
between plasma testosterone level and delinquency in adolescent males (van
Bokhoven et al., 2006). Testosterone also showed a relationship to criminal violence
in female inmates (Dabbs & Hargrove, 1997) and sexual violence and recidivism in
male sex offenders (Studer, Aylwin, & Reddon, 2005).
7
In many types of DSD, prenatal levels of androgens are thought to be affected.
Therefore, DSD constitutes a possibility to study effects of androgen exposure on sexdifferentiated traits. To our knowledge, the effect of prenatal androgens on criminal
behavior has not yet been studied. The aim of this study was hence to investigate the
influence of prenatal androgens on criminal behavior. We expected prenatal
androgens to increase criminal behavior. Consequently, we predicted: (a) an increased
rate of convictions of individuals diagnosed with disorders were prenatal androgens
are higher than normal, i.e., CAH and female hermaphroditism, and (b) a decrease of
conviction in individuals with disorders were prenatal androgens are low or cannot act
on target tissue due AR insufficiency, i.e., KS, hypospadias, ‘Other malformations of
penis’ and AIS.
To be able to prevent crime, insight in the underlying risk factors is needed.
Overall, the outcomes of DSD are not very well understood; most focus has been on
predictors for later sex reassignment (Lee, Houk, Ahmed, & Hughes, 2006). Some
studies have considered psychological outcomes (e.g. Schützmann, Brinkmann,
Schacht, & Richter-Appelt, 2009). Better understanding of the connection between
DSD and criminal behavior may also lead to better management and prevention of
unfavorable outcomes of DSD.
Method
Ethics
The regional Ethics Committee at the Karolinska Intitutet approved the study
(2009-1562-31/5). The data was merged and anonymized by an independent
government agency (Statistics Sweden), and the code linking the personal
identification numbers to the new case numbers was destroyed immediately after
merging. Therefore, informed consent was neither required, nor possible.
National Registers
The study was conducted by linkage of several longitudinal nationwide
population-based registers in Sweden: the National Patient Register (held by the
National Board of Health and Welfare) contains nearly all inpatient and day surgery
records since 1964 and outpatient records since 2001; the Medical Birth Register
(National Board of Health and Welfare) holds information about all births in Sweden
since 1973; the Multi-Generation Register (Statistics Sweden) contains information
about relationships between people born after 1932, and nationally registered after
1961, and their parents or adoptive parents; Migration records (Statistics Sweden)
contains registered migrations since 1901; the Integrated Database for Labour
Market Research (Statistics Sweden) has data of income, education, occupation,
employment status, social transfers, etc. from year 1990 to 2009; the Register of
Education (Statistics Sweden) holds information about highest finished education
level for the years 1985–1989; the Population and Housing Census (Statistics
Sweden) contains individual, household and dwelling data for year 1960–1990; the
National Crime Register (Swedish National Council for Crime Prevention) covers all
registered convictions between the years 1973–2009 and the Cause of Death Register
(National Board of Health and Welfare) which contains all registered deaths for the
years 1952–2010 and their causes.
In Sweden, every resident receives a unique ten-digit personal identity number.
This constitutes a key to interconnect different records, and enables register research.
8
Identification of study population
The study had a population-based matched cohort design. People with DSD
diagnoses (see Table 2) were identified in the National Patient Register (n = 18,030),
the Medical Birth Register (n = 8,234) and a quality register (n = 560) containing
CAH patients (held by clinical specialists). Six-thousand four-hundred and thirty-one
subjects were present in more than one register and 20,373 subjects were identified in
total. In these registers, discharge diagnoses are coded according to the 7 th, 8th, 9th and
10th versions of the International Classification of Diseases (ICD). Diagnostic codes
of interest were grouped as CAH, ‘other adrenogenital disorders’, AIS, hypospadias,
‘other malformations of penis’, hermaphroditism and KS according to the ICD-10
manual (see Table 2).
Table 2. Diagnostic codes in ICD of included disorders.
Diagnosis group
Diagnosis name
ICD10
Congenital adrenogenital Congenital adrenogenital disorders
hyperplasia (CAH)
associated with enzyme deficiency
Salt-losing congenital adrenal hyperplasia
21-Hydroxylase deficiency
adrenal pseudohermaphroditism, female
Other adrenogenital
Other adrenogenital disorders
disorders
Adrenogenital disorder, unspecified
Androgen insensitivity Androgen resistance syndrome
syndrome (AIS)
Testicular feminization (syndrome)
Male pseudohermaphroditism with androgen
resistance
Other specified androgen resistance
syndrome
Hypospadias
Hypospadias, balanic
Hypospadias, penil
hypospadias, penoscrotal
hypospadias, perineal
Congenital chordee
Other hypospadias
Hypospadias, unspecified
Other malformations of Other congenital malformations of penis
penis
Other specified congenital malformations of
male genital organs
Congenital malformation of male genital
organ, unspecified
Concealed penis
Micropenis
Hermaphroditism
Hermaphroditism, not elsewhere classified
Male pseudohermaphroditism, not elsewhere
classified
Female pseudohermaphroditism, not
elsewhere classified
Pseudohermaphroditism, unspecified
Indeterminate sex, unspecified
Klinefelter's syndrome Klinefelter's syndrome karyotype 47,XXY
(KS)
Klinefelter's syndrome, male with more than
two X chromosomes
Klinefelter's syndrome, male with 46,XX
karyotype
Klinefelter's syndrome, unspecified
Diagnostic code
ICD version
ICD-9 fr 1987
ICD-8
E25.0
E25.0A
E25.0B
E25.0C
E25.8
E25.9
E34.5
E34.5A
2552
2552
2552
2552
2552
2552
2578
2578
255C
255C
255.01
255.08
255.08
255.02
757W
257.98
E34.5B
2578
257W
E34.5W
2578
Q54.0
Q54.1
Q54.2
Q54.3
Q54.4
Q54.8
Q54.9
Q55.6
7526
7526
7526
7526
7526
7526
7526
7528
752G
752G
752G
752G
273
752.00
752.2
752.2
752.21
752.22
752.63
752.29
752.29
752W
Q55.8
Q55.9
Q56.0
7528
7528
7527
752.64
752.08
Q56.1
7527
752.71
Q56.2
Q56.3
Q56.4
Q98.0
Q98.1
7527
7527
7527
752.72
752.08
752.08
Q98.2
Q98.4
752H
ICD-7
757.26
757.21
757.24
9
Exclusions
The study population was restricted to individuals born before 1994, so that all
individuals were at least 15 years (the age of criminal responsibility in Sweden) at the
end of the follow-up in 2009. Six-thousand five-hundred and eighty-eight cases born
after 1994 were excluded.
