1014991

research-article2021
AUT0010.1177/13623613211014991AutismDemetriou et al.

Original Article

Autism

Autism spectrum disorder: 1­–15

© The Author(s) 2021
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DOI: 10.1177/13623613211014991
https://doi.org/10.1177/13623613211014991

in neuropsychological and self-report journals.sagepub.com/home/aut

measures of executive and

non-executive cognitive function

Eleni A Demetriou1, Karen L Pepper1, Shin Ho Park1,

Liz Pellicano2 , Yun Ju C Song1, Sharon L Naismith1,
Ian B Hickie1, Emma E Thomas1 and Adam J Guastella1

Abstract
Sex differences in autism may in part be understood by an atypical sex profile of executive function and non-executive
function. In this study, we compared females and males with autism against non-autistic individuals on neuropsychological
and self-report measures to examine whether any sex differences in executive function and non-executive function
might be unique to autism. Our study showed a significant overall female advantage for measures of psychomotor
speed, cognitive flexibility, verbal learning and memory and semantic fluency. There was no significant interaction effect
between diagnosis and sex. No sex differences were observed on the self-report measure of executive function. Our
results suggest that while females show different cognitive performance to males, these sex differences were not specific
to the autistic cohort.

Lay abstract
Research comparing females and males with a diagnosis of autism suggests that there are sex differences in some
characteristics such as behaviour regulation. One area not studied in detail is whether females and males with autism
perform differently in tests of cognitive ability. The results of previous research are quite mixed. One explanation
may be that some research comparing females and males with autism did not include a neurotypical control group for
comparison. As a result, it is not clear whether the sex differences in cognitive ability observed in people with autism
are similar to differences between neurotypical males and females. To better understand whether there are unique
differences between males and females with autism, it is important to also compare them with neurotypical males and
females. In our research, we included a neurotypical group and compared males and females with and without a diagnosis
of autism. We found that the sex differences in autism are similar to what we observe in males and females without
autism. Our study showed that compared with males, females (with and without autism) do better in assessments
of processing speed, cognitive flexibility, verbal learning and memory and semantic fluency. Our results suggest that
although females show different cognitive performance to males, these sex differences were not specific to the group
with a diagnosis of autism.

Keywords
autism spectrum disorder, Behavioural Rating Inventory of Executive Function, Cambridge Neuropsychological Test
Automated Battery, executive function, sex differences

1
The University of Sydney, Australia Corresponding author:
2
Macquarie University, Australia Adam J Guastella, Michael Crouch Chair in Child and Youth Mental
Health, Brain and Mind Centre, Children’s Hospital Westmead Clinical
School, Faculty of Medicine and Health, The University of Sydney,
Camperdown, Sydney, NSW 2050, Australia.
Email: adam.guastella@sydney.edu.au
2 Autism 00(0)
Autism spectrum disorder (ASD) is a neurodevelopmental
condition with a strong male bias, currently at about three
males to every one female (Loomes et al., 2017). This sex
bias may be due to a range of factors. These include genetic
and/or neurobiological differences as, for example,
described in the ‘imprinted-X liability model’ (Skuse,
2000), ‘the male brain theory’ (Baron-Cohen et al., 2005)
and the ‘female protective effect theory’ (Ferri et al., 2018;
Frazier et al., 2014). These aetiological factors may thus
contribute to the observed differences in the symptom pro-
file of ASD females where diagnosis is generally made
later in life (Ferri et al., 2018; Jamison et al., 2017) and is
characterised by more severe symptomatology with sig-
nificant co-occurring difficulties (Dworzynski et al., 2012;
Ferri et al., 2018). Alternatively, difference may be due to
diagnostic or clinician biases in the characterisation of
ASD (Van Wijngaarden-Cremers et al., 2014), sex-related
sociocultural and environmental moderators (Kreiser &
White, 2014) and gender roles (Reilly et al., 2016).
Methodological differences in study design (Hyde, 2016)
may also contribute to observed differences between
females and males with ASD. In ASD, sex differences
have also been reported on informant behavioural ratings
of ASD symptomatology (Torske et al., 2018), adaptive
behaviour and executive function (EF; White et al., 2017);
however, the factors contributing to these differences are
still undetermined.
To understand better the aetiology of sex differences,
there has been growing interest in identifying the charac-
teristics that might differentiate autistic males and females,
including neurocognitive performance. Yet, despite exten-
sive research on group differences in ASD, comparison of
sex differences on neuropsychological assessments and
self/informant appraisals of cognitive function has been
limited. The examination of neurocognitive performance
is particularly pertinent given the reported relationship
between neuropsychological measures and ASD aetiology
such as theory of mind (Pellicano, 2007). Furthermore, sex
differences in the subjective self-assessments of ASD may
inform on underlying self-referential processes guiding
these (Burrows et al., 2017; Lombardo et al., 2007) and
may provide an additional framework to understand the
factors that lead to a higher male prevalence in autism.
Research evaluating behavioural and performance-based
measures of EF generally reflects low intercorrelations
(Demetriou, Song, et al., 2018; Gardiner et al., 2017;
McAuley et al., 2010) and highlights the importance of uti-
lising multiple types of measures. This is particularly per-
tinent in ASD given suggestions of biased self-perception
in autistic individuals who may report a more positive self-
evaluation on a range of variables, including cognitive per-
formance (Furlano et al., 2015). Typically however,
research on cognitive function in ASD focuses on one
assessment type with fewer studies evaluating both neuro-
cognitive and behavioural measures.
Broadly, the study of cognition is subsumed under dis-
crete cognitive functions and a distinction is generally
made between executive and non-executive function (non-
EF) domains. EF refers to the capacity to respond adap-
tively and engage in goal-directed, purposeful behaviours
(Lezak et al., 2012). Core EFs as identified in the ‘unity
and diversity’ model include mental set shifting, working
memory (WM) and response inhibition (Miyake et al.,
2000). Further research of the factors identified in the
‘unity and diversity model’ (Miyake & Friedman, 2012)
verified the shifting and WM factors (noted as shifting-
specific factor and updating-specific factor) and a com-
mon shared factor. The latter encapsulates all variability of
the response-inhibition factor in the original model. These
factors account for much of the individual differences in
EF performance and contribute to higher-order EF
domains, including fluency/generativity, concept forma-
tion and planning (Diamond, 2013). Much of the research
of EF domains in ASD is based on the above factor models
proposed by Miyake and Diamond, with the core EF
domains, set shifting, WM and response inhibition, receiv-
ing the most attention.
In addition to EF, the Diagnostic and Statistical Manual
of Mental Disorders (5th ed.; DSM-5; American Psychiatric
Association (APA), 2013) defines five cognitive non-EF
domains – complex attention, learning and memory, visuo-
perceptual functions, language and social cognition – as
the key neurocognitive domains important in normative
behaviour and psychopathology. In cognitive science (and
also adopted in DSM-5), a distinction is usually made
between WM and short-term memory (STM). STM typi-
cally refers to a maintenance memory system that holds
information chunks (generally up to seven) for a brief
period. WM has been defined as the STM system respon-
sible for active maintenance and manipulation of informa-
tion (McCabe et al., 2010). WM has been generally
regarded as an EF process in part because of its active role
in information processing. Despite representing different
constructs, the distinction between STM and WM is not
clearly maintained in research (Aben et al., 2012). In ASD,
there is a well-established pattern for overall difficulties in
EF compared with neurotypical populations (Demetriou,
Lampit, et al., 2018); however, research on cognitive sex
differences in ASD is limited.
In terms of cognition, most sex-related research in
ASD has focused on neuropsychological assessments of
children, with fewer studies assessing cognitive sex dif-
ferences in adults, where overall, the research findings are
equivocal. In a cohort of autistic participants younger than
the age of 18, Frazier and colleagues (2014) showed that
females had significantly lower verbal/non-verbal and
overall intelligence quotient (IQ) in comparison with
males. These findings are somewhat disputed as they rep-
resent a very specific genetic and geographical cohort and
thus may be subject to ascertainment bias (Howe et al.,
Demetriou et al. 3
2014). Comparable outcomes for verbal IQ were, how-
ever, reported in a second study of children with ASD
recruited from the general community (van Ommeren
et al., 2016). Another study of autistic children aged
7–14 years, showed that females perform poorly on cogni-
tive flexibility measures in comparison with males
(Memari et al., 2013). In autistic adult males and females
(Lehnhardt et al., 2016), it was shown that females per-
formed better on verbal fluency tests of EF, whereas males
showed superior verbal abilities as assessed by verbal IQ
tasks. In contrast, Lai and colleagues (2017) did not find
any sex differences across any IQ indices or on a response
inhibition task. A possible reason for the mixed findings
in the ASD literature is that some studies have failed to
include a sex-matched neurotypical comparison group.
For example, cognitive sex differences in 3-year-old chil-
dren with ASD (Zwaigenbaum et al., 2012) dissipated
once they were compared with a comparison group of
neurotypical children of similar age and intellectual abil-
ity. In a study of adults aged 19 years and older, which
included comparisons with neurotypical adults (Kiep &
Spek, 2017), no significant main or interaction effects for
gender and diagnosis were observed for the EF domains
of planning, mental flexibility and WM. Two other studies
however, reported a significant sex with diagnosis inter-
action effect for EF measures of response inhibition
(Lemon et al., 2011) and cognitive flexibility (Bölte et al.,
2011). In Lemon et al. (2011), autistic females reported
poorer response inhibition compared with autistic males
and typical females, whereas in Bölte et al. (2011), autis-
tic females showed better cognitive flexibility compared
with autistic males, whereas the reverse was true in the
typical comparison group. Overall, evidence for sex dif-
ferences in cognitive EF and non-EF in ASD groups is
mixed, particularly for the EF domain of cognitive flexi-
bility. Although there is a trend for a female advantage for
verbal fluency tasks and a male advantage on verbal IQ
indices, these findings may in part be confounded by
methodological differences, including developmental
changes and type of comparison group. Studies reported
above, which examine sex differences in ASD and com-
pare with a neurotypical control group, are summarised in
Table 1.
In contrast to the mixed ASD findings, cognitive sex
differences in the normative population traditionally report
a female advantage for verbal domains and a male advan-
tage for visuospatial tasks (Gur et al., 2012; Hyde, 2016).
This finding has been confirmed in recent meta-analyses
(Miller & Halpern, 2014), although the causal explana-
tions of such differences and the research itself are still
debated. For example, contrary to the traditional view of
biological heritability of sex differences, it has been pro-
posed that ‘inherited’ socio-environmental factors have a
pivotal role in maintaining sex differences (Fine et al.,
2017). Potential biases, however, may also influence the
study of normative sex differences and include gender
socialisation roles (Reilly et al., 2016) or methodological
differences in study design such as type of assessment
measures and task characteristics (Lejbak et al., 2011;
Reed et al., 2017; Reilly et al., 2016). Given the observa-
tion of sex differences in the normative population,
reported sex differences in ASD may be magnified in the
absence of a comparison neurotypical group.
Consistent with the above observation, a recent meta-
analysis of 13 studies that included comparisons with neu-
rotypical individuals (Hull et al., 2016) did not identify a
distinct cognitive sex profile in autism. Specifically, no sex
differences were identified for IQ (effect size synthesised
on 13 studies) or for the key ASD domains of social com-
munication (synthesised on five studies) and restricted and
repetitive patterns and interests (synthesised on four stud-
ies). In their systematic review, Hull et al. (2016) reported
trends for sex differences in EF in ASD for cognitive flex-
ibility (female advantage) and response inhibition (male
advantage) and on a visuospatial task (male advantage).
In addition to neuropsychological assessments, subjec-
tive ratings of cognitive ability have been of increasing
interest in the autism field particularly given some support
that they may represent a more ecologically valid assess-
ment of cognitive difficulties (Albein-Urios et al., 2018;
Wallace et al., 2016). Support, however, for superior eco-
logical validity remains equivocal, with some studies
reporting significant differences between informant and
self-report evaluations of EF (McAuley et al., 2010) and
poor correlations between behavioural and performance-
based measures (Chan et al., 2009; Mackinlay et al., 2006;
Toplak et al., 2013). Most studies of behavioural measures
of EF examine differences between the ASD cohort and
neurotypical comparison groups or the normative stand-
ardisation sample. EF difficulties based on informant rat-
ings of the Behavioural Rating Inventory of Executive
Function (BRIEF; Roth et al., 2005) were reported in chil-
dren, adolescents (de Vries & Geurts, 2015; Gilotty et al.,
2002; Mackinlay et al., 2006) and adults (Wallace et al.,
2016) with ASD. Research, however, on sex differences in
ASD using behavioural ratings has been limited. A study
that utilised informant ratings (White et al., 2017) found
that parents rated females to have significantly higher lev-
els of executive difficulties despite performing at compa-
rable levels of intellectual functioning as males. A second
study (Torske et al., 2018) reported a trend for girls to be
rated by parents as more impaired on planning and organ-
ising ability but did not identify any other sex differences
on informant ratings of EF. These sex differences may be
explained by the more severe symptomatology observed in
females with ASD (Jamison et al., 2017) but may also
reflect biases on the expected behaviours of females com-
pared with males. Contrary to the above, a study using
informant ratings for children up to the age of 18 (Huizinga
& Smidts, 2010) reported that boys were significantly
 4

Table 1.  Summary of studies on sex differences in autism spectrum disorder.

Study Diagnostic groups Cognitive function Factor group Factor sex Interaction: Group × Sex
2 2 2
Bölte et al. ASD (females) N = 21 IQ (non-verbal) F = 2.18, p = 0.11, η p  = 0.04 F = 0.10, p = 0.77, η p  = 0.00 F = 0.07, p = 0.79, η p  = 0.00
(2011) ASD (males) N = 35
TYP (females)* N = 23
TYP (males)* N = 35
*siblings with no ASD
diagnosis
2 2 2
  Wisconsin Card Sorting Test F = 3.17, p = 0.07, η p  = 0.03 F = 0.09, p = 0.75, η p  = 0.03 F = 0.24, p = 0.63, η p  = 0.00
(perseveration errors)
2 2 2
  Trail Making Test (TMT-B-TMT-A) F = 3.45, p = 0.04, η p  = 0.04 F = 1.98, p = 0.16, η p  = 0.02 F = 3.91, p = 0.04, η p  = 0.04
ASD females were faster than ASD males
TYP males were faster than TYP females
2 2 2
  Embedded Figures Test F = 1.82, p = 0.17, η p  = 0.02 F = 0.02, p = 0.88, η p  = 0.00 F = 0.02, p = 0.88, η p  = 0.00
2 2 2
  Block Design Test F = 0.08, p = 0.77, η p  = 0.00 F = 1.09, p = 0.30, η p  = 0.01 F = 5.56, p = 0.02, η p  = 0.05
ASD males performed better than ASD females
TYP females performed better than TYP males
Goddard ASD (females) N = 12 IQ No significant difference between  
et al. (2014) ASD (males) N = 12 ASD and TYP
TYP (females) N = 12 t = 0.12, p = 0.94
TYP (males) N = 12
  Autobiographical Memory Cueing Task F(1, 44) = 9.18, p = 0.004, η2 = 0.17 F(1, 44) = 5.30, p = 0.026, η2 = 0.11 F(1, 44) = 4.24, p = 0.045, η2 = 0.09
ASD females produced more autobiographical
memories than ASD males
No differences between TYP females and TYP males
  Semantic Fluency (Animals category) Not significant: p > 0.05 F(2,43) = 3.69, η2 = 0.65, p = 0.03 Not significant: p > 0.05
Females better than males
Kiep and ASD (females) N = 40 Tower of Hanoi F(8,122) = 1.09, p = 0.377, η2 = 0.067 F(8,122) = 1.25, p = 0.276, η2 = 0.076 F(8,122) = 1.25, p = 0.621, η2 = 0.049
Spek (2017) ASD (males) N = 99 (planning task)
TYP (females) N = 25
TYP (males) N = 35
  Wisconsin Card Sorting Test F(7, 184) = 0.9, p = 0.507, η2 = 0.033 F(7, 184) = 0.677, p = 0.691, F(7, 184) = 1.229, p = 0.289, η2 = 0.045
η2 = 0.025
  Working Memory Index – WAIS III F(2, 192) = 0.007, p = 0.993, η2 = 0.000 F(2, 192) = 1.96, p = 0.144, η2 = 0.020 F(2, 192) = 0.58, p = 0.994, η2 = 0.001
  Fluency F(4, 188) = 5.635, p = 0.00, η2 = 0.107 F(4, 188) = 1.739, p = 0.143, F(4, 188) = 0.188, p = 0.944, η2 = 0.004
η2 = 0.036

(Continued)
Autism 00(0)
 Demetriou et al.

Table 1. (Continued)
Study Diagnostic groups Cognitive function Factor group Factor sex Interaction: Group × Sex

Lai et al. ASD (females) N = 32 IQ  

(2012) ASD (males) N = 32 No significant difference between female
TYP (females) N = 32 ASD, male ASD, female TYP or male TYP
TYP (males) N = 32 groups (statistical tests not reported)
  Go–No-Go Task F(1, 121) = 6.51, p = 0.012, η2 = 0.051 F(1, 121) = 0.25, p = 0.621, η2 = 0.002 F(1, 121) = 0.34, p = 0.564, η2 = 0.003
Commission errors
  Go–No-Go Task F(1, 121) = 17.25, p < 0.001, η2 = 0.125 F(1, 121) = 3.52, p = 0.063, η2 = 0.028 F(1, 121) = 0.08, p = 0.779, η2 = 0.001
Omission errors
  Phonemic Fluency F(1, 122) = 0.19, p < 0.668, η2 = 0.002 F(1, 121) = 6.51, p = 0.012, η2 = 0.051 F(1, 121) = 1.17, p = 0.282, η2 = 0.009
Lemon et al. IQ  
(2011) WISC: no significant differences
Statistical tests not reported
Lemon et al. EF Stop Task F(3, 19) = 3.87, p = 0.026  
(2011) (response inhibition) ASD females were slower than TYP
females: p = 0.002, Cohen’s d = 1.30
TYP males: p = 0.025, Cohen’s d = 0.86
No significant difference between
ASD males and TYP males: p = 0.919,
Cohen’s d = 0.05
Sedgewick ASD (females) N = 13 IQ Not significant Not significant Not significant
et al. (2016) ASD (males) N = 10 WAIS p > 0.18 p > 0.33 p > 0.33
TYP (females) N = 10
TYP (males) N = 32
Solomon ASD (females) N = 20 IQ TYP group > ASD group: p < 0.05 Not reported  
et al. (2012) ASD (males) N = 20 WASI
TYP (females) N = 19
TYP (males) N = 17

ASD: autism spectrum disorder; TYP: non-autistic participants; IQ: intelligence quotient; TD: typically developing; WAIS-III: Wechsler Adult Intelligence Scale–Third Edition; WISC: Wechsler Intelligence Scale for Children; EF:
executive function; WASI: Wechsler Abbreviated Scale of Intelligence.
5
6 Autism 00(0)
more impaired than girls on almost all of the BRIEF clini-
cal scales.
In summary, there is limited extant research on sex dif-
ferences in autism, with only few studies focusing on
potential underlying factors such as neurocognitive func-
tioning that may contribute to the behavioural phenotype.
Methodological differences in the autism literature of cog-
nitive sex differences limit generalisation of findings. The
goal of this study therefore was to assess for sex differ-
ences in autism across a range of cognitive EF and non-EF
domains and evaluate whether they contribute to an atypi-
cal cognitive profile in autism. We aimed to address limita-
tions of some previous research by including a neurotypical
comparison group, selecting a homogeneous age cohort
above the age of 16 to control for potential sex-related
developmental differences and by utilising measures
across both verbal and visuospatial domains of EF and
non-EF. Our measures consisted of both neuropsychologi-
cal assessments and self-evaluations, the latter based on
the BRIEF (Roth et al., 2005). Our neuropsychological
measures of non-EF mapped on the domains outlined in
the DSM-5 and included measures of complex attention,
verbal and visuospatial learning and memory and language
(fluency construct). A detailed analysis of sex differences
in social cognition measures is in preparation by our group
and was not included in this study. The inclusion of EF
measures in our study was informed in part by the findings
of a meta-analysis of EF in ASD (Demetriou, Lampit,
et al., 2018). In that study, broad difficulties in EF were
identified with no evidence for differential impact of dis-
crete EF sub-domains. Furthermore, our study did not
include measures of response inhibition based on the find-
ings of the revised unity in diversity model (Friedman
et al., 2008). In this model, response inhibition was identi-
fied as a common shared factor with no unique contribu-
tion to the EF construct. Response inhibition and WM
were, however, assessed in our study by self-appraisals of
EF behavioural ratings. Given the mixed findings in the
extant literature, we based our hypotheses on the overall
findings of the meta-analysis and systematic review by
Hull and colleagues (2016), and statistical analyses were
conducted with an alpha of <0.05.
First, our primary hypothesis was that we should see a
significant interaction effect for sex by diagnosis for our
measures of psychomotor speed and cognitive flexibility
with females with ASD performing better than males with
ASD and a reverse trend expected for sex differences in
neurotypical individuals. Second, aligned with trends in
the typical population, we expected an overall female
advantage on neuropsychological measures of verbal
domains and a male advantage for visuospatial tasks.
Third, consistent with normative findings for the EF self-
report measure (Roth et al., 2005), we expected a signifi-
cant sex effect for the BRIEF clinical scales of ‘emotional
control’, that is, the capacity to regulate and modulate
emotional responses, and ‘initiate’, that is, the capacity to
commence a task and engage in appropriate problem-solv-
ing strategies (Roth et al., 2005). A male advantage was
reported for the former and a female advantage for the lat-
ter scale.
Method
Community involvement
There is no community involved in this study.
Participants
Ethics approval was obtained by the University’s ethics
committee. Informed consent was obtained directly from
each participant prior to inclusion in the study. A cohort of
youth and adults (N = 128; age: M = 24.8, SD = 6.6 years;
age range: females: 16–38, males: 16–47, 41.4% female)
were recruited for the study. The ASD group (N = 69, age:
M = 24.4, SD = 7.5 years, age range: females: 16–38, males:
16–47, 36.2% female; n = 25) was a convenience sample
presenting for treatment and/or social skills development
at a University clinic (Clinic). Non-autistic participants for
the ASD comparison group (TYP; N = 59, age: M = 25.3,
SD = 5.2, age range: females: 18–30, males: 18–42, 47.5%
female, n = 28) were recruited through advertising at a
number of different university websites. All participants
were screened and excluded from the study if they had
intellectual disability (IQ < 70) or reported current sub-
stance dependence.
Non-autistic participants were excluded if they reported
a mental health diagnosis (past or current), had another neu-
rodevelopmental condition or were currently experiencing
significant levels of depression, anxiety or stress as meas-
ured by the standardised instruments: Depression, Anxiety
and Stress Scale (DASS-21; Lovibond & Lovibond, 1995)
and the Social Interaction Anxiety Scale (SIAS; Mattick &
Clarke, 1998). The autistic participants also completed the
same symptom-severity questionnaires. Participants met
criteria for the primary presenting disorder of ASD based on
clinical diagnoses made by qualified clinicians on standard-
ised clinical interviews based on the DSM-5 (APA, 2013)
and diagnostic assessment instruments. The ASD diagnosis
was confirmed following completion of the Autism
Diagnostic Observation Schedule–Second edition (ADOS-
2; Lord et al., 2012) and the Social Responsiveness Scale
(SRS; Constantino & Gruber, 2005). Interviews were under-
taken with the participants, and where possible, additional
information, including developmental history, was obtained
from parents, carers and previous diagnostic assessments.
The assessment battery comprised a combination of
diagnostic assessments, neuropsychological tests and self-
report measures of executive and non-EF. Trained post-
graduate research students conducted all assessments in
Demetriou et al. 7

person over two sessions at the Clinic. Participants were
seen individually within quiet (though not soundproof)
rooms with typical indoor lighting. None of the partici-
pants reported sensory discomfort and no participant was
observed to be distressed during testing.
The neuropsychological test battery included a brief IQ
test, the Wechsler Test of Adult Reading (WTAR; Wechsler,
2001) and a comprehensive battery of verbal and non-ver-
bal tests of EF and non-EF. The WTAR is a single word-
reading test and provides a valid and reliable assessment of
general intellectual functioning (Wechsler, 2001) although
some research suggests it may be less appropriate for
autistic people (see ‘Limitations’ section). The non-EF
measures consisted of tests of psychomotor speed (Trail
Making Test–Part A (TMT-A)), visuospatial learning/STM
(Paired Associate Learning (PAL) and Spatial Span (SSP))
and verbal learning/STM (Logical Memory (LM), Rey
Auditory-Verbal Learning Task (RAVLT)). EF measures
assessed the domains of mental flexibility (Trail Making
Test–Part B (TMT-B)), sustained attention (Rapid Visual
Information Processing (RVP-A)), attentional shifting
(Intra-Extra Dimensional (IED)) and phonetic and seman-
tic fluency (Controlled Oral Word Association Test
(COWAT)). The self-report ratings of EF were based on
the BRIEF (Roth et al., 2005). Supplementary Table S1
includes a more detailed description of each of the specific
measures.
examined main effect differences for diagnosis, sex and
the interaction of diagnosis with sex, across all measures
of EF and non-EF. Significant demographic moderators
(Education) were incorporated in the analysis as covari-
ates. Each neuropsychological measure was included in
the MANCOVA as a discrete variate; measures were not
combined into an overall index. Pillai’s Trace was utilised
to assess the significance of the overall main (diagnosis,
sex) and interaction (diagnosis with sex) effects. Follow-up
statistical analyses (ANOVA) utilised the Bonferroni cor-
rection for multiple comparisons and examined the
between-subject effects of the individual neuropsychologi-
cal measures. Significance findings are reported for
p < 0.05.
Results
Demographics
Results are summarised in Tables 2 and 3, and comparisons
were made between the autistic and non-autistic groups.
There were no significant differences in the sex representa-
tion between groups, χ2 = 1.65, p = 0.199. We examined
whether autistic females and males differed significantly on
symptom/trait severity based on the ADOS (t(1,
55) = −0.884, p = 0.381) and SRS scores (t(1, 60) = −0.522,
p = 0.604) and found no significant differences. We also
examined correlations between the ADOS and EF and

Data analysis
Data analysis was performed using the IBM SPSS Statistics Table 2.  Sex distribution.
version 24. Univariate analysis of variance (ANOVA) Gender ASD TYP Total
examined for differences across the demographics of intel-
lectual functioning (IQ/WTAR) and Years of Education Female 25 28 53
  % Total 19.5 21.9 41.4
(Education). Education and IQ were examined as potential
Male 44 31 75
moderators of cognitive function performance. Age differ-
  % Total 34.4 24.2 58.6
ences were assessed based on the Mann–Whitney test. The
Total 69 59  
Pearson Chi-Square Test Statistic of Independence (χ2)
  53.9 46.1  
assessed sex representation across the diagnostic groups.
Multivariate analysis of covariance (MANCOVA) ASD: autism spectrum disorder; TYP: non-autistic participants.

Table 3. Demographics.

Demographic ASD (N = 69) TYP (N = 59)   Statistical analysis 

variables
M SD M SD
Age 24.4 7.5 25.3 5.2 U = 1,567.0, p = 0.025
Predicted IQ 107.7 8.4 107.2 8.3 F(1, 126) = 0.12, p = 0.730
Years of education 12.5 2.1 14.3 2.1 F(1, 126) = 22.89, p < 0.001
ADOS Female 9.5 3.1 — — t(1, 55) = −0.884, p = 0.381
ADOS Male 9.9 3.1 — —
SRS Female 102.3 32.9 — — t(1, 60) = −0.522, p = 0.604
SRS Male 95.1 28.2 — —

ASD: autism spectrum disorder; TYP: non-autistic participants; SD: standard deviation; IQ: intelligence quotient; ADOS: Autism Diagnostic
Observation Schedule; SRS: Social Responsiveness Scale.
8 Autism 00(0)
non-EF cognitive tests. Significant associations were
observed between the ADOS and non-EF tests of process-
ing speed (TMT-A, r = 0.406, p < 0.01), attentional pro-
cesses (RVP-A, r = −0.273, p < 0.05) and structured STM
for immediate (Logical Memory I (LMI), r = −0.277,
p < 0.05) and delayed memory (Logical Memory 2 (LM2),
r = −0.291, p <  0.05). No significant associations were
observed with any of the EF cognitive tests.
An ANOVA using the Bonferroni test indicated that the
mean score for Education for the autistic group (M = 12.5,
SD = 2.1) was significantly lower compared with the non-
autistic group (M = 14.3, SD = 2.1), F(1, 126) = 22.89,
p < 0.001, η2 = 0.154. Education was included as a covari-
ate in all subsequent multivariate analyses. No significant
effects were observed for IQ (WTAR), ASD: M = 107.7,
SD = 8.4, TYP: M = 107.2, SD = 8.3, F(1, 126) = 0.120,
p = 0.730, η2 = 0.001. The Mann–Whitney test showed a
significant effect for Age, ASD: M = 24.4, SD = 7.5, range
= 16–47; TYP: M = 25.3, SD = 5.2, range = 18–42,
U = 1,567.0, z = −2.245, p = 0.025. Preliminary analyses
with Age as an additional covariate revealed no significant
effects on sex differences.
A significant difference between autistic females and
autistic males was observed on the DASS Depression:
Females: M = 28.2, SD = 12.6, Males: M = 18.9, SD = 12.7,
F(1, 59) = 7.67, p = 0.007, and DASS Anxiety: Females:
M = 21.7, SD = 11.9, Males: M = 14.6, SD = 10.1, F(1,
59) = 6.08, p = 0.017 (see Supplementary Tables S4 and
S5). The examination of the covariate effects of Depression
and Anxiety indicated, however, that they did not have a
moderating effect on overall sex differences. We have
reported the MANCOVA analysis with Education as the
only covariate, in order to preserve power.
Sex differences across autistic and non-autistic
cohorts
Results are summarised in Table 4. A significant overall
main effect for diagnosis for the neuropsychological meas-
ures (Pillai’s Trace: F(12, 112) = 3.45, p < 0.001,
ηp2  = 0.270) revealed broad difficulties in cognitive EF and
non-EF for the autistic group compared with the non-autis-
tic group. As this study focuses on sex differences only, we
have not reported a detailed analysis of the diagnostic dif-
ferences between autistic and non-autistic individuals. A
summary of outcome measures by diagnosis for this sam-
ple is presented in Supplementary Tables S2 and S3. A sig-
nificant overall main effect for sex was also observed
(Pillai’s Trace: F(12, 112) = 2.52, p = 0.006, ηp2  = 0.212);
however, the diagnosis by sex interaction was not signifi-
cant (Pillai’s Trace: F(12, 112) = 0.62, p = 0.826,
ηp2  = 0.062). The interaction effect sizes for almost all of
the individual neurocognitive measures were very small
( ηp2  < 0.04). Post hoc power analysis (conducted with
G*Power software) indicated that a sample size of
N > 4000 would be required for the above interaction
effects to reach significance. This suggests that the non-
significant sex by diagnosis interaction finding may reflect
a true lack of an interaction effect although we acknowl-
edge that it may also be a consequence of the study been
underpowered to detect small effect sizes. However, given
the trend in the normative literature (see ‘Discussion’ sec-
tion) for converging outcomes in areas where a traditional
male or female advantage has been observed (Hyde, 2016),
we suggest that our findings reflect a lack of sex differ-
ences in ASD for psychomotor speed and cognitive flexi-
bility. The results indicate that our first hypothesis of a
significant sex by diagnosis interaction for psychomotor
speed and cognitive flexibility is not supported in this
study.
Our second hypothesis of sex differences based on pro-
cessing mode (verbal vs visuospatial) was partially sup-
ported. The between-groups main effects for sex revealed
an overall female advantage for the verbal measures of:
verbal learning-structured (LM I): F(1, 123) = 6.30,
p = 0.013, ηp2  = 0.049; verbal learning-unstructured
(RAVLT): F(1, 123) = 6.22, p = 0.014, ηp2  = 0.048; and
semantic fluency (COWAT Semantic): F(1, 123) = 4.62,
p = 0.034, ηp2  = 0.036. A female advantage was observed
for mental flexibility (TMT-B): F(1, 123) = 6.01, p = 0.016,
ηp2  = 0.047, which has a significant verbal processing
component. Contrary to our prediction, none of our visuos-
patial measures identified a male advantage.
Our third hypothesis for expected sex differences on the
BRIEF (female advantage for the ‘initiate’ clinical scale
and a male advantage for the ‘emotional control’ scale)
was also not supported. A significant overall effect for
diagnosis was observed for the two composite indices of
the BRIEF (Pillai’s Trace: F(2, 81) = 18.36, p < 0.001,
ηp2  = 0.312), with each of the Metacognition Index (MI),
F(1, 82) = 24.88, p < 0.001, ηp2  = 0.233, and Behavioural
Regulation Index (BRI), F(1, 82) = 36.13, p < 0.001,
ηp2  = 0.306, reaching significance. The sex main effect
(Pillai’s Trace: F(2, 81) = 1.09, p = 0.340, ηp2  = 0.026) and
the sex by diagnosis interaction (Pillai’s Trace: F(2,
81) = 1.17, p = 0.316, ηp2  = 0.028) were not significant for
the BRIEF MI and BRIEF BRI respectively, or any of the
clinical scales (Sex: Pillai’s Trace: F(9, 73) = 1.83,
p = 0.078, ηp2  = 0.184; Sex × Diagnosis: Pillai’s Trace:
F(9, 73) = 1.29, p = 0.255, ηp2  = 0.138). The results are
summarised in Table 5.
Discussion
Our study examined broad sex differences in cognitive
function in autistic and non-autistic youth and adults. An
examination of sex differences in symptom severity in
autistic individuals indicated that both males and females
were comparable on symptomatology. Any cognitive dif-
ferences observed could therefore be attributed to atypical
cognitive styles. For neuropsychological performance
measures, we predicted a significant sex by diagnosis
Table 4.  Cognitive non-EF and EF domains.
Demetriou et al.

ASD TYP Between-subject factors

Cognitive function domain sex M SD M SD Main effect Sex × Diagnosis interaction

Cognitive control  
  Psychomotor speed Female 31.1 14.5 20.8 4.8 F(1, 123) = 12.94, p < 0.001, η2 = 0.095a F(1, 123) = 0.160, p = 0.690, η p2  = 0.001
  Male 37.3 20.2 23.3 6.9 F(1, 123) = 4.05, p < 0.001, η2 = 0.032b  
  Sustained attention Female .875 .071 .924 .040 F(1, 123) = 12.91, p = 0.046, η2 = 0.095a F(1, 123) = 0.488, p = 0.486, η p2  = 0.004
  Male .888 .053 0931 .041 F(1, 123) = 0.442, p = 0.508, η2 = 0.004b  
Verbal learning and STM  
  Verbal learning (structured) Female 42.0 12.8 43.8 8.4 F(1, 123) = 1.33, p = 0.251, η2 = 0.011a F(1, 123) = 0.588, p = 0.445, η p2  = 0.005
  Male 35.1 12.9 41.1 10.5 F(1, 123) = 6.30, p = 0.013, η2 = 0.049b  
  Verbal STM (structured) Female 24.4 11.5 28.1 7.2 F(1, 123) = 3.62, p = 0.059, η2 = 0.029a F(1, 123) = 0.206, p = 0.651, η p2  = 0.002
  Male 20.4 9.9 26.9 7.9 F(1, 123) = 3.53, p = 0.063, η2 = 0.028b  
  Verbal learning (unstructured) Female 54.6 11.3 59.5 6.7 F(1, 123) = 7.33, p = 0.008, η2 = 0.056a F(1, 123) = 0.509, p = 0.477, η p2  = 0.004
  Male 48.7 12.4 57.3 7.3 F(1, 123) = 6.22, p = 0.014, η2 = 0.048a  
  Verbal STM (unstructured) Female 11.5 3.9 12.9 2.9 F(1, 123) = 6.46, p = 0.012, η2 = 0.050a F(1, 123) = 0.553, p = 0.458, η p2  = 0.004
  Male 10.0 4.1 12.6 2.7 F(1, 123) = 2.46, p = 0.119, η2 = 0.020b  
Visuospatial learning and STM  
  Visuospatial learning Female 7.9 9.9 5.6 8.3 F(1, 123) = 4.05, p = 0.046, η2 = 0.032b F(1, 123) = 4.103, p = 0.045, η p2  = 0.032
  Male 23.1 33.7 3.7 4.6 F(1, 123) = 3.88, p = 0.051, η2 = 0.031b  
  Visuospatial STM Female 6.2 1.4 7.6 1.1 F(1, 123) = 27.35, p < 0.001, η2 = 0.182a F(1, 123) = 0.044, p = 0.834, η p2  < 0.001
  Male 6.6 1.3 7.8 1.2 F(1, 123) = 1.80, p = 0.182, η2 = 0.014b  
EF  
  Mental flexibility Female 71.8 42.7 45.8 10.2 F(1, 123) = 13.03, p < 0.001, η2 = 0.096a F(1, 123) = 0.0, p = 0.998, η p2  < 0.001
  Male 85.8 39.2 54.7 17.8 F(1, 123) = 6.01, p = 0.016, η2 = 0.047b  
  Attentional shifting Female 23.3 20.5 15.6 14.2 F(1, 123) = 3.88, p = 0.051, η2 = 0.031a F(1, 123) = 0.415, p = 0.521, η p2  = 0.003
  Male 28.6 30.4 13.7 11.8 F(1, 123) = 0.422, p = 0.517, η2 = 0.003b  
  Phonemic fluency Female 34.1 13.6 41.8 7.8 F(1, 123) = 19.28, p < 0.001, η2 = 0.136a F(1, 123) = 1.043, p = 0.309, η p2  = 0.008
  Male 31.5 9.6 43.7 11.4 F(1, 123) = 0.111, p = 0.740, η2 = 0.001b  
  Semantic fluency Female 21.0 5.8 23.1 4.4 F(1, 123) = 6.22, p = 0.014, η2 = 0.048a F(1, 123) = 0.331, p = 0.566, η p2  = 0.003
  Male 18.5 4.9 21.7 5.3 F(1, 123) = 4.62, p = 0.034, η2 = 0.036b  

EF: executive function; ASD: autism spectrum disorder; TYP: non-autistic participants; STM: short-term memory.
a
Diagnostic main effect. bSex main effect.
9
 10

Table 5.  Self-report measures of EF.

ASD TYP Main effect Sex × Diagnosis interaction

BRIEF cognitive function domain Sex M SD M SD

BRIEF
  Behavioural Regulation Index Female 65.2 11.7 39.9 10.0 F(1, 82) = 36.13, p < 0.001, η2 = 0.306a F(1, 82) = 1.93, p = 0.168, η p2  = 0.023
  Male 59.8 13.9 40.8 8.9 F(1, 82) = 0.428, p = 0.515, η2 = 0.005b  
  Metacognition Index Female 82.0 19.6 54.3 11.8 F(1, 82) = 24.88, p < 0.001, η2 = 0.233a F(1, 82) = 0.274, p = 0.602, η p2  = 0.003
  Male 82.0 16.1 56.2 15.5 F(1, 82) = 0.226, p = 0.635, η2 = 0.003b  
Clinical scales
 Inhibit Female 15.8 4.2 11.0 2.4 F(1, 81) = 13.82, p < 0.001, η2 = 0.146a F(1, 81) = 0.789, p = 0.377, η p2  = 0.010
  Male 14.9 3.5 11.2 2.4 F(1, 81) = 0.116, p = 0.735, η2 = 0.001b  
 Shift Female 14.5 2.9 8.0 2.5 F(1, 81) = 50.95, p < 0.001, η2 = 0.386a F(1, 81) = 3.45, p = 0.065, η p2  = 0.041
  Male 12.7 2.8 8.5 1.9 F(1, 81) = 0.901, p = 0.345, η2 = 0.011b  
  Emotional control Female 22.5 5.3 13.7 4.1 F(1, 81) = 21.40, p < 0.001, η2 = 0.209a F(1, 81) = 1.52, p = 0.222, η p2  = 0.018
  Male 20.0 5.9 13.8 4.1 F(1, 81) = 0.796, p = 0.375, η2 = 0.010b  
 Self-monitor Female 12.4 2.4 7.3 1.9 F(1, 81) = 32.62, p < 0.001, η2 = 0.287a F(1, 81) = 0.952, p = 0.332, η p2  = 0.012
  Male 12.1 3.5 8.1 1.8 F(1, 81) = 0.209, p = 0.649, η2 = 0.003b  
 Initiate Female 17.9 4.8 10.6 2.5 F(1, 81) = 24.73, p < 0.001, η2 = 0.234a F(1, 81) = 1.54, p = 0.219, η p2  = 0.019
  Male 17.5 4.0 12.2 3.9 F(1, 81) = 0.595, p = 0.443, η2 = 0.007b  
  Working memory Female 17.5 4.7 10.7 3.4 F(1, 81) = 25.71, p < 0.001, η2 = 0.241a F(1, 81) = 1.09, p = 0.298, η p2  = 0.013
  Male 16.1 3.8 10.7 2.5 F(1, 81) = 0.429, p = 0.514, η2 = 0.005b  
 Plan/organise Female 20.4 5.2 12.7 2.9 F(1, 81) = 1.43, p = 0.235, η2 = 0.017a F(1, 81) = 1.08, p = 0.302, η p2  = 0.013
  Male 20.6 4.7 14.6 4.7 F(1, 81) = 19.86, p < 0.001, η2 = 0.197b  
 Task/monitor Female 11.4 3.3 8.7 2.2 F(1, 81) = 12.95, p = 0.001, η2 = 0.138a F(1, 81) = 0.101, p = 0.752, η p2  = 0.001
  Male 11.9 2.2 8.7 F(1, 81) = 0.320, p = 0.573, η2 = 0.004b  
 Organisation/materials Female 14.9 4.5 11.6 2.0 F(1, 81) = 10.49, p = 0.002, η2 = 0.115a F(1, 81) = 0.728, p = 0.396, η p2  = 0.009
  Male 15.9 3.9 11.2 3.0 F(1, 81) = 0.154, p = 0.696, η2 = 0.002b  

EF: executive function; BRIEF: Behavioural Rating Inventory of Executive Function; ASD: autism spectrum disorder; TYP: non-autistic participants.
a
Diagnosis main effect. bSex main effect.
Autism 00(0)
Demetriou et al. 11
interaction effect for EF, overall female advantage for ver-
bal tasks and male advantage for non-verbal tasks. For the
self-report measure (BRIEF), we predicted sex differences
in ASD for the clinical scales of emotional control and ini-
tiate. Only our second hypothesis was partially supported.
Contrary to our predictions, we did not find a significant
sex by diagnosis interaction effect for our measures of psy-
chomotor speed and cognitive flexibility. Instead, an over-
all female advantage was observed on measures of
psychomotor speed, cognitive flexibility, two measures of
verbal learning and memory and for semantic fluency.
The findings on cognitive flexibility (as measured by
reasoning speed) and verbal tasks are consistent with
trends in the general normative population (Gur et al.,
2012). It is of note, however, that there was no persistent
female advantage across verbal tasks or male advantage
for visuospatial tasks. Moderating factors leading to null
results may relate to gender atypical brain cognitive pro-
cesses (Svedholm-Häkkinen et al., 2018), converging
trends in gender socialisation (Halari et al., 2005) or may
be due to the specific cognitive measures assessed in the
study.
In their study, Svedholm-Häkkinen and colleagues
(2018) reported cognitive processes in some males and
females may be more aligned with the opposite sex than
their biological sex. Although their research did not
extend to specific cognitive tasks as measured in this
study, such atypicalities could potentially moderate find-
ings on cognitive sex differences. In relation to gender
socialisation, there is growing support of converging out-
comes in areas where a traditional male or female advan-
tage was observed. Hyde (2016) refers to meta-analytic
studies indicating an attenuation in effect sizes of sex dif-
ferences due to improved performance by females in tasks
with a traditional male advantage. The three-dimensional
(3D) rotation task was an example where improved per-
formance by females led to a significant reduction on
observed sex differences over the last 30 years in a task
with a traditional male advantage task. This was attributed
to the formal introduction of this topic in the school cur-
riculum making it accessible to both males and females. It
suggests that sex differences may be influenced by social
or educational changes. The lack of expected normative
trends for a male advantage for the visuospatial tasks in
this study may also be due to the tasks used here, com-
pared with other studies (Pletzer et al., 2017). Hyde (2016)
in summarising a number of meta-analytic studies reported
variations on effect sizes from null to large depending on
the tasks assessed. Potentially, the verbal and non-verbal
tasks utilised in our study may better capture female rather
than male advantage.
The female advantage in specific verbal tasks and cog-
nitive flexibility observed in our study may in part be
explained by sex differences in neural circuitry. A
functional neuroimaging study (Hill et al., 2014) of WM
tasks identified different areas of activation by males and
females. Males recruited more parietal/visuospatial areas
of the brain, whereas females recruited prefrontal/hip-
pocampal areas associated with phonological tasks sug-
gesting that females may perform better on tests of verbal
STM. Comparably, Ingalhalikar and colleagues (2014)
reported sex differences in cortical and cerebellar connec-
tivity which they related to enhanced perception in males
and superior analytical/intuitive processes in females, the
latter potentially accounting for our observed sex differ-
ences in cognitive flexibility. A recent neuroimaging study
identified a significant sex by diagnosis interaction for
frontal tracks (Zeestraten et al., 2017), which may also in
part explain our findings for EF domains of fluency and
cognitive flexibility.
Furthermore, our hypothesis for sex differences on the
self-report measure was also not supported. An examina-
tion of differences within the autistic cohort revealed simi-
lar self-reports of executive dysfunction that was
significantly higher than the non-autistic comparison
group but did not differ by sex. The reported significant
(albeit small) normative sex difference for the ‘emotional
control’ and ‘initiate’ clinical scales (Roth et al., 2005) was
not extended to the autistic individuals in this study. These
results suggest that males and females with autism report
similar difficulties in executive functioning in real-world
situations. Our findings also suggest that the reported sex
differences in EF based on parental ratings (White et al.,
2017) may reflect informant cognitive biases in the evalu-
ation of males and females with autism.
Commensurate with our overall findings, recent
research suggests sex differences in autistic individuals
reflect normative trends, thus highlighting the importance
of including a non-autistic normative comparison group.
Such trends have been reported for specific cognitive
tasks, for example, visuospatial rotational task (Rohde
et al., 2017), broader social traits such as social motivation
and friendship (Sedgewick et al., 2016) and brain neurobi-
ology (Ecker et al., 2017).
Limitations
There are a number of limitations in our study. First, the
lack of a significant sex by diagnosis effect may relate to
the lower power of this study compared with the much
larger sample sizes required to detect a significant small
effect (more than 3000 based on power analysis).
Consequently, potential atypical sex differences in autism
may not have been detected in our study. Furthermore, the
effect size for the sex factor reported here is larger than
generally reported in the literature. This may relate to con-
founding variables associated with smaller sample sizes
(Button et al., 2013) and propensity for effect sizes to be
12 Autism 00(0)
inflated in such studies. We note, however, that our find-
ings on sex differences are generally consistent with the
broader literature and large effect sizes on sex differences
have been reported in the literature for specific tasks. For
example, two metanalytic studies reported in Hyde (2016)
(Linn & Petersen, 1985; Voyer et al., 1995) report large
effect sizes for the mental rotation (Cohen’s d = 0.73 and
0.51, respectively) but smaller effect sizes for other cogni-
tive functions (e.g. mathematics performance, Cohen’s d
= 0.05, Lindberg et al.). Second, our autistic group did not
include individuals with intellectual difficulties and, over-
all, they showed a relatively high IQ; thus, our results can-
not extend to the broader autistic population with
intellectual difficulties. It is also noted that single word-
reading estimates for IQ (WTAR) may be less appropriate
for individuals with autism, particularly, given the gener-
ally high correlations between word-reading tests and
level of education. Third, in our sample, there were signifi-
cant differences on Education, which may have been
driven by our recruitment of non-autistic comparison
group through university websites. Nevertheless, as our
autistic group had, on average, completed secondary
school-level education, this education difference may be
less pronounced in our sample. Fourth, our cognitive test
battery was not exhaustive. Other cognitive domains that
could be assessed include WM, response inhibition,
higher-order EFs such as concept formation and ‘hot’ EFs.
Fifth, we note that self-report evaluations of EF can be
challenging for individuals with EF difficulties and for
autistic individuals and the use of such evaluations may
have influenced the results. Finally, we did not control for
the use of medication, which may have a confounding
effect on test performance.
Conclusion and future directions
Our study suggests sex differences in cognitive EF and
non-EF in autistic adults as evidenced by an overall
female advantage on specific measures of psychomotor
speed, cognitive flexibility, verbal learning and memory
and semantic fluency. These differences were not, how-
ever, unique to autistic participants and followed a similar
sex difference pattern for non-autistic individuals.
Contrary to other research advocating a distinct male
brain profile (Baron-Cohen et al., 2005), our findings do
not support the view of atypical sex differentiation of cog-
nitive function in autism on the specific measures exam-
ined in the study. Although we utilised an extensive
battery of neurocognitive tests and examined all clinical
scales of the behavioural self-report measures, limitations
as discussed above may have influenced this study’s out-
comes. Future studies of sex differences in autistic indi-
viduals would benefit from collaborations to ensure larger
sample sizes and from utilising a multidimensional assess-
ment protocol. Importantly, inclusion of a non-autistic,
normative comparison group to allow examination of a
diagnosis with sex interaction will permit more conclu-
sive statements on atypical sex differences in autism.
Such studies should aim to be longitudinal in nature to
examine whether sex differences in cognitive profiles
emerge at different stages of development (Mandy et al.,
2018). Enhancing the research design to incorporate a
more comprehensive assessment protocol across both
neuropsychological and behavioural measures and con-
trolling for potential neurobiological and sociocultural
moderators can contribute to a better understanding of sex
differences in autism and inform diagnostic and interven-
tion strategies.
Acknowledgements
We acknowledge a National Health and Medical Research
Council (NHMRC) postgraduate scholarship to E.A.D.
(GNT1056587), a National Health and Medical Research Council
Australian Fellowship (APP1136259) to I.B.H. and Australian
Research Council (ARC) Linkage Project grants (LP110100513;
LP110200562), a National Health and Medical Research Council
Career Development Fellowship (APP1061922) and a Project
Grant (1043664; 1125449) to A.J.G.
Declaration of conflicting interests
The author(s) declared the following potential conflicts of inter-
est with respect to the research, authorship, and/or publication of
this article: Professor Ian Hickie was an inaugural Commissioner
on Australia’s National Mental Health Commission (2012–18).
He is the Co-Director, Health and Policy at the Brain and Mind
Centre (BMC) University of Sydney, Australia. The BMC oper-
ates an early-intervention youth services at Camperdown under
contract to headspace. Professor Hickie has previously led com-
munity-based and pharmaceutical industry-supported (Wyeth,
Eli Lily, Servier, Pfizer, AstraZeneca) projects focused on the
identification and better management of anxiety and depression.
He was a member of the Medical Advisory Panel for Medibank
Private until October 2017, a Board Member of Psychosis
Australia Trust and a member of Veterans Mental Health Clinical
Reference group. He is the Chief Scientific Advisor to, and a 5%
equity shareholder in, InnoWell Pty Ltd. InnoWell was formed
by the University of Sydney (45% equity) and PwC (Australia;
45% equity) to deliver the $30 M Australian Government-funded
Project Synergy (2017–20; a three-year program for the transfor-
mation of mental health services) and to lead transformation of
mental health services internationally through the use of innova-
tive technologies.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
ORCID iDs
Liz Pellicano https://orcid.org/0000-0002-7246-8003
Adam J Guastella https://orcid.org/0000-0001-8178-4625
Supplemental material
Supplemental material for this article is available online.
Demetriou et al. 13
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