Journal of Clinical Child & Adolescent Psychology

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Rigidity and Sensory Sensitivity: Independent

Contributions to Selective Eating in Children,
Adolescents, and Young Adults

Hana F. Zickgraf, Emily Richard, Nancy L. Zucker & Gregory L. Wallace

To cite this article: Hana F. Zickgraf, Emily Richard, Nancy L. Zucker & Gregory L. Wallace
(2020): Rigidity and Sensory Sensitivity: Independent Contributions to Selective Eating in
Children, Adolescents, and Young Adults, Journal of Clinical Child & Adolescent Psychology, DOI:
10.1080/15374416.2020.1738236

To link to this article: https://doi.org/10.1080/15374416.2020.1738236

Published online: 19 Mar 2020.

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JOURNAL OF CLINICAL CHILD & ADOLESCENT PSYCHOLOGY
https://doi.org/10.1080/15374416.2020.1738236

Rigidity and Sensory Sensitivity: Independent Contributions to Selective Eating

in Children, Adolescents, and Young Adults
a
Hana F. Zickgraf , Emily Richardb, Nancy L. Zucker c
, and Gregory L. Wallace b

a
Department of Psychiatry and Behavioral Neuroscience, Pritzker School of Medicine, University of Chicago; bDepartment of Speech,
Language and Hearing Sciences, The George Washington University; cDepartment of Psychiatry and Behavioral Sciences, Duke University

ABSTRACT
Objective: Selective or “picky” eating (SE) refers to rejection of a wide range of familiar and
unfamiliar foods based on aversions to their sensory properties. When severe, SE can cause
symptoms of avoidant/restrictive food intake disorder (ARFID), including weight loss, nutritional
deficiencies, and/or psychosocial impairment. SE is highly prevalent in autism spectrum disorder
(ASD) compared to both typical development and other developmental disorders. A possible
explanation for the high prevalence of SE in ASD is the effect of core ASD symptoms, repetitive/
restrictive behaviors (e.g., rigidity), and sensory sensitivity on feeding behaviors. These traits are
found not only in ASD but also in other clinical groups and the general population, albeit often at
subclinical levels. Identifying mechanisms of SE across various populations is critical to inform
intervention approaches.
Methods: In 263 unselected children ages 5–17, 534 unselected college students ages 18–22, 179
children with anxiety/obsessive spectrum disorders ages 5–17, and 185 children with ASD ages
4–17, we explored the unique contributions of sensory (i.e., oral texture and olfactory) sensitivities
and rigidity as predictors of self/parent-reported SE.
Results: In each sample, rigidity and oral texture sensitivity, controlling for olfactory sensitivity,
age, and gender, emerged as significant, independent predictors of SE.
Conclusions: This is the first study to highlight the importance of cognitive/behavioral rigidity to
SE, and one of the first to illustrate the domain-specificity of the relationship between sensory
sensitivity and SE.

Introduction also vary in the food variety present in their diet,

Food neophobia, or rejection of novel foods or their
ingredients, is part of typical development, peaking
during the toddler years and gradually decreasing
across later childhood (e.g., Birch et al., 1996;
Carruth et al., 2004). Food neophobia is a highly
conserved behavior that is evident in every omnivor-
ous species and is protective against the accidental
ingestion of toxins (Ventura & Worobey, 2013). The
developmental window during which humans express
heightened food neophobia coincides with toddlers’
increasing physical independence and ability to self-
feed. During development, as children are exposed to
a variety of foods and become familiar with the foods
in their environment, the expression of food neopho-
bia declines (e.g., Pliner & Loewen, 1997). Yet, food
neophobia is also an individual difference, with some
children demonstrating more pervasive avoidance that,
at the extreme, may impair functioning. In addition to
their initial willingness to taste a novel food, children
sometimes based on aversions to sensory properties
or presentation/preparation of foods, a term referred
to as picky or selective eating.
Problematically, the meaning of picky or selective
eating is variably defined across studies and historically,
different authors and studies have used different sever-
ity thresholds or levels to group participants on picky
eating behavior (Taylor et al., 2015). This has contrib-
uted to confusion about how to differentiate feeding
problems from developmentally typical neophobic eat-
ing in young children and/or from benign individual
differences in food preference and dietary variety in
children, adolescents, and adults (e.g., Eddy et al.,
2019). However, it appears clear that: (1) a subset of
children demonstrate greater selective and neophobic
eating than their same-aged peers, usually beginning
before age five and in some cases persisting throughout
development into adulthood, and (2) selective/picky
eating is associated with psychosocial impairment and
reduced dietary variety/quality in some cases or