Information about death dates and migration were found in the Cause of Death
Register and the Total Population Register respectively. People who died or
emigrated before the study period began in 1973 were excluded (n = 11 and n = 20,
respectively).
Only people born in Sweden were included in the study, for three reasons. First,
since DSD occurs during fetal development, and the diagnosis is often acquired in
childhood, it is possible for immigrants to obtain a DSD diagnosis that is not recorded
in Sweden. To include immigrants as controls would therefore increase the risk of
false negatives. Second, there is also a risk for the group emigrating from their
homeland to be subject to selection bias, not being representative for the total
population. Third, to settle in a new country often includes being confronted with a
strained situation, and this could be a possible confounder. Therefore, 1144
immigrants with DSD diagnosis were excluded from the study.
Cases with more than one DSD diagnosis (n = 501) that were incongruent were
excluded from further analysis (n = 7), i.e., CAH and AIS, CAH and KS, ‘other
adrenogenital disorders’ and AIS, ‘other adrenogenital disorders’ and KS, or AIS and
KS. Forty-one cases diagnosed with both CAH and AIS were detected, but since 35
were part of the CAH quality register and the CAH diagnose was considered reliable,
only 6 cases of these were excluded. One case diagnosed with both KS and AIS was
excluded. There were no cases with both CAH and KS diagnoses, nor any cases with
‘other adrenogenital disorders’ and AIS or KS.
In cases that had more than one diagnosis, but where the diagnoses were not
considered incongruent, the patients were excluded from the diagnose group that
represented a less severe phenotype or had less explanatory power in regard to
etiology (see Table 3).
Women were excluded from diagnosis groups with male diagnoses, i.e., KS (n =
12), hypospadias (n = 117) and ‘other malformations of penis’ (n = 18).
Table 3. Excluded diagnoses.
Primary diagnoses
Hermaphroditism
Excluded diagnoses
Other malOther
Hypospadias formations of adrenogenital
penis
disorders
CAH
10
10
4
200
AIS
28
33
6
0
KS
0
4
1
0
Hypospdias
31
0
109
0
Other malformation of penis
1
0
0
0
Identification of population-based control group
For each case one hundred controls from the general population (without any of
the DSD diagnoses) were matched by birth year and gender. They were randomly
selected from the Multi-Generation Register and the Population and Housing Census.
10
Outcome measures
Data on all convicts from January 1 st, 1973 to December 31st, 2009 was
obtained from the National Crime Register. The outcome any crime was defined as
any notation in the register. Violent crime was defined as murder, manslaughter,
filicide, assault, illegal threat, violation of a person’s/woman’s integrity, robbery,
arson, threat and violence against an officer, kidnapping, illegal restraint, illegal
coercion and intimidation. The outcome Sex crime was defined as rape, sexual
coercion, sexual abuse of a dependent adult, sexual abuse of a child, sexual
intercourse with a child, sexual harassment, buying of sexual service from a child,
sexual intercourse with offspring/sibling and pimping. The outcome measures were
dichotomized (as any crime or no crime, etc.).
Covariates
Parents’ education was used as a proxy to control for differences between cases
and controls in socioeconomic status. For a subgroup of the population (subject n =
8,800, controls n = 853,497), born year 1970–2004, information about parents were
extracted from the Multi-Generation Register. Parents’ education level, achieved
when the child was 15 years of age, was thereafter collected from the Integrated
Database for Labour Market Research (year 1990–2009) and the Register of
Education (year 1985–1989, Statistics Sweden). Education level was coded from one
to seven, where one represented lower secondary school shorter than nine years and
seven represented PhD studies. The parent who had achieved the highest education
was kept in the analysis.
Statistical analyses
The association between having been diagnosed with any DSD and any crime,
violent crime or sex crime was estimated with conditional logistic regression, using
the logistic command in SAS version 9.3. Odds ratios were calculated for groups
divided according to their estimated prenatal androgen level, in order to answer the
hypotheses. In the high-androgen group patients diagnosed with CAH, ‘other
androgenital disorders’ and women diagnosed with hermaphroditism were included.
Patients diagnosed AIS, hypospadias, ‘other malformations of penis’, KS and men
diagnosed with hermaphroditism were included in the low-androgen group. Since it
is uncertain whether prenatal androgen levels are affected in ‘other andrenogenital
disorders’, analyses were conducted both with and without this group included.
