Social Science & Medicine 74 (2012) 1667e1674

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Social Science & Medicine

journal homepage: www.elsevier.com/locate/socscimed

Autism spectrum disorders: Toward a gendered embodiment model

Keely Cheslack-Postava a, *, Rebecca M. Jordan-Young b
a
Paul F. Lazarsfeld Center for the Social Sciences, Columbia University, 420 W, 118th Street, Mail Code 3355, New York, NY 10027, United States
b
Department of Women’s, Gender, and Sexuality Studies, Barnard College, Columbia University, New York, NY, United States

a r t i c l e i n f o a b s t r a c t

Article history: One of the most consistent observations in the epidemiology of autism spectrum disorders (ASD) is the
Available online 12 July 2011 preponderance of male cases. A few hypotheses have been put forth which attempt to explain this
divergence in terms of sex-linked biology, with limited success. Feminist epidemiologists suggest the
Keywords: importance of investigating specific mechanisms for male-female differences in health outcomes, which
Autism spectrum disorders may include sex-linked biology and/or gender relations, as well as complex biosocial interactions.
Gender
Neither domain has been systematically investigated for autism, and the possible role of gender has been
Sex
particularly neglected. In this article, we posit hypotheses about how social processes based on
Biosocial
Gender socialization
perception of persons as male or female, particularly patterns of social and physical interaction in early
Diagnostic bias development, may affect the observed occurrence and diagnosis of ASD. We gesture toward an
Developmental context embodiment model, incorporating hypotheses about initial biological vulnerabilities to autism e which
may or may not be differentially distributed in relation to sex biology e and their interactions with
gender relations, which are demonstrably different for male and female infants. Toward building such
a model, we first review the epidemiology of ASD with an eye toward male-female differences, then
present a theory of gender as a “pervasive developmental environment” with relevance for the excess
burden of autism among males. Finally, we suggest research strategies to further investigate this issue.
Ó 2011 Elsevier Ltd. All rights reserved.

Introduction
Autistic disorder (which we also refer to as autism) is charac-
terized by impaired development in social interaction and
communication, accompanied by patterns of repetitive behavior or
restricted interests, appearing before age 3. The broader category
“autism spectrum disorders” (ASD) encompasses autistic disorder,
Asperger syndromeewhere language develops typically, despite
other impairmentseand Pervasive Developmental Disorder Not
Otherwise Specified (PDD-NOS), diagnosed where some, but not all
criteria for an autism diagnosis are present. A complex set of
genetic factors is believed to play an important role in the etiology
of these conditions; however, given that autism is a complex trait
with great variability in specific manifestations, and because of the
diversity of genetic associations that have been suggested thus far,
a role for environmental factors, broadly construed, is also virtually
certain (Balaban, 2006).
Autism is diagnosed behaviorally based on a variety of symp-
toms and signs that vary by age. For example, an infant with autism
* Corresponding author.
E-mail address: kc2497@columbia.edu (K. Cheslack-Postava).
may not respond to his/her name, while a toddler may have
delayed speech, fail to engage in “pretend” play, or line up toys
obsessively. An older child or adult may have difficulty “getting”
jokes, engaging in conversation, and forming friendships. Cognitive
impairment is present in a substantial proportion of cases. The ‘gold
standard’ instruments for diagnosis are a standardized clinical
interview, the Autism Diagnostic Interview-Revised (ADI-R) and an
observation of set activities, the Autism Diagnostic Observation
Schedule (ADOS); a variety of other scales and instruments are used
for clinical, epidemiological, or screening purposes. A key charac-
teristic of all such instruments is that they are to some extent
subjective, relying on parental, caregiver, or self-report and/or
clinician observation and assessment.
One of the most consistent observations in the epidemiology of
ASDs is the preponderance of male cases. A comprehensive review
of 43 studies published between 1966 and 2008 found male:female
(M:F) ratios ranging from 1.33:1 to 16:1, with a mean of 4.2:1;
among studies reporting on ASDs combined, the median ratio was
4.0:1 (Fombonne, 2009). This disparity is even greater among
Asperger syndrome and “high functioning” autism cases where it
can approach 10:1 (Fombonne, 1999).
Several hypotheses have been advanced to explain the male-
female (MeF) disparity in ASD diagnoses. Among the most

0277-9536/$ e see front matter Ó 2011 Elsevier Ltd. All rights reserved.
doi:10.1016/j.socscimed.2011.06.013
1668 K. Cheslack-Postava, R.M. Jordan-Young / Social Science & Medicine 74 (2012) 1667e1674
widely cited is Baron-Cohen’s et al. (2005) “extreme male brain”
hypothesis. Baron-Cohen holds that there is an “essential differ-
ence” between male and female cognitive and affective styles, with
males oriented toward understanding and building law-like
systems (systemizing), and females oriented toward under-
standing and predicting humans (empathizing). ASDs, in this
model, reflect deficits in the cognitive processes of “empathizing”,
and strengths in “systemizing” (Baron-Cohen, 2009). Baron-Cohen
further suggests that the “male brain” pattern reflects the orga-
nizing action of testosterone on the developing fetal brain, and has
reported some correlations between steroids in amniotic fluid and
sex-typed behavior in infants and young children (Knickmeyer
et al., 2006; Knickmeyer, Baron-Cohen, Raggatt, & Taylor, 2005;
Knickmeyer, Baron-Cohen, Raggatt, Taylor, & Hackett, 2006).