CONTACT Hana F. Zickgraf zickgraf@uchicago.edu 5941 S. Maryland Ave, MC 3077, Chicago, IL 60637
© 2020 Society of Clinical Child & Adolescent Psychology
2 H. F. ZICKGRAF ET AL.
contexts (e.g., Cardona Cano et al., 2015; Mascola et al.,
2010; Wildes, et al., 2012; N. Zucker et al., 2015).
Although definitions are variable, up to 30% of children
and adults are identified as selective or picky eaters
using a deliberately broad criterion (e.g., agreement
on a true/false or dichotomized likert-type scale; Ellis
et al., 2017; Taylor et al., 2015; Zickgraf et al., 2016).
Picky or selective eating is more prevalent in vulnerable
populations. For example, across studies, 60–70% of
school-aged children with autism spectrum disorder
(ASD) are described as “picky eaters” by their parents
(e.g., Kral et al., 2013; Marí-Bauset et al., 2014). This
rate far exceeds the prevalence among not only indivi-
duals from the general population but also other atypi-
cally developing groups (Beighley et al., 2013).
Prior to the 2013 introduction of Avoidant Restrictive
Food Intake Disorder (ARFID) to the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition
(DSM-5; APA, 2013), infants and children up to age 6
with severely limited dietary variety due to rejection of
familiar and unfamiliar foods (e.g., selective or picky
eating) could be diagnosed with Feeding Disorder of
Infancy and Early Childhood (FDIEC). FDIEC in infants
and toddlers, and severe selective or picky eating in
children with ASD and other developmental disabilities
have historically been treated by feeding disorder specia-
lists using escape extinction and reinforcement-based
procedures to shape acceptance of a wider range of
foods (e.g., Lukens & Silverman, 2014). In the feeding
disorder literature, the term “selective eating” is more
commonly used than “picky eating.” ARFID was intro-
duced to DSM-5 in response to clinical need, and the
recognition that nutritional and psychosocial impair-
ment due to severe selective or picky eating (among
other eating restrictions that can cause ARFID) can
develop across the lifespan and onset is not limited to
children under six or those with developmental disabil-
ities (APA, 2013). Typically developing school-aged chil-
dren, adolescents, and adults with severe selective or
picky eating often present for treatment at eating dis-
order focused centers (e.g., Nicely et al., 2014; Zickgraf,
Lane-Loney, et al., 2019). In the eating disorder litera-
ture, severe SE that can lead to ARFID has variously
been referred to as “selective/neophobic eating” and
“sensory sensitivity.” Given the relatively large evidence
base suggesting that subclinical selective or picky eating
exists on a continuum with the severe manifestation
potentially causing feeding and eating disorder symp-
toms, we will use “selective eating” (SE) in this manu-
script to refer to the full severity range of this eating
restriction (e.g., Ellis et al., 2017; Wildes et al., 2012;