Earlier studies have also shown an increased risk for crime in men with KS
(Stochholm et al, 2012), therefore the analysis were repeated with and without this
group too. Odds ratios were also calculated for each diagnostic group separately, due
to the possible clinical interest in information about the risk associated with each
diagnose.
Moreover, analyses were conducted for the subgroup of the population where
information about parents’ highest education was available, both with and without
parents’ education included in the model. Thereafter, the odds ratios of these repeated
analyses were compared to reveal if controlling for education lead to differences in
levels of significance of any OR.
11
Results
Groups divided according to estimated prenatal androgen level
In the group of people diagnosed with disorders associated with high androgens,
1,523 cases were compared with 152,300 age- and gender-matched controls from the
general population. Two hundred and thirty-four cases and 20,954 controls had been
convicted for any crimes, whereas 35 cases and 2,894 controls had been convicted for
violent crimes and 5 cases and 211 controls had been convicted for sex crimes. There
were no significant increased risks for any crime, violent crime, or sex crime for the
total group. However, there was a small but increased risk that women in this group
had been convicted for committing at least one crime, and that men had been
convicted for sex crimes (see Table 4).
When ‘other adrenogenital disorders’ were excluded from this group, 1,076
cases and 107,600 controls remained. There were no significant increased risks for
any of the studied variables.
Two thousand and five hundred ninety seven cases in the group diagnosed with
disorders associated with low androgens (n = 11,104) had committed any crime,
compared to 252,120 of the controls (n = 1,110,400). Sexual offences had been
committed by 52 cases and 3,027 controls. There was a minimal significant increase
in risk for any crime, and significant increased risk for sex crimes, but not for violent
crimes, among individuals diagnosed with disorders associated with low prenatal
androgen levels.
If men with KS where excluded from the group (n = 884), there were no
significant increased risk for either any crime, violent crime or sex crime for the cases
(n = 10220) compared to controls (n = 1022000).
Groups divided according to diagnosis
One thousand six individuals diagnosed with CAH were compared with 100 age- and
gender-matched controls each, selected from the general population. One hundred and
thirty-five subjects diagnosed with CAH were convicted for committing any crime, 19
were convicted for committing at least one violent crime, and three for sex crimes,
compared to 13,343, 1,956 and 116 respectively of the controls. No increased risk for
any crime or violent crime was found after matching for sex and birth year. There was
a tendency towards an increased risk for sex crime even if this risk was not
statistically significant (see Table 5).
In the group with ‘other adrenogenital disorders’ (n = 447), 92 subjects with the
diagnosis had been convicted for committing at least one crime, 15 subjects had been
convicted for violent crimes, and two subjects had been convicted for sex crimes.
Corresponding numbers for controls were 7,083, 887 and 95 respectively. The risk
that an individual diagnosed with ‘other adrenogenital disorders’ had been convicted
for any crime or violent crimes was significantly increased compared to controls, but
the increased risk for sex crimes was not significant.
Individuals with androgen insensitive syndrome (n = 783) had no significant
increased risk for any crime, violent crime or sex crime.
There were no differences between men with hypospadias (n = 7,690) and
general population controls in regard to the risk for any crime, violent crime and sex
crime.
Among the men diagnosed with ‘other malformations of penis’ (n = 1,709), 432
had been convicted for any crime, compared to 39,664 of the controls. There was a
12
very small but significant increased risk for any crime, but no increased risk of being
convicted for violent crimes or sex crimes for cases compared to controls.
Individuals diagnosed with hermaphroditism (n = 108) did not differ from
controls in regard to incidence of any crimes or violent crimes. The OR for sex crimes
was not possible to calculate due to no incidence.
Two hundred and eighty-two men with KS (n = 884) had been convicted for any
crime compared with 25,185 of the controls, 71 KS individuals had at least one
violent conviction, as 4,888 of the controls. Eighteen subjects had been convicted for
sexual offences, which was also true for 290 controls. The statistical analyses showed
that the incidence of any crime, violent crime, or sex crime was significantly
increased for men with KS compared to controls.
Table 4. Descriptive statistics and OR for any crime, violent crime and sex crime for
groups divided according to estimated prenatal androgen level
Androgen level and sex
Frequency
Case
High androgens
Control
Any crime
Case
%
Control
%
OR
95 % CI
1523
152300
234 15.36%
20954 13.76%
1.14 0.99 1.31
Men
586
58600
147 25.09%
13955 23.81%
1.07 0.89 1.29
Women
937
93700
1076
107600
Men
364
Women
7.47%
1.27 1.02 1.58
142 13.20%
13871 12.89%
1.03 0.86 1.23
36400
81 22.25%
8533 23.44%
0.94 0.73 1.20
712
71200
61
5338
7.50%
1.16 0.89 1.51
Low androgens
11104
1110400
2597 23.39%
252120 22.71%
1.04 1.00 1.09
Men
10728
1072800
2558 23.84%
249159 23.23%
1.04 0.99 1.08
376
37600
39 10.37%
10220
1022000
9844
376
High androgens (other adrenogenital disorders excluded)
Women
Low androgens (KS excluded)
Men
Women
Androgen level and sex
9.28%
8.57%
6999
7.88%
1.36 0.97 1.89
2315 22.65%
226935 22.20%
1.03 0.98 1.08
984400
2276 23.12%
223974 22.75%
1.02 0.97 1.07
37600
39 10.37%
Frequency
Case
High androgens
87
Control
2961
2961
7.88%
1.36 0.97 1.89
Violent crime
Case
%
Control
%
OR
95 % CI
1523
152300
35
2.30%
2894
1.90%
1.22 0.87 1.70
Men
586
58600
25
4.27%
2303
3.93%
1.09 0.73 1.63
Women
937
93700
10
1.07%
591
0.63%
1.70 0.91 3.19
1076
107600
20
1.86%
2007
1.87%
1.00 0.64 1.55
Men
364
36400
13
3.57%
1540
4.23%
0.84 0.48 1.46
Women
712
71200
7
0.98%
467
0.66%
1.50 0.71 3.18
Low androgens
11104
1110400
558
5.03%
54961
4.95%
1.02 0.93 1.11
Men
10728
1072800
555
5.17%
54641
5.09%
1.02 0.93 1.11
376
37600
3
0.80%
320
0.85%
0.94 0.30 2.94
10220
1022000
487
4.77%
50073
4.90%
0.97 0.89 1.07
9844
984400
484
4.92%
49753
5.05%
0.97 0.89 1.07
376
37600
3
0.80%
320
0.85%
0.94 0.30 2.94
High androgens (other adrenogenital disorders excluded)
Women
Low androgens (KS excluded)
Men
Women
Androgen level and sex
Frequency
Sex crime
Case
Control
Case
High androgens
1523
152300
5
0.33%
211
0.14%
2.37 0.98 5.77
Men
586
58600
5
0.85%
207
0.35%
2.43 1.00 5.92
Women
937
93700
0
0.00%
4
0.00%
High androgens (other adrenogenital disorders excluded) 1076
107600
3
0.28%
116
0.11%
2.59 0.82 8.16
Men
364
36400
3
0.82%
114
0.31%
2.65 0.84 8.36
Women
712
71200
0
0.00%
2
0.00%
Low androgens
11104
1110400
52
0.47%
3027
0.27%
1.72 1.31 2.27
Men
10728 1072800
52
0.48%
3026
0.28%
1.72 1.31 2.27
0
0.00%
1
0.00%
Women
376
37600
%
Control
%
OR
95 % CI
Low androgens (KS excluded)
10220 1022000
34
0.33%
2736
0.27%
1.24 0.89 1.75
Men
9844
984400
34
0.35%
2736
0.28%
1.24 0.89 1.75
Women
376
37600
0
0.00%
1
0.00%
13
Table 5. Descriptive statistics and OR for any crime, violent crime and sex crime for
each diagnosis, respectively.
Condition and sex
Congenital adrenogenital disorders
Frequency
Case Control
Case
(%)
Any crime
Control (%)
OR
95 % CI
1006
100600
135 13.42%
13343 13.26%
1.01 0.85
1.22
Men
364
36400
81 22.25%
8533 23.44%
0.94 0.73
1.20
Women
642
64200
54
4810
7.49%
1.13 0.86
1.50
Other adrenogenital disorders
447
44700
92 20.58%
7083 15.85%
1.38 1.09
1.73
Men
222
22200
66 29.73%
5422 24.42%
1.31 0.98
1.75
Women
225
22500
26 11.56%
1661
7.38%
1.64 1.09
2.47
Androgen insensitivity syndrome
783
78300
126 16.09%
12462 15.92%
1.01 0.84
1.23
Men
407
40700
87 21.38%
9501 23.34%
0.89 0.70
1.13
Women
Hypospadias men
376
37600
39 10.37%
2961
7.88%
1.36 0.97
1.89
7690
769000
1752 22.78%
173868 22.61%
1.01 0.96
1.07
Other malformations of penis men
1709
170900
432 25.28%
39664 23.21%
1.12 1.00
1.25
108
10800
12 11.11%
1469 13.60%
0.79 0.44
1.45
Men
38
3800
5 13.16%
941 24.76%
0.46 0.18
1.18
Women
Klinefelter's syndrome men
70
7000
7 10.00%
528
7.54%
1.36 0.62
2.99
884
88400
282 31.90%
25185 28.49%
1.18 1.02
1.36
Hermaphroditism
Condition and sex
Congenital adrenogenital disorders
Frequency
Case Control
Case
8.41%
(%)
Violent crime
Control (%)
OR
95 % CI
1006
100600
19
1.89%
1956
1.94%
0.97 0.62
1.53
Men
364
36400
13
3.57%
1540
4.23%
0.84 0.48
1.46
Women
642
64200
6
0.93%
416
0.65%
1.45 0.64
3.25
Other adrenogenital disorders
447
44700
15
3.36%
887
1.98%
1.72 1.02
2.88
Men
222
22200
12
5.41%
763
3.44%
1.61 0.89
2.89
Women
225
22500
3
1.33%
124
0.55%
2.44 0.77
7.72
Androgen insensitivity syndrome
783
78300
24
3.07%
2421
3.09%
0.99 0.66
1.49
Men
407
40700
21
5.16%
2101
5.16%
1.00 0.64
1.56
Women
Hypospadias men
376
37600
3
0.80%
320
0.85%
0.94 0.30
2.94
7690
769000
373
4.85%
38427
5.00%
0.97 0.87
1.08
Other malformations of penis men
1709
170900
89
5.21%
9025
5.28%
0.99 0.80
1.22
108
10800
2
1.85%
251
2.32%
0.79 0.20
3.23
Men
38
3800
1
2.63%
200
5.26%
0.49 0.07
3.56
Women
Klinefelter's syndrome men
70
7000
1
1.43%
51
0.73%
1.98 0.27 14.49
884
88400
71
8.0%
4888
5.5%
Frequency
Case Control
Case
Hermaphroditism
Condition and sex
Congenital adrenogenital disorders
(%)
Sex crime
Control (%)
1.49 1.17
OR
1.91
95 % CI
1006
100600
3
0.30%
116
0.12%
2.59 0.82
8.17
Men
364
36400
3
0.82%
114
0.31%
2.65 0.84
8.36
Women
642
64200
0
0.00%
2
0.00%
Other adrenogenital disorders
447
44700
2
0.45%
95
0.21%
2.11 0.52
8.59
Men
222
22200
2
0.90%
93
0.42%
2.17 0.53
8.83
Women
225
22500
0
0.00%
2
0.01%
Androgen insensitivity syndrome
783
78300
2
0.26%
109
0.14%
1.84 0.45
7.45
Men
407
40700
2
0.49%
108
0.27%
1.86 0.46
7.54
Women
Hypospadias men
376
37600
0
0.00%
1
0.00%
7690
769000
30
0.39%
2111
0.27%
1.42 0.99
2.04
Other malformations of penis men
1709
170900
2
0.12%
503
0.29%
0.40 0.10
1.59
108
10800
0
0.00%
14
0.13%
Men
38
3800
0
0.00%
14
0.37%
Women
Klinefelter's syndrome men
70
7000
0
0.00%
0
0.00%
884
88400
18
2.04%
290
0.33%
Hermaphroditism
6.32 3.91 10.21
14
Covariates
Groups divided according to androgen levels
There were no differences in which odds ratios that reached significance levels
between the analyses where parents’ education were controlled for and in the analyses
where it was not (see Appendix).
However, there were differences between the analyses where the total
population was included and where only the sample with information about parents’
education was included. In the smaller sample, the risk for sex crimes for patients
with high androgens was significant in both the sample where ‘other andrenogenital
disorders’ was included and where it was not. Though the other significant risks in the
total sample were not significant in the sample where information about parents’
education was known (see Appendix, table 6-8).
Groups divided according to diagnosis
As for the groups divided according to androgen levels, there were no
differences in significance level between the odds ratios adjusted for parents’
education and the crude odds ratios in the analysis where groups were divided
according to diagnosis.
Moreover, the risk for sex crimes in individuals with CAH were increased and
reached significance level in the smaller sample. The same was true for individuals
with other congenital disorders. Furthermore, there was no increased risk for any
crime in individuals with ‘other malformation of penis’ in the smaller sample (see
Appendix, table 9-11).
Discussion
Do prenatal androgens affect criminal behavior?
We studied the risk for crime in individuals diagnosed with DSD, with the
hypotheses that criminal behavior would be (a) increased in conditions associated
with higher levels of androgens during fetal development, and (b) decreased in
conditions where androgens are lower than normal. The findings did not support these
predictions, as there was no significant increase of the risk for any crime, violent
crime or sex crime in the group diagnosed with disorders associated with increased
prenatal androgens, nor did the result show a decrease of crime incidence in
conditions where prenatal androgens are expected to be lowered.
Women with disorders associated with high levels of androgens during fetal
development had a small increased risk for any crime, even if this risk did not reach
significance level in the group where ‘other andrenogenital disorders’ were excluded.
Men in the high-androgen group had an increased risk for committing sex crimes, but
neither was this risk significant when excluding other andrenogenital disorders. These
results indicate an effect of circulating testosterone on criminal behavior, rather than
an effect of prenatal androgen levels, since androgens are most likely raised later in
life and not during fetal development in conditions diagnoses with ‘other
andrenogenital disorders’. Unfortunately, the etiology of ‘other andrenogenital
diorders’ cannot be established with certainty, as the diagnosis can indicate many
different conditions, in some cases even regular CAH (Fahlhammar, H., MD PhD,
personal correspondence). Effects of either increased levels of prenatal or circulating
androgen can therefore not be excluded, considering sex crimes in men, or any crime
15
in women. Speaking in favor of the latter interpretation is that this is consistent with
some earlier studies that found a positive correlation between testosterone and
invasive sex crimes among male sexual offenders (Studer et al., 2005) and aggressive
dominant behavior among female inmates (Dabbs & Hargrove, 1997). Medication
that suppresses testosterone production also tends to lessen the risk of relapse in men
convicted for sex crimes (Briken & Kafka, 2007). If circulating androgens have an
affect on criminality, this could also affect other DSD conditions since other DSD
patients are treated with testosterone medication (e.g. KS). The effect of this
medication on crime should therefore be further studied.
Another possibility is that there could be a nonlinear influence of prenatal
androgens, only affecting women that normally would not be exposed to androgens
prenatally, but which cannot explain the variation in crime among men (the increased
incidence of sex crimes in high-androgen men may then be affected by other factors
than prenatal androgens). This effect may be mediated by a more male behavior
pattern at large that also can lead to higher incidence of crime. For example, studies
have shown that CAH girls often prefer boys as playmates (e.g. Long, Wisniewski &
Migeon, 2004), and it is conceivable that CAH girls therefore develop a more male
behavior pattern regarding crime through social learning (Bandura, Ross, & Ross,
1961).
The risk for any crime, and sex crime was raised in conditions associated with
low prenatal androgen. These are mostly explained by the high incidence of crime in
individuals with KS, as the odds ratios are no longer significant when this group is
excluded from the analysis. The high risk for crime connected to KS is probably
caused by other factors than lowered prenatal androgen exposure (these are discussed
below), even if this possibility cannot be excluded based on the results from the
current study. The unsignificant result in the group with other conditions than KS
associated with low prenatal androgens nevertheless indicates that decreased prenatal
androgen levels do not affect the risk for crime.
Other possible relations
The findings in the current study may have other explanations than altered sex
hormones, e.g. psychiatric comorbidity. Some studies have shown a high incidence of
psychiatric disorders in DSD patients (Johannsen, Ripa, Mortensen, & Main, 2006;
Liang et al., 2008). Psychiatric disorders might affect crime, especially severe,
chronic conditions as bipolar disorders and schizophrenia (Fazel, Gulati, Linsell,
Geddes, & Grann, 2009; Fazel, Lichtenstein, Grann, Goodwin, & Långström, 2010).
Whether psychiatric comorbidity mediates the effect of DSD on crime should be
further investigated. Other explanations could involve stigmatization of DSD patients,
which may lead to isolation and in turn lower socio-economic status (SES), possibly
affecting rates of crime. Moreover, one study shows sub-normal intelligence scores
for women with CAH (Johannsen, Ripa, Reinisch, et al., 2006), which also might
affect criminal behavior directly or mediated by SES.
Difficulties with using DSD as a model for androgen influence
There are some problems associated with using DSD as a model for androgen
influence. First, many other factors that follow from DSD may also contribute to an
increase or decrease of the risk for crime, which may confound the results and make
them harder to interpret. Moreover, since DSD conditions are quite rare the sample
size is not very big, which makes it hard to detect changes with small effect sizes. The
diagnoses also have varying etiology and phenotypes (e.g. the diagnose
16
hermaphroditism can indicate several conditions and hypospadias and ‘other
malformations of penis’ can both be an isolated phenomena or be part of more
complicated syndromes). Consequently, it is not always possible to nail other factors
that might be involved. Furthermore, not all cases with hypospadias and ‘other
malformations of penis’ are caused by altered sex hormones, but may have genetic
origins. These causes are hard to separate, and therefore they can blend out the
possible organizing effect of decreased androgens during fetal development. Another
complicating factor is that the influence of androgens on the development of sex
organs not necessary needs to have the same effects on the sex differentiation of the
brain, since these processes occur during different time periods (Houk, Hughes,
Ahmed, & Lee, 2006). Levels of circulating hormones during childhood, adolescence
and adulthood may also vary, both as a result of natural changes, but also as an effect
of medication. For example, patients with CAH are often treated during their whole
life with glucocorticoids, which reduces androgen production to normal or even
subnormal proportions, but if adherence to treatment is low, levels of androgens can
rise (Fahlhammar, H., MD PhD, lecture at Karolinska University Hospital, March 24,
2012). Consequently, circulating hormonal levels can be both increased and decreased
in the patient group, which makes it hard to know how postnatal hormonal status
influence the risk for crime. These different obstacles induce difficulties in the use of
DSD as a model to study the role of androgens in sex differentiated behaviors.
Finally, results of the current study should be interpreted with much caution, as one
must consider that repeated significance tests may inflict the result, exaggerating the
risk for false results reaching significance levels.
Crime in individuals with disorders of sex development
‘Other adrenogenital disorders.
There was an increased risk for any crime and violent crime associated with
‘other androgenital conditions’. As described above, ‘other andrenogenital disorders’
constitutes a diverse group of conditions, where the etiology is unclear. Because of
this reason, it is hard to consider other possible explanations of the results other than
the ones already discussed.
‘Other malformations of penis’.
A potential explanation of the small increased risk for crime in general
associated with the group diagnosed with ‘other malformations of penis’ could be that
the diagnoses are more common among children with low birth weight, which is
associated with lower SES of the mother (van den Berg, van Eijsden, Vrijkotte, &
Gemke, 2012). Low birth weight can also lead to other outcomes, e.g. attention
deficit/hyperactivity symptoms (Hultman et al., 2007), which some studies show are
related to higher rates of crime (Fletcher & Wolfe, 2009; Mannuzza, Klein, &
Moulton, 2008). It is important to consider the small effect when interpreting the
result, and it should be taken with much caution.
Klinefelter’s syndrome.
The incidence of convictions for any crime, violent crime and sex crime was
increased for men diagnosed with KS. Previous studies have reported similar results
(Schröder, de la Chapelle, Hakola, & Virkkunen, 1981; Stochholm et al., 2012).
Unfavorable socio-economic conditions are proposed as an explanation to increased
rates of crime. In the current study, parents’ education was used to control for socioeconomic factors, since DSD are congenital disorders and can have an effect on for
17
example educational outcomes of the affected individual. Controlling for parents’
education in a subgroup of the total sample did not lower the increased risk associated
with KS for any parameter studied. Hence, home environment factors cannot explain
the increased crime rates. On the contrary, lower SES caused by factors involved in
the disease seems to have an impact. In Stochholm et al’s study, adjustment for socioeconomic factors associated with the KS individual and not his parents reduced the
estimated risk for all crimes, but it was still significantly increased for the subgroups
sexual abuse and arson. Lower SES caused by factors linked with the chromosome
aneuploidy may in other words be a likely explanation to higher crime rates in general
for men with KS, but does not constitute a sufficient explanation to increased
incidence of arson and sexual abuse.
There are no clear explanations to why sexual abuse is increased. In general,
information about sexual function in men with KS is sparse. The disorder often leads
to reduced fertility and small testis (Acherman & Hughes, 2011). There are some
descriptions in the literature of different or deviating sexual behavior in KS, but only
based on small samples and case reports (Herzog & Money, 1993; Knecht, 1993).
Stochholm et al. (2012) suggest that feelings of being sexually different may lead to
misinterpretation of sexual signals, or frustration, which in turn can result in socially
and legally unacceptable ways of achieving sexual satisfaction. Another question that
ought to be further investigated is how testosterone treatment of KS affects incidence
of sex crime.
Only a small proportion of all men with KS receive a diagnosis. Chromosomal
abnormalities may be discovered in connection to criminal investigation, which could
explain a higher rate of crime among men with KS. To control for this, Stochholm et
al. (2012) omitted cases convicted in close proxy to the diagnose date. This hardly
changed their result. This implies that higher detection rate does not explain the
increased risk for crime associated with KS. Moreover, chromosomal analyses are not
part of the normal procedure in forensic investigations in Sweden (Eriksson, Å., PhD,
personal correspondence).
Conclusions
In conclusion, this population-based study of prenatal androgens and risk for
crime did not identify an increased risk for crime in individuals diagnosed with
disorders associated with higher prenatal androgens, nor was a decreased risk for
individuals with lower androgen levels found. The hypotheses could therefore not be
confirmed.
The results propose an activating effect of circulating testosterone on criminal
behavior, which should be further studied. Possibly, the result could also be explained
by a nonlinear influence of prenatal androgens, only affecting women that normally
would not be exposed to androgens prenatally, but which cannot explain the variation
in crime among men.
We also found an increased risk for any crime and violent crime in ‘other
androgenital disorders’, a small increased risk for any crime in ‘other malformations
of penis’, and an increased risk for any crime, violent crime and sex crime in men
with KS.
Even if the results did not suggest an effect of prenatal androgens at large, the
size of some groups are not very large, and there can still be small effects of prenatal
androgen, which are not detected. Nevertheless, it is possible to conclude that the
results of this study indicate that the potential effect of dissimilar prenatal androgen
levels cannot explain the big sex differences in criminal behavior.
18
To further elucidate how prenatal androgens affect incidence of crime in DSD,
future research needs to employ bigger samples to be able to find changes with small
effect sizes. In order to avoid higher rates of crime in DSD because of disease-specific
reasons, it is important to focus on mediators of the increased risk, which could lead
to improvements of treatment and possibly, prevention of crime caused by diseasespecific pathways. Moreover, the etiology of DSD needs to be additionally
investigated, to better be able to separate different causes of DSD. It is also desirable
to direct interest to a broader spectrum of long-time outcomes of DSD, both for the
interesting possibility of studying the influence of sex hormones on development but
also to further advance the management of patients with DSD.
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21
Appendix
Table 6. The total study population without parents' education included in the model.
Androgen level and sex
Any crime
Violent crime
OR 95 % CI
OR 95 % CI
High androgens
1.14 0.99 1.31
1.22 0.87 1.70
Men
1.07 0.89 1.29
1.09 0.73 1.63
Women
1.27 1.02 1.58
1.70 0.91 3.19
High androgens (other adrenogenital disorders excluded) 1.03 0.86 1.23
1.00 0.64 1.55
Men
0.94 0.73 1.20
0.84 0.48 1.46
Women
1.16 0.89 1.51
1.50 0.71 3.18
Low androgens
1.04 1.00 1.09
1.02 0.93 1.11
Men
1.04 0.99 1.08
1.02 0.93 1.11
Women
1.36 0.97 1.89
0.94 0.30 2.94
Low androgens (KS excluded)
1.03 0.98 1.08
0.97 0.89 1.07
Men
1 0.97 1.07
0.97 0.89 1.07
Women
1.36 0.97 1.89
0.94 0.30 2.94
Sex crime
OR 95 % CI
2.37 0.98 5.77
2.43 1.00 5.92
2.59 0.82
2.65 0.84
8.16
8.36
1.72 1.31
1.72 1.31
2.27
2.27
1.24 0.89
1.24 0.89
1.75
1.75
Table 7. The sample with information about parents' education, without parents' education included in the model.
Androgen level and sex
Any crime
Violent crime
Sex crime
OR 95 % CI
OR 95 % CI
OR 95 % CI
1.15 0.88 1.49
0.80 0.41 1.56
4.52 1.09 18.69
High androgens
1.23 0.87 1.74
0.83 0.39 1.77
4.66 1.12 19.39
Men
1.06 0.69 1.63
0.72 0.18 2.91
Women
0.89 0.46 1.74
4.98 1.20 20.68
High androgens (other adrenogenital disorders excluded) 1.15 0.87 1.51
1.23 0.85 1.78
0.94 0.44 2.01
5.15 1.23 21.54
Men
1.05 0.67 1.64
0.78 0.19 3.14
Women
1.00 0.95 1.06
0.97 0.88 1.08
1.00 0.63 1.57
Low androgens
1.00 0.95 1.06
1.00 0.95 1.06
1.00 0.63 1.57
Men
1.10
0.70
1.72
0.83
0.21
3.37
Women
0.99 0.94 1.04
0.95 0.85 1.05
0.71 0.41 1.23
Low androgens (KS excluded)
0.99 0.93 1.04
0.95 0.85 1.05
0.71 0.41 1.23
Men
1.10 0.70 1.72
0.83 0.21 3.37
Women
Table 8. The sample with information about parents' education, with parents' education included in the model.
Androgen level and sex
Any crime
Violent crime
Sex crime
OR 95 % CI
OR 95 % CI
OR 95 % CI
1.11 0.85 1.45
0.76 0.39 1.47
4.39 1.06 18.21
High androgens
1.17 0.82 1.66
0.76 0.35 1.62
4.42 1.06 18.48
Men
1.04 0.67 1.59
0.69 0.17 2.78
Women
0.84 0.43 1.64
4.81 1.16 20.04
High androgens (other adrenogenital disorders excluded) 1.11 0.84 1.46
1.18 0.81 1.71
0.87 0.40 1.86
4.94 1.18 20.73
Men
1.02
0.65
1.60
0.74
0.18
3.00
Women
1.00 0.94 1.05
0.97 0.87 1.07
0.99 0.63 1.56
Low androgens
0.99 0.94 1.05
0.97 0.87 1.07
0.99 0.63 1.56
Men
1.09 0.69 1.70
0.83 0.20 3.35
Women
0.98 0.93 1.04
0.94 0.84 1.04
0.70 0.41 1.22
Low androgens (KS excluded)
0.98 0.93 1.04
0.94 0.84 1.04
0.70 0.41 1.22
Men
1.09 0.69 1.70
0.83 0.20 3.35
Women
22
Table 9. The total study population without parents' education included in the model.
Condition and sex
Any crime
Violent crime
OR 95 % CI
OR
95 % CI
Congenital adrenogenital disorders
1.01 0.85 1.22 0.97 0.62
1.53
Men
0.94 0.73 1.20 0.84 0.48
1.46
Women
1.13 0.86 1.50 1.45 0.64
3.25
Other adrenogenital disorders
1.38 1.09 1.73 1.72 1.02
2.88
Men
1.31 0.98 1.75 1.61 0.89
2.89
Women
1.64 1.09 2.47 2.44 0.77
7.72
Androgen insensitivity syndrome
1.01 0.84 1.23 0.99 0.66
1.49
Men
0.89 0.70 1.13 1.00 0.64
1.56
Women
1.36 0.97 1.89 0.94 0.30
2.94
Hypospadias men
1.01 0.96 1.07 0.97 0.87
1.08
Other malformations of penis men
1.12 1.00 1.25 0.99 0.80
1.22
Hermaphroditism
0.79 0.44 1.45 0.79 0.20
3.23
Men
0.46 0.18 1.18 0.49 0.07
3.56
Women
1.36 0.62 2.99 1.98 0.27
14.49
Klinefelter's syndrome men
1.18 1.02 1.36 1.49 1.17
1.91
OR
2.59
2.65
Sex crime
95 % CI
0.82
8.17
0.84
8.36
2.11
2.17
0.52
0.53
8.59
8.83
1.84
1.86
0.45
0.46
7.45
7.54
1.42
0.40
0.99
0.10
2.04
1.59
6.32
3.91
10.21
Table 10. The sample with information about parents' education, without parents' education included in the model.
Condition and sex
Any crime
Violent crime
Sex crime
OR 95 % CI
OR
95 % CI
OR
95 % CI
Congenital adrenogenital disorders
1.17 0.89 1.55 0.92 0.47
1.79 4.98 1.20
20.70
Men
1.23 0.85 1.78 0.94 0.44
2.01 5.15 1.23
21.54
Women
1.10 0.70 1.75 0.87 0.22
3.53
Other adrenogenital disorders
1.17 0.49 2.81
Men
1.18 0.38 3.69
Women
1.17 0.27 5.03
Androgen insensitivity syndrome
0.91 0.71 1.17 0.85 0.51
1.43
Men
0.85 0.63 1.14 0.85 0.49
1.49
Women
1.10 0.70 1.72 0.83 0.21
3.37
Hypospadias men
0.99 0.93 1.05 0.93 0.82
1.05 0.85 0.48
1.49
Other malformations of penis men
1.04 0.91 1.18 1.05 0.83
1.33 0.30 0.04
2.16
Hermaphroditism
0.16 0.02 1.15
Men
Women
0.52 0.07 3.87
Klinefelter's syndrome men
1.26 1.00 1.60 1.58 1.08
2.32 7.64 3.31
17.66
Table 11. The sample with information about parents' education, with parents' education included in the model.
Condition and sex
Any crime
Violent crime
Sex crime
OR 95 % CI
OR
95 % CI
OR
95 % CI
Congenital adrenogenital disorders
1.13 0.85 1.50 0.87 0.45
1.70 4.79 1.15
19.92
Men
1.18 0.81 1.71 0.87 0.40
1.86 4.94 1.18
20.73
Women
1.07 0.68 1.71 0.84 0.21
3.39
Other adrenogenital disorders
1.15 0.48 2.79
Men
1.04 0.33 3.31
Women
1.11 0.26 4.82
Androgen insensitivity syndrome
0.90 0.71 1.16 0.84 0.50
1.41
Men
0.83 0.62 1.13 0.84 0.48
1.47
Women
1.09 0.69 1.70 0.83 0.20
3.35
Hypospadias men
0.98 0.92 1.04 0.92 0.81
1.04 0.84 0.47
1.48
Other malformations of penis men
1.04 0.92 1.19 1.06 0.84
1.34 0.30 0.04
2.14
Hermaphroditism
0.15 0.02 1.12
Men
Women
0.56 0.08 4.17
Klinefelter's syndrome men
1.30 1.02 1.65 1.65 1.12
2.43 7.96 3.43
18.47