Several serious weaknesses with this line of thinking must be
noted, however, beginning with the observation that the concepts
of “systemizing” and “empathizing” are not well-specified (Grossi &
Fine, in press). Further, Baron-Cohen’s studies have not been
independently replicated, and have been faulted on extensive
methodological grounds (Grossi & Fine, in press; Jordan-Young,
2010). Finally, a systematic analysis of studies linking sex-typed
cognitive traits in humans with pre-natal steroid hormone expo-
sures suggests that pre-natal steroids probably do not make
a meaningful contribution to MeF cognitive differences (Jordan-
Young, 2010).
Early hormone exposures could alternatively alter expression of
specific disease related genes, either increasing or decreasing risk
(Kaminsky, Wang, & Petronis, 2006). Specific mechanisms are as yet
undetermined, but could include sensory perception, neuroendo-
crine reward processes involved in social-emotional interaction
and learning, or factors related to ease of building or pruning neural
connections, to name a few (see the risk model developed by
Dawson (2008) for elaboration). Genetic sex could also affect risk
for ASD through X-linked traits. Having two X chromosomes
protects females from some X-linked disordersdknown or
hypothesized mechanisms include genes outside the pseudoauto-
somal region that escape X-inactivation; genes expressed only from
the paternally inherited allele through imprinting, a parent-specific
process of gene silencing; and production of some level of func-
tional gene product. For example, Fragile X syndrome, involving
mutations in the FMR1 gene on the long arm of the X chromosome
resulting in decreased levels of its protein product, affects females
more rarely and less severely than males, and as many as 30% of
those with Fragile X are also diagnosed with ASDs (Marco & Skuse,
2006). However, only a small percentage of ASD cases overall have
been associated with X-linked disorders. More perfunctory theories
include disruptions in the vasopressin system or a protective role of
oxytocin (Carter, 2007) and sex differences in neurodevelopmental
susceptibility to environmental insults (Dean & McCarthy, 2008).
Varying degrees of evidence support each of these theories, but
to date, none has provided a strong account for MeF differences in
autism. While it is beyond the scope of this article to evaluate this
evidence, what these theories hold in common is that they place
the mechanisms responsible for these observed discrepancies
firmly in the realm of sex-linked biology (“sex”), which is concep-
tualized as distinct from the social realm of MeF difference
(“gender”). However, considering how social as well as biological
forces might be acting to cause observed disparity may provide
new insights into its etiology.
Though sex and gender may be conceptually distinct, they are in
practice often inseparable (see Springer, Stellman, and Jordan-
Young, 2011). Even if an investigator posits a mechanism
involving sex chromosomes, the identities of which are laid down
prior to the possibility of any socialization, gene expression is
influenced by experience and learning, as has been demonstrated
in multiple animal (Majdan & Shatz, 2006; Mello, 2002; Sng &
Meaney, 2009) and human (Karmiloff-Smith, 2007) studies.
Moreover, most studies of genetics and health involve behavioral or
other phenotypic outcomes that are measured at the level of the
whole organism (i.e., the individual). At this level, it is not possible
to separate the individual’s gendered biography from their biology
e in fact, from the moment of birth, gendered processes literally
become biological (see (Fausto-Sterling, 2005; Jordan-Young, 2010).
For other purposes, we might follow Springer et al. (2011) and use
the composite term “sex/gender” to highlight the fundamental
entanglements of these domains while generally avoiding the
stand-alone term “sex.” Below, though, we develop a conceptual
model that is meant to reflect the underlying mechanisms through
which sex and gender become sex/gender e that is, the moment(s)
of their entanglement. Thus, we do use the term “sex,” though we
caution that its use in the abstract model should not distract from
the principle that it will generally not be possible to actually assess
sex apart from gender. Moreover, when we use the stand-alone
term “gender,” we refer not to properties of individuals (as in
gender identity or gender roles), but rather to higher-order
processes of interaction and norms, specifically patterns of early
interaction with adults that systematically differ by the perceived
sex/gender of the child.
Before proceeding further, we find it important to clarify the
relationship between the argument we advance here, and prior
models of autism that invoked the social environment, specifically
parentechild relations. As Siller and Sigman (2002, p. 78) have
noted, " The possible contributions of parents to their [autistic]
children’s development have been neglected, probably because of
a sensitivity of investigators, clinicians, and parents to previous,
fallacious, psychogenic theories of autism." In contrast to prior
"psychogenic" theories that have blamed parenting styles, espe-
cially of mothers, for autism, we wish to be clear that our model
does not concern deficits in parenting in any sense. Instead, it
engages the idea that “normal" and normative parenting, like all
other family and community relations, is gendered, meaning that
boy and girl children, on average, encounter different experiences,
interactions, and environments. Moreover, we assert that those
aspects of the social environment that differ, on average, for boys
and girls are not enough in and of themselves to generate ASDs:
there must be some sort of underlying vulnerability.
Epidemiology of ASD and maleefemale comparisons
ASDs are characterized by marked heterogeneity in symptoms,
developmental course, and associated co-morbidities. By way of
example, subsets of cases experience developmental regression;
differences in head circumference, serotonin levels, and immuno-
logical parameters; epilepsy, gastrointestinal complaints, and sleep
disturbances (Levy, Mandell, & Schultz, 2009; Newschaffer et al.,
2007). Some heterogeneity likely stems from the exponential
increase in recognized cases from 1943 when Kanner published the
first case series of eleven patients with “autistic disturbances”
(Kanner, 1943), to a 1966 survey of autism in the UK reporting
a prevalence of 0.04% (Fombonne, 2003), to a 2009 CDC publication
estimating ASD prevalence at 1% of U.S. 8-year olds (Autism and
Developmental Disabilities Monitoring Network, 2009). The
extent to which changes in diagnostic criteria, awareness, de-
stigmatization, and diagnostic substitution can account for the
trend is not certain.
Etiology also appears heterogeneous. Approximately 10% of
cases are linked to recognized genetic syndromes, and associations
with genes or loci on nearly every chromosome have been reported
(Abrahams & Geschwind, 2008). With technological advances, rare
copy number variations (CNVs) e insertions or deletions of
 K. Cheslack-Postava, R.M. Jordan-Young / Social Science & Medicine 74 (2012) 1667e1674
relatively large segments of DNA e have emerged as possibly
important. Yet, because CNVs have been found in a wide variety of
locations in the genome, and in unaffected subjects, they may have
limited explanatory power (Abrahams & Geschwind, 2008). Several
pre-natal exposures have also been implicated, including thalido-
mide, anti-convulsant drugs, and immune factors (Newschaffer
et al., 2007); however these encompass a very small subset of
total cases. The most consistently identified risk factors for ASD are
having an affected sibling, older parental ages, and male sex/
gender, with the former two hypothesized to arise from genetic
factors. Meanwhile, in trying to determine the mechanisms behind
the MeF disparity, it makes sense to ask whether there is
systematic variation in M:F ratios for ASD which may provide
insight about the role of sex/gender in etiology and diagnosis, and
would suggest that mechanisms associating sex/gender with
autism risk are subject to modification.
There are in fact several instances of such variation in M:F ratios.
A number of examples suggest that in the presence of additional
developmental insults or delays, M:F ratios for autism are lower
(though there are exceptions; see for example Schendel, Autry,
Wines, and Moore (2009) regarding major birth defects). Intellec-
tual disability (ID, also referred to as mental retardation or cogni-
tive impairment, typically IQ below 70 or equivalent developmental
test performance) is one of the most prevalent co-morbidities to
ASD. M:F ratios decline with increasingly severe ID (Fombonne,
1999; Nicholas et al., 2008; Volkmar, Szatmari, & Sparrow, 1993;
Yeargin-Allsopp et al., 2003). For example, M:F ratios in ASD
among 3e10 year olds in Atlanta were 6.7:1 among children
without ID, 4.4:1 in those with IQ 50e70, and 1.3:1 among those
with IQ < 20 (Yeargin-Allsopp et al., 2003). The correlation between
epilepsy and ID likely explains a reported M:F ratio of 2:1 for autism
with epilepsy versus 3.5:1 without (Amiet et al., 2008). Lower M:F
ratios have also been reported among cases with dysmorphic
features or microcephaly (Miles et al., 2005), and various studies
have found associations between autism and obstetric and peri-
natal complications (reviewed in: (Bilder, Pinborough-Zimmerman,
Miller, & McMahon, 2009; Kolevzon, Gross, & Reichenberg, 2007)).
In a cohort of over 400,000 births in metropolitan Atlanta, Schendel
and Bhasin (2008) found that M:F ratios for autism decreased with
decreasing birth weight or gestational age, among all children with
autism and by presence of ID or other developmental disability.
These observations collectively suggest that while there is some-
thing protective about being female with regard to ASD, that
protective element is less functional when accompanied by other
impairments or vulnerabilities. If there are subtle protective
elements of female gender socialization, then infants affected by ID,
or prematurity, for example, may be less able to benefit from such
experiences. Neonatal interventions common to both male and
female infants with early pre-term birth or other complications
could also plausibly reduce MeF differences in early social
environment.
Differences in M:F ratios for ASD across other social categories
such as race, socioeconomic status (SES), or immigrant status could
reflect variation in the social structuring of gender, and a corre-
sponding impact on developmental or diagnostic processes. A
range of studies have explored variation in ASD diagnoses across
single dimensions of social difference. Several have reported asso-
ciations of autism with measures of higher SES, though not all
studies find such an association (see Durkin et al., 2010 for
summary and references). Researchers tend to conclude that such
associations reflect ascertainment bias, however Durkin et al.
reported a positive gradient in ASD prevalence by SES even among
children who had not previously received a diagnosis (Durkin et al.,
2010). Higher prevalence has also been reported in some immi-
grant minority groups (Keen, Reid, & Arnone, 2010), which is
1669
somewhat at odds with the pattern of higher prevalence among
socially advantaged groups. The intersection of sex/gender with
race, SES, or immigrant status, though on occasion presented
descriptively (see for instance (Bhasin & Schendel, 2007)), has not
been systematically explored as a potential window on the joint
roles of multiple social processes in ASD risk and diagnosis.
Gender as a “Pervasive Developmental Environment”:
potential roles of gendered social processes in producing M:F
patterns in autism
In the following sections, we introduce a simplified model of
developmental trajectories for an infant with underlying suscepti-
bility for ASD that may or may not eventually lead to an ASD
diagnosis (Fig. 1). Given the etiologic heterogeneity of ASDs, and the
large and uncertain array of candidates for the specific disruptions
underlying ASDs, we cannot be certain about specific elements in
the diagram. For example, we expect that an accurate model would
require multiple different forms of initial vulnerability, any of
which might be differentially distributed by (genetic) sex, or not.
However, we can identify points where gendered social processes,
functioning through adult perception of, response to and interac-
tion with an infant may interact with biology producing probabi-
listic ‘switches’ whereby males end up both more likely than
females to express ASD symptoms, and more likely to be diagnosed,
given expression of symptoms.
Our aim, then, is not to create a singular model of development
in autism but instead to show the structure of developmental
cascades that always involve both biological and environmental
factors. Social interactions have material effects on the developing
brain, which in turn affect the biological substrate at the next level
of development. Indeed, brain development requires interactions.
As Karmiloff-Smith has noted, "the neonate cortex is neither
localized nor very specialized at birth. This allows interaction with
the environment to play a crucial role in gene expression and in the
Fig. 1. Hypothesized model for effects of gender environment on developmental and
diagnositic trajectories for an infant with initial underlying susceptibility for ASD,
which may or may not be differentially distributed by genetic sex. Adult perception of,
response to, and interaction with the infant is shaped by perceived gender, so that
certain types of interaction are more common with male than female infants, and vice
versa. Some element(s) of this differential social environment that is more frequently/
intensely experienced by female infants acts as a protective factor, muting the emer-
gence or expression of ASD-related symptoms. Among children who express symp-
toms of ASD compatible with diagnosis, recognition and identification is more likely
among males. The model is simplified to focus on gendered environment in that it
excludes other environmental or contextual inputs which may affect probability of
symptom expression or diagnosis. Additionally, it is expected, given etiologic hetero-
geneity of ASDs, that hypothesized gender-linked mechanisms may be operant under
some forms of initial underlying vulnerability but not others.
1670 K. Cheslack-Postava, R.M. Jordan-Young / Social Science & Medicine 74 (2012) 1667e1674
ultimate cognitive phenotype.. epigenesis is probabilistic, and
gene expression is activity-dependent" (Karmiloff-Smith, 2007, p.
84). As we explore below, empirical evidence on gender and social
interactions demonstrates that experiences potentially impinging
on the ultimate cognitive phenotype are profoundly shaped by
gender.
Hypothesizing developmental mechanisms: sex and gender in
interaction
Many developmental scenarios could explain a "true" difference
in rates of autism between males and females. Here, we suggest
three plausible scenarios involving the presence of initial
biologically-based vulnerabilities, related for example to sensory
and/or information processing abilities. Such vulnerabilities may or
may not be sex-linked. That is, initial "vulnerable" phenotypes may
be randomly distributed among male and female infants, but MeF
differences might emerge via interaction of vulnerabilities with
gendered aspects of the developmental context. The first scenario
thus begins with vulnerabilities that are randomly distributed
among males and females, then expressed differentially as ASD
symptoms because of gendered socialization, resulting in increased
M:F ratios. A second scenario would involve vulnerabilities that are
more prevalent in males, but are amplified through gendered
socialization. A third scenario would involve vulnerabilities that are
more prevalent in males but unaffected by socialization.
In the first two scenarios, biological vulnerabilities play a role in
disparities without constituting an "innate" sex difference in
autism. This is more obvious in the first scenario, where initial
vulnerabilities are randomly distributed, but it is also the case when
the initial vulnerabilities are not randomly distributed, so long as
the final MeF difference in autism emerges only in the context of
gender-differentiated socialization. That is, the model treats the
developmental context as a crucial component in the development
of autism, not a lesser "modifier" of a biological substrate conceived
as prior to and separate from developmental context. Both
hypotheses explain disparities in autism by taking seriously
extensive data demonstrating pervasive gender differences in
children’s early socialization. Currently, however, only the third
scenario is represented in the literature. By omitting gendered
socialization from the array of factors considered in producing MeF
differences, researchers make the implicit assumption that it has no
effect.
Gender socialization occurs through interactions with other
people, as well as through exposure to different physical environ-
ments, even from very young ages. As an example of the latter,
studies have found pronounced differences in the toys and physical
environments of girl versus boy infants (Nash & Krawczyk, 1994;
Pomerleau, Bolduc, Malcuit, & Cossette, 1990). In this discussion
we focus on social interactions, encompassing both verbal and
physical exchanges. These are shaped by a wide range of factors
that include characteristics of the infant, as well as the intentions,
implicit beliefs, and sensitivity (i.e., skill in perceiving and decoding
infant cues) of the infant’s social partner. There is evidence that the
latter three factors are all influenced by the perceived gender of the
infant. Scores of studies have documented parents’ differential
socialization of boys and girls (Fine, 2010; Harris, 2009), though the
degree and precise domains of differential treatment are somewhat
controversial. One meta-analysis suggests that while there is
evidence of parents’ sex-typed perception and encouragement of
sex-typed activity, they may treat boys and girls more or less
similarly in most other broad domains, including overall amount
of interaction; achievement encouragement; restrictiveness
versus encouragement of independence; warmth, nurturance, and
responsiveness; disciplinary strictness; and clarity of
communication (Lytton & Romney, 1991). Notably, that review
found larger sex-typing effects for younger children, and for studies
where parents are actually observed, rather than queried (Lytton &
Romney, 1991).
Suggestive evidence that gender socialization may be relevant
for traits related to autism is provided by studies of subtle differ-
ences in how adults communicate with infants of different genders.
A recent study of 6377 infant-mother dyads from the (U.S.)
nationally-representative Early Childhood Longitudinal Study Birth
Cohort found that verbal stimulation has a strong positive effect on
infants’ social-emotional and cognitive development, and also
found a small but significant bias toward mothers offering more
verbal stimulation to girls than boys (Page, Wilhelm, Gamble, &
Card, 2010). Likewise, a recent observational study of 36 infant-
mother dyads found that "Mothers of daughters made more
interpretations and engaged in more conversation with their
daughters, whereas mothers of sons made more comments and
attentionals, which were typified by instructions rather than
conversation" (Clearfield & Nelson, 2006, p. 127). Mothers also
spent more time engaged in activity with daughters versus
watching sons (Clearfield & Nelson, 2006). In this study, investi-
gators did not find maleefemale differences in infant contact/
proximity to mothers or looking behavior (Clearfield & Nelson,
2006), however individual children were not observed over time.
In a longitudinal study in which infants were observed within days
of birth by an adult interactor unaware of child’s sex, male and
female infants did not exhibit any significant differences in mutual
eye gaze with the adult; however, by four months of age differences
in eye contact behavior appeared, these being accounted for by an
increase in eye contact made by girls (Leeb & Rejskind, 2004). While
this study did not directly measure adult behavior in relation to
child gender, it is compelling in demonstrating infant differences by
gender emerging only after inception of the earliest social inter-
actions, in a behavior with direct relevance to ASD, namely eye
contact.
Another body of research has documented that attributions of
gender profoundly shape the way observers perceive emotions and
behavior in children. Often referred to as “baby X studies,” such
research involves creatively manipulating the perceived sex of
identical infants or very small children, and analyzing how
observers describe or react to the children when labeled as female
versus male. One well-known study involved a short film of a baby
in an infant seat presented with four different stimuli ea teddy
bear, a jack-in-the-box, a doll, and a buzzer e each presented
several times in succession. More than 200 observers were
randomly assigned the information that the child was a boy versus
a girl, without making an obvious point of this. There were
remarkable differences in the way that observers saw the same
infant when they thought they were watching “David” versus
“Dana,” especially when presented with the child’s somewhat
ambiguous response to the jack-in-the-box. Those observers who
thought they were watching “David” were much more likely to
describe the child as “angry,” while those who thought they were
watching “Dana” described the child as “afraid” (Condry & Condry,
1976). Subsequent studies have extended these observations,
including by controlling for actual variations in infant characteris-
tics (e.g., (Culp, Cook, & Housley, 1983; Delk, Madden, Livingston, &
Ryan, 1986; Donovan, Taylor, & Leavitt, 2007; Lyons & Serbin, 1986;
Seavey, Katz, & Zalk, 1975; Sidorowicz & Lunney, 1980)). On the
other hand, one review of infant gender labeling studies concluded
that overall effects, though present, were not strong or consistent
(Stern & Karraker, 1989) belying the limitations of this experimental
method for understanding real-world phenomena. Nonetheless,
a clue about how differences in perception of infant expressions by
perceived gender may translate to differences in response is given
 K. Cheslack-Postava, R.M. Jordan-Young / Social Science & Medicine 74 (2012) 1667e1674
by a study of Donovan et al. (2007) who found that mothers of 6-
month old infants were more sensitive to changes in facial
expressions of a similarly-aged infant when the child was pre-
sented as female.
It is not clear precisely what effect described differences in adult
perception, response or interaction might have on infants with ASD
vulnerabilities. For one thing, none of these studies focused on
children at risk for ASD, and may not be generalizable. Nonetheless,
sex-typing may condition responses to both gender-typical and
gender atypical behaviors in vulnerable girls, in ways that consti-
tute early, naturalistic interventions by parents and caregivers.
Siller and Sigman (2002), in a longitudinal study, found that among
children with autism, levels of synchronization between caregiver
interactions and child’s focus of attention during play were asso-
ciated with gains in joint attention and language up to 16 years
later. If findings of increased sensitivity to female infants extend to
focus of attention, then female infants may experience on average
higher levels of such synchronization. Additionally, a focus of
parental participation in early intervention for ASD is to adapt
interactive styles to promote early social engagement and
communication (Dawson, 2008). Studies above suggest that the
social environment of a female infant may provide on average more
bids for social engagement, whether through format of speech,
play, or eye contact. Another possibility is that certain behav-
iorsdlike eye contact, or vocal response to questionse may be
more heavily ‘coached’ in girls, so that behaviors appear more
‘typical’ and may mask other ASD symptoms. While the studies
discussed here have important limitations and the potential rele-
vance of any specific scenario to ASD is unknown, the main point is
that development is a "looping process" in which gender is a crit-
ical, ongoing factor: it shapes initial social and tactile input that the
child receives from human interaction, as well as other people’s
responses to the child’s behaviors, in an iterative manner.
Gender bias in diagnosis
Some of the observed MeF difference in autism may stem from
parents’, clinicians’, and others’ different perceptions and expec-
tations for boys versus girls, beginning in early infancy. Lest readers
are tempted to speculate that gender labeling is a thing of the past,
it is worth noting that recent studies generally indicate labeling
effects as strong as those found in the earliest studies, more than 30
years ago. Reliance on cognitive schemas about gender to label
behavior not only affects how we perceive specific people and their
actions, it loops back to reinforce belief in fundamental, generalized
gender differences. Importantly, this process leads people to
discount actual evidence of intra-sex variability and inter-sex
similarity, and operates even in the face of commitments to simi-
larity or a ‘wish’ for similarity. That is, being egalitarian in orien-
tation doesn’t seem to affect gender labeling very much (Fine,
2010).
Infants randomly labeled as male are perceived to be stronger
and more masculine than infants labeled as female (Burnham &
Harris, 1992), and newborn girls are described as littler, softer,
and more finer featured, even in when they do not differ on any
objective measures (Rubin, Provenzano, & Luria, 1974). Mothers in
one study were asked to estimate how capable their infants would
be in crawling up a ramp; mothers exaggerated their infant sons’
physical abilities, while underestimating their girls’ abilities, rela-
tive to objective tests of infants’ abilities made immediately
following these estimates (Mondschein, Adolph, & Tamis-LeMonda,
2000).
In terms of how gendered expectations might affect ASD diag-
nosis, the simplest and most likely scenario is that ASD, as
a syndrome that is commonly and epidemiologically associated
1671
with males, would be more readily recognized in male versus
female children, given equal presentation of symptoms. Well-
documented examples of disease being more readily diagnosed in
males due to such labeling effects include heart disease (Goldberg,
2002; Institute of Medicine, 2003) and HIV/AIDS (Goldstein &
Manlowe, 1997). The extremely prolific citation, both within and
outside psychology, of Baron-Cohen’s theory of autism as repre-
senting an “extreme male brain”, lend credence to this scenario.
Conversely, we should not discount the possibility that parents
would be likely to notice and be concerned about traits if they are
"gender atypical." In this case, ASD symptoms (such as disliking
touch or difficulty displaying mutuality in interaction) might raise
concern at a lower threshold in girls as opposed to boys. This would
run counter to the observed trend of a higher M:F ratio. Yet again,
given the association of autism with males, parents and clinicians
may more readily label an uncommunicative girl as “timid” or “shy”
rather than entertaining a diagnosis of ASD.
Another possibility is that given the same underlying deficits,
“female autism” tends to look different than “male autism” in terms
of symptom expression, resulting in female cases that share these
deficits but go undiagnosed or receive alternative diagnoses. Nearly
two decades ago, Kopp and Gillberg described six girls who met
diagnostic criteria for autism, but took several years of clinical
encounters to receive autism diagnoses (Kopp & Gillberg, 1992).
Likely contributing to the delay were qualitative differences in
these girls’ behavior versus the expected behavioral presentation
that these authors described. Their social impairment was
described as tending “more toward ‘clinging’ to other people,
imitating their speech and movements without a deeper under-
standing., and only brief periods of aloofness” (Kopp & Gillberg,
1992, p. 96). They also showed high frequency of language use,
though often echolalic and uncommunicative, as opposed to
muteness more common in males. Despite such suggestive
evidence, there is still a dearth of research on MeF differences in
presentation (Thompson, Caruso, & Ellerbeck, 2003), a clear
impediment being that recognized female cases are likely to be
those most similar to male cases. Lack of knowledge about the
nature and extent of such differences may contribute to the
observed M:F disparity.
Some evidence of gender bias in identification of ASD exists. The
United States Centers for Disease Control and Prevention’s Autism
and Developmental Disabilities Monitoring Network consists of
sites in several U.S. states that conduct surveillance to identify
children with ASDs. Beginning in 2000, school and medical records
of 8-year-old children have been periodically examined to deter-
mine the prevalence of children meeting a study case definition for
ASD (Autism and Developmental Disabilities Monitoring Network,
2009). Because identification is not dependent on previous diag-
nosis, this method may allow detection of diagnostic biases,
although case identification still depends on relevant behaviors
having been recorded, and a record existing in the first place. For
children born in 1994, the median age of diagnosis was a half-year
later in girls than in boys (Shattuck et al., 2009), and boys with ASD
were significantly more likely to have been so identified than were
girls (Mandell et al., 2009). Although in other studies, reports of
later age or longer time to diagnosis in girls versus boys failed to
reach statistical significance (Mandell, Listerud, Levy, & Pinto-
Martin, 2002; Mandell, Novak, & Zubritsky, 2005; Ouellette-Kuntz
et al., 2009), significance may be affected by low numbers of
female cases and study designs dependent on prior diagnosis with
ASD. Two recent studies compared rates of ASD diagnosis among
siblings of children with ASD (Constantino, Zhang, Frazier,
Abbacchi, & Law, 2010) and subjects from the 14,000 member
Avon Longitudinal Study of Parents and Children (ALSPAC) (Russell,
Steer, & Golding, in press) in males and females who showed
1672 K. Cheslack-Postava, R.M. Jordan-Young / Social Science & Medicine 74 (2012) 1667e1674
symptoms of autism derived from other study measures. 27% of
female siblings (versus 47% of males) who scored above cut-offs on
quantitative scales of social communication or responsiveness, or
showed a history of language delay and autistic speech character-
istics had received an ASD diagnosis (Constantino et al., 2010). In
ALSPAC, 18% of girls, versus 37% of boys who showed develop-
mental impairments most predictive of ASD diagnosis had actually
received such a diagnosis in the community (Russell et al., in press).
These observations suggest that ASD-related characteristics can be
more readily observed and/or more rapidly translated into clinical
diagnoses for boys than for girls; this could occur through differ-
ential interpretation of behaviors or levels of awareness and
concern on the part of caregivers, educators, or clinicians.
Estimating Cumulative impact on observed M:F ratios
The lines of thought entertained here raise the question of what
proportion of the observed discrepancy in diagnoses may be
attributed to social processes related to gender. While such esti-
mates involve considerable speculation, it is helpful to examine the
range of possibilities. To do so, we define three M:F ratios. Mo:Fo is
the observed ratio of males to females among cases receiving
diagnoses in the community. Me:Fe is the ratio of males to females
among persons in the population expressing symptoms of autism
sufficient for diagnosis, irrespective of actually receiving a diag-
nosis; and Ms:Fs is the ratio of males to females among persons with
Fig. 2. Calculated range of M:F ratios for A) expression of ASD symptoms compatible with diagnosis; and B) underlying susceptibility to ASD; assuming a 4:1 observed M:F ratio.
underlying susceptibility, irrespective of whether or not they
express symptoms.
The ratio Me:Fe can then be determined if we know Mo:Fo and
the probabilities of diagnosis for males (dm) and females (df),
respectively, who show symptoms of ASD:
Mo Fo df
Me : Fe ¼ : ¼ Mo : Fo 
dm df dm
We assume Mo:Fo to be 4:1, and plot Me:Fe over a range of values of
df/dm in Fig. 2A. Limited data suggest that df/dm may fall between
0.5 (Constantino et al., 2010; Russell et al., in press) and 0.75
(OR ¼ 1.35 for previous diagnosis in males versus females (Mandell
et al., 2009)), giving Me:Fe values ranging from about 2:1 to 3:1.
Ms:Fs is then a function of Me:Fe and risks in males (rm) and
females (rf) of expressing autism symptoms, given underlying
susceptibility:
Me Fe
Ms : Fs ¼ : ¼ Me : Fe  RRf vs;m
rm rf
In Fig. 2B, we begin with several values for Me:Fe ranging from 2
to 3.2. For each of these values, we plot Ms:Fs for RRf vs.m values
ranging from 1 to 0.5, assuming that being female is a protective
factor, associated with a relative risk below 1. These equations show
that the relationship between observed M:F ratios and M:F ratios
for underlying susceptibility to ASD depends on levels of diagnostic
 K. Cheslack-Postava, R.M. Jordan-Young / Social Science & Medicine 74 (2012) 1667e1674
bias and the relative effect of gendered social environment on
symptom expression. Assuming reasonable values for these vari-
ables results in Ms:Fs ranging from 3:1 to much closer to 1:1, sug-
gesting that underlying biologic susceptibility may well be
approximately equally distributed with respect to biologic sex.
Questions and strategies for research
Clearly, the role of gender in ASD etiology and diagnosis is ripe
for further research. With regard to diagnosis, questions remain as
to whether, and to what extent, girls are under-diagnosed, which
may vary by population, time period, case definition, and methods
used for diagnosis or case ascertainment. It is difficult to imagine
a scenario through which population-level screening or surveil-
lance could be conducted in a manner truly blinded as to sex/
gender. Therefore, the best approach for population-based esti-
mates probably derives from comparisons of community diagnosis
with estimates for “true” ASD status obtained using more general
criteria. It is also important to gain a better understanding of
whether ASDs manifest differently in a subset of girls, and if so, to
develop strategies for identifying this subset. An alternative
approach would involve examining whether professional percep-
tion of ASD symptoms varies by sex/gender of the subject, e.g., by
presenting vignettes that vary only in whether a girl or boy is
described, an approach previously used to investigate race and SES
in autism and ADHD diagnosis (Cuccaro et al., 1996). The role of
perceived sex/gender in clinical assessment could be even more
directly explored by presenting video footage of clinical interac-
tions which are digitally manipulated to vary the apparent gender
of the subject. Because parental efforts may be key in obtaining an
ASD diagnosis, MeF disparity in ASD-specific concern elicited by
potentially related symptoms or behaviors among parents is also
relevant.
The epidemiology of MeF differences in ASD has been reason-
ably well explored with respect to intellectual disability and related
factors. Differences in M:F ratios for ASD across other social cate-
gories such as race, SES, or immigrant status have been less
explored and could reflect variation in the social performance of
gender, and a corresponding impact on developmental or diag-
nostic processes. It would be useful to position such analyses
against a backdrop of information on variation in gendered
socialization across these categories. It may also be informative to
explore change over time, and across any of these categories
attention should be paid to formally testing significance for any
evidence of variation. Finally, variation by sex/gender in associated
features, biomarkers, co-morbidities and developmental trajecto-
ries could be cataloged. Gaining a better understanding overall of
heterogeneity in this ratio should provide clues about underlying
mechanisms.
Testing the hypothesis that female gender socialization acts as
a protective factor for ASD will be theoretically and logistically
challenging, and will need to include the following steps: 1) Iden-
tification of specific socially-based exposures associated with
gender, particularly in infancy, that could hypothetically affect
probability of ASD manifestation in a vulnerable infant; for
example, interpretive versus instructive statements. 2) Qualitative
and quantitative measurement of exposure to these factors in
infants at risk for ASD, which will include observing interaction
with caregivers in as naturalistic a setting as possible. In order to
gain sufficient power, given low overall prevalence of ASDs,
a prospective approach could focus on a high-risk population, such
as “baby sibs” of children with ASD diagnoses. However, because
the additional cases from such families will by definition arise from
“multiplex” (more than one child affected) families, which may
have different etiology than simplex families, results from this
1673
approach may not be widely generalizable. A retrospective case-
control design could capitalize on archives of video footage of
young children prior to diagnosis, but would require sufficient
footage of typical interaction with caregivers and would not allow
observation of a standard set of activities. 3) Assess association
between exposures and outcome. Because exposures of interest are
likely to be experienced by all infants to varying degrees, this will
involve determining whether there is a threshold above which
certain exposures become protective. The ultimate test of any such
identified protective ‘exposures’ would be to incorporate them into
the design of randomized intervention studies. If this approach was
able to help identify elements of an effective very early intervention
that could improve developmental trajectories for some children at
risk of ASDs, it would be the ultimate proof of utility for this
biosocial approach from a public health perspective.
Conclusion
The case of autism illustrates how gender theory can be used not
just to more precisely illuminate the nature and etiology of male-
female health differentials, but also contribute to fundamental
knowledge of specific developmental disorders, and the complex
interaction of biology and the social environment. Our argument is
fully biosocial, and our main points in advancing it are to articulate
a model for autism, specifically for explaining the male-female
disparities in prevalence, that does not exclude social-
environmental variables, and is therefore more biologically satis-
fying; and to demonstrate concrete mechanisms whereby autism
may become more prevalent in males as a result of social structures
and processes related to gender. What we have presented suggests
a domain of research questions and strategies specific to ASDs that
have as of yet been little explored; and a theory of gender as
a pervasive developmental environment with potential broader
applicability to understanding differential health states for males
and females, particularly those arising in early life.
Acknowledgments
The authors thank the Robert Wood Johnson Foundation Health
& Society Scholars program and the Foundation for Worker,
Veteran, and Environmental Health for financial support. We thank
participants in the Gender and Health Working Group at Columbia
University for their many helpful comments during the develop-
ment of this paper.
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