Zickgraf et al., 2016; Zickgraf & Schepps, 2016;
N. Zucker et al., 2015).
The role of emotional reactions, most commonly
anxiety, in driving food avoidance has been emphasized
in the early literature on subclinical SE in typically
developing children (e.g., Taylor et al., 2015). In con-
trast, within the ASD and, more recently, in the eating
disorder literature, SE is usually considered to be driven
by sensory experiences, in isolation or in association
with emotional reactions. For example, in their dimen-
sional model of ARFID eating restrictions, Thomas and
colleagues refer to the presentation of ARFID charac-
terized by SE as “sensory sensitivity” and suggest that
this is the key mechanism implicated in the eating
restriction (Thomas et al., 2017). This terminology has
since been adopted in several clinical phenomenology
studies of ARFID (e.g., Dumont et al., 2019; Reilly et al.,
2019). Similarly, prior studies have linked sensory sen-
sitivities to SE not only in children with ASD (e.g.,
Chistol et al., 2018; Dovey et al., 2019; Kral et al.,
2013; Nadon et al., 2011) but also in typically develop-
ing children (e.g., Nederkoorn et al., 2019; Steinsbekk
et al., 2017). In two cross-sectional studies of children,
sensory sensitivity has been shown to fully mediate the
relationship between anxiety and SE (Farrow &
Coulthard, 2012; Zickgraf & Elkins, 2018). However,
the amount of variance in SE predicted by sensory
sensitivity is relatively small, indicating that other,
unmeasured predictors are present (e.g., Zickgraf &
Elkins, 2018).
Cognitive components, such as cognitive flexibility,
the ability to switch between mental tasks or states,
may play a role in the development or maintenance of
SE. This neuropsychological function is believed to
underlie and/or contribute to psychopathological symp-
toms of cognitive and behavioral rigidity, including repe-
titive behaviors, restricted interests, obsessions and
compulsions, perfectionism, and difficulty coping with
novelty, change, or unexpected events (e.g., Kashdan &
Rotterberg, 2010; Schultz & Searleman, 2002). Cognitive/
behavioral rigidity is a shared phenotypic trait across
ASD and anorexia nervosa, although it has yet to be
explored in populations with ARFID or subclinical
symptoms like SE (e.g., Westwood, Eisler, et al., 2016,
Westwood, Stahl, et al., 2016; Zucker & Losh, 2008;
Zucker et al., 2007). Case studies of ARFID characterized
by SE and research on nonclinical child and adult selec-
tive eaters document rigidity around how food is pre-
pared or presented (e.g., eating only certain brands of
a preferred food, difficulty eating preferred foods in
unfamiliar restaurant settings) and difficulty transition-
ing between meals and other activities, in addition to
aversive responses to the sensory properties of food
(Bryant-Waugh, 2013; Chiarello, et al., 2018; Kauer
et al., 2015; Mascola et al., 2010; Zickgraf, Murray,

et al., 2019). Treatments for ARFID in both neurotypical
and ASD populations emphasize cognitive interventions
including enhancing flexibility and promoting disconfir-
mation learning, rather than sensory habituation alone,
although as noted above, the dominant treatment mod-
ality for severe SE in very young children and children
with developmental delays does not emphasize cognitive
change, likely due to the often limited verbal and/or
cognitive capacities of this population (e.g., Chiarello
et al., 2018; Dumont et al., 2019; Kuschner et al., 2017;
Lukens & Silverman, 2014; Thomas & Eddy, 2018;
N. L. Zucker et al., 2018).
A possible explanation for the very high prevalence
of SE in people with ASD is the impact of core ASD
symptoms, including not only sensory sensitivities but
also restrictive/repetitive behaviors, particularly insis-
tence on sameness. Taking a dimensional, transdiag-
nostic perspective, these traits are found not only in
ASD but also in other clinical groups and in the
general population, albeit often at subclinical levels.
The current study seeks to challenge the current focus
on sensory sensitivity as the primary driver of SE and
resulting ARFID in the eating disorder literature by
exploring cognitive/behavioral rigidity as an addi-
tional predictor of SE in typically developing children,
children with anxiety and OC-spectrum disorders,
and young adults, as well as children with ASD.
Identifying contributors to SE across various popula-
tions and developmental stages is critical to inform
the intervention approach and choice. Because ARFID
is a lifespan diagnosis, it is necessary to explore
whether the same candidate contributors predict SE
severity across age groups. Identifying transdiagnos-
tic, neuropsychological correlates of SE is a necessary
first step to understanding the key mechanisms
involved in the etiology and maintenance of disor-
dered eating symptoms. These contributors can then
guide the development of interventions that target the
underlying mechanisms of expressed behavioral and
cognitive symptoms (e.g., Sanislow et al., 2010).
By examining two potential predictors of SE in chil-
dren and young adults who are beyond the develop-
mental window where SE is expressed, we sought to
identify factors that contribute to the maintenance of
SE into age groups where it is less normative and
potentially more likely to contribute to a subclinical
impairment or even ARFID. This is the first study to
date to explore the independent contributions of sen-
sory sensitivity and cognitive/behavioral rigidity to SE
in samples with typical development, OCD/anxiety,
or ASD.
The current study has two broad aims. The first is to
explore, in a conceptual replication across four samples
RIGIDITY AND SENSORY SENSITIVITY 3
differing in age and diagnosis, the relationships
between specific domains of sensory sensitivity and
SE, and for the first time, the relationship between
cognitive rigidity and SE. We hypothesize that smell
and oral texture sensitivity will be uniquely related to
SE, as these are the sensory modalities most involved in
choosing and experiencing foods, and that cognitive
rigidity will be a significant, independent predictor of
the severity of SE across samples.
The second broad aim is to explore group differences
in the degree of SE and the standardized effect sizes for
sensory sensitivity and cognitive rigidity between general
samples of young adults and children/adolescents.
Zickgraf and Elkins (2018) highlighted differences in
the strength of the relationship between sensory sensi-
tivity and SE between children ages 7–17 and young
adult college students, as well as sample differences in
the degree of SE reported. A comparison between young
adults and a representative, rather than clinical, sample
of children will help to clarify whether the difference in
degree of SE and strength of the sensory sensitivity/SE
relationship observed by Zickgraf and Elkins (2018) was
due to age-related developmental differences or to the
anxiety/OC-spectrum diagnoses in the child sample
(note that the child and adolescent samples in the cur-
rent study are the same as those whose data were used in
Zickgraf & Elkins, 2018). We hypothesize that while
children/adolescents and young adults will differ in
degree of SE, the predictors of SE will remain consistent
across all four samples.
Methods
This study is a secondary analysis of data from four
samples, each recruited separately for studies with their
own specific aims. HFZ collected data from the anxiety/
OC-spectrum, representative, and college student sam-
ples. GLW collected data from the ASD sample.
Different measures of sensory sensitivity, cognitive
rigidity, and selective eating were used in the samples
recruited by HFZ and GLW. Details for each of these
samples and their respective measures are provided
below.
Participants
Anxiety/OC-Spectrum Clinic Sample
Parents of children ages 5–17 were recruited at
a university-based tertiary anxiety/OCD clinic to parti-
cipate in a study on the temperamental correlates of
selective eating. The main eligibility criterion was hav-
ing a primary diagnosis of an anxiety disorder (general-
ized anxiety, specific phobia, separation anxiety,
4 H. F. ZICKGRAF ET AL.
selective mutism, social anxiety), obsessive-compulsive
disorder, tic disorder, or trichotillomania/excoriation
disorder. Children and parents were approached in
the clinic waiting room. Parents provided written
informed consent, and children provided verbal and
written assent. Parents were paid 5 USD as an incentive
for participation and completed paper-and-pencil sur-
veys. A total of 224 families were approached, and 203
(90.6%) consented. Of these, 21 did not return their
completed surveys, resulting in a completion rate of
81.3%. Three participants with missing data on one or
more study variables were excluded from the analyses,
resulting in a final sample size of 179. A majority of
survey respondents (77.0%) were mothers. Data on
parents’ educational attainment were available from
a subset of participants (69.5%) who completed demo-
graphic data collection during the clinic’s intake proce-
dure; more than 75% of mothers and fathers had
a four-year college degree or higher education.
Children were 58.1% male, 41.3% cisgender female,
and 0.6% transgender female with a mean age of
11.85 (3.48) years. Data from a subset of this sample
were used in a previous study exploring the mediation
of the anxiety/selective eating relationship by sensory
over-responsivity (Zickgraf & Ellis, 2018).
Representative Sample
Parents of children ages 5–17 years living in the United
States were recruited online from a commercial survey
participant panel service (Qualtrics INC) recruited to be
nationally representative on geographical region, educa-
tion attainment, and race/ethnicity. The surveys were
completed online in a single sitting. A total of 2688
panel workers were screened, of whom 2088 (56.6%)
were ineligible because they did not have children
between ages 5–17, 456 (28.5%) did not consent to parti-
cipate in research, 470 (29.4%) consented but did not
complete the survey, and 169 (6.3%) failed embedded
attention checks or finished the survey in under 5 min.
Of the final 505, 242 were randomized to respond to a set
of survey instruments that did not include the SensOR or
AQ. The present sample includes 263 parents, 191
(72.6%) of whom were mothers. Parents were asked to
report how many eligible children they had (e.g., ages
5–17). A random number generator was used to choose
an integer between 1 and the number reported (inclusive);
parents were instructed to answer the survey questions
about the child whose place in the birth order of eligible
children corresponded to the generated number. Parents
were asked to enter the selected child’s name, initials, or
a nickname, which was then piped into the text of all
questions. The children were 47.5% male and 47.5%
female; due to an error in the survey, data on child gender
were missing for 13 children (4.9%). Parent respondents
reported educational attainment ranging from less than
high school (2.3%), high school education (25.9%) some
college (22.8%), two-year college degree (13.7%), four-
year college degree (21.7%), master’s degree (11.8%),
and doctoral degrees (1.5%).
Undergraduate Sample
Five hundred and thirty-four undergraduates enrolled
in psychology courses at the University of Pennsylvania
were recruited during the fall 2016 semester to partici-
pate in research for course credit. Twenty-four partici-
pants (4.5%) with missing data on study variables were
excluded. Participants were 71.0% female and 29.0%
male, and had a mean age of 19.94 (2.27) years; 97.3%
were ages 18–22. These participants were initially
recruited for a study of parent/child resemblance in
eating behaviors (Elkins & Zickgraf); their data were
also used in a study exploring the mediating role of
sensory sensitivity in the selective eating/anxiety rela-
tionship (Zickgraf & Elkins, 2018). Data on parental
education were not available from this sample of parti-
cipants; however, biological parents of 109 participants
(20.4% of the sample) participated in the study of
parent/child resemblance in eating behaviors, and
these parents reported high educational attainment
(88% with a four-year degree or higher education)
and family income (72% with household income
greater than 100,000 USD per year; Elkins & Zickgraf,
2018). This is consistent with the demographics of the
University of Pennsylvania undergraduates (Chetty
et al., 2017).
Children with ASD Sample
One hundred and eighty-five parents of 4- to 17-year-
old children with ASD (134 male, 72%), recruited
through advertisements in a community ASD clinic
newsletter, completed anonymous, one-time online
questionnaires about their children’s eating habits and
were paid 10 USD as an incentive to participate in this
study. Inclusion criteria were not only a community-
based diagnosis of ASD but also an elevated score on
the Autism Quotient-10 (Allison et al., 2012), a brief
ASD screening tool. Additionally, children currently on
a special diet (e.g., a gluten-free diet) or who had lost
five or more pounds in the month prior to screening
were excluded from participation. Two hundred and
twenty-four parents reported that their child had
a diagnosis of ASD, but 27 did not pass AQ-10 screen-
ing criteria and 12 children were on a special diet and/
or had lost five or more pounds in the last month and
were therefore excluded from study participation. The
final sample of children had a mean age of 8.65 (3.04)
 RIGIDITY AND SENSORY SENSITIVITY 5

years. In this sample, 65% of respondents indicated that internal consistency in this sample (smell sensitivity:
maternal education was a four-year college degree or α = .90; oral texture sensitivity: α = .91). There was
higher education attainment. no measure of non-oral texture sensitivity in the ASD
sample.

Measures
Sensory Sensitivity
In the non-ASD samples, sensory sensitivity to oral
texture, non-oral texture, and smell was assessed using
items from the SensOR (SensOR; Schoen et al., 2008).
The SensOR has seven domains, assessing discomfort
or distress in response to taste, texture (including oral
and non-oral texture), smell, audition, vision, kines-
thetic/body positioning, and movement. In the present
study, we used the full smell scale (5 items, including
“scented soaps” and “air fresheners”), and split the
texture scale into oral (86 items, e.g., “brushing teeth,”
“lumpy food,” “crumbs on face/mouth”) and non-oral
textures (29 items, e.g., “getting a haircut,” “seams in
clothing,” “fuzzy textures”). Because the SensOR items
are dichotomous, alpha was computed based on poly-
choric matrices. In the undergraduate sample, oral tex-
ture α =.77, non-oral texture α = .94, smell α = .88. In
the clinical sample, oral texture α = .78, non-oral tex-
ture α = .96, smell α = .91. In the representative sample,
oral texture α = .82, non-oral texture α = .94,
smell α = .92.
In the ASD sample, smell and oral texture sensitiv-
ities and their impacts were assessed using 10 total
items (5 items each) adapted from the Eating Habits
Survey (Wildes et al., 2012). Example items include: “Is
your child sensitive to the smells of food?” and “Does
sensitivity to food textures keep your child from eating
a variety of foods?” These scales demonstrated excellent
Selective Eating
In the non-ASD samples, selective eating was measured
using the three-item picky eating (PE) subscale of the
nine-item ARFID screen (NIAS; Zickgraf & Ellis, 2018).
The NIAS-PE scale is a self-report measure of selective
or picky eating, validated in adults, that has been mod-
ified for parent-report about children (Zickgraf &
Elkins, 2018). The three items (e.g., “My child is
a picky eater,” “My child dislikes most of the foods
that other kids his/her age eat,” and “My child refuses
to eat everything but a short list of preferred foods”) are
scored on a 0–5 Likert-type scale and summed for
a score ranging from 0 to 15. In the undergraduate
sample, the self-report version showed good internal
consistency: α = .85, and the parent-report version
showed good internal consistency in the clinical
(α = .94) and representative (α = .91) samples. See
Table 1 for item means and ranges from the three
non-ASD samples.
In the ASD sample, picky eating was assessed using
two items (“My child enjoys a wide variety of foods”
and “My child decides that s/he doesn’t like a food,
even without tasting it”) from the Food Fussiness scale
of the Children’s Eating Behavior Questionnaire
(CEBQ; Wardle et al., 2001). The frequency of occur-
rence of behaviors was rated on a 5-point Likert-type
scale ranging from “Never” to “Always.” Although the
child NIAS and CEBQ have not been validated against
each other, the adult versions of the SE subscales of the

Table 1. Demographic characteristics (age, gender) and scores on measures of rigidity, sensory processing, and picky eating.
Anxiety/OC Spectrum Clinic Sample Representative Sample Undergraduate Sample ASD Sample
N 179 263 510 185
Age 11.85 (3.48) 10.62 (3.96) 19.93 (2.27) 8.65 (3.04)
Gender ratio (M:F) 1.39 1.0 0.41 2.63
SensOR oral texture (0–1) .09 (.15) .18 (.23) .17 (.15) –
SensOR non-oral texture .10 (.11) .12 (.17) .28 (.25) –
(0–1)
SensOR smell .12 (.25) .07 (.18) .08 (.20) –
(0–1)
AQ attention switching 2.18 (2.00) 1.85 (1.94) 4.87 (2.07) –
(0–10)
NIAS-PE 6.16 (4.92) 7.52 (4.62) 4.42 (3.70) –
(0–15)
Smell sensitivity – – – 2.88 (1.20)
(1–5)
Oral texture sensitivity – – – 2.76 (1.24)
(1–5)
Flexibility Scale-Revised Total Score – – – 44.86 (8.65)
(0–81)
CEBQ picky eating (1–5) – – – 3.13 (1.06)
Data are represented as mean (standard deviation).
6 H. F. ZICKGRAF ET AL.
two measures are strongly correlated: r = .69 (Zickgraf
& Ellis, 2018). See Table 1 for item means and ranges
from the ASD sample.
Rigidity
In the non-ASD samples, rigidity was measured using the
attention-switch subscale of the adult self-report and
child/parent-report versions of the 50-item Autism
Quotient (AQ; Auyeung et al., 2008; Woodbury-Smith
et al., 2005). The AQ is a screening instrument designed
to identify possible cases of ASD in undiagnosed popula-
tions and to measure phenotypic ASD traits in individuals
who do not meet diagnostic criteria for ASD. The atten-
tion switching subscale assesses both cognitive and beha-
vioral rigidity. Sample items include “I enjoy doing things
spontaneously” and “I find it easy to do more than one
thing at once.” Items are scored on a 1–4 Agree/Disagree
scale, and dichotomized, such that strongly agree and
agree = 1 and strongly disagree and disagree = 0.
Because the items are binary, polychoric alpha was used
to assess internal consistency. The attention switching
subscale showed adequate consistency in the undergrad-
uate (.64) and anxiety/OC-spectrum (.65) sample, and
good internal consistency in the representative sample
(α = .84). The alpha coefficients in the present samples
are consistent with the prior literature and suggest better
internal consistency than has been reported in other large
undergraduate samples (Hurst et al., 2007).
Within the ASD sample, the Flexibility Scale-Revised
(Strang et al., 2017) was used to assess various forms of
inflexibility. The Flexibility Scale-Revised is a valid and
reliable (Cronbach’s α = .75-.91) 27-item parent-report
questionnaire that assesses multiple aspects of behavioral
flexibility for children (i.e., Routines/Rituals, Transitions/
Change, Special Interests, Social Flexibility, and
Generativity) and importantly, does not include any con-
tent related to food choice or eating behaviors. For the
current study, the total score was used as the primary global
flexibility-related correlate of interest in SE behaviors. The
Table 2. Correlations between selective eating and predictor variables (age, gender, rigidity, and sensory
processing).
Anxiety/OC Spectrum Clinic Sample
NIAS-PE
Age −.08
Gender −.03
Rigidity .25***
Oral texture .45***
Smell .12
Non-oral texture .33***
***p <.001, **p <.01, *p <.05
In the anxiety/OC spectrum clinic sample, representative sample, and undergraduate sample, rigidity was measured using the AQ
attention switching scale, oral texture, smell, and non-oral texture sensitivity were measured using the respective SensOR subscales,
and selective eating was measured using the NIAS-PE. In the ASD sample, rigidity was measured using the Flexibility Scale-Revised
Total Score, and oral texture and smell sensitivity were measured using the respective subscales of the Eating Habits Survey.
total score was used because it showed the strongest corre-
lation with the Behavior Rating of Executive Functioning
Shift scale (Gioia et al., 2000) a gold-standard self-/parent-
report measure of cognitive flexibility and rigidity.
Data Analysis
Analyses were conducted separately in each sample. To
explore specific aim 1, zero-order correlations among the
predictors and dependent variables (NIAS-PE in the non-
ASD samples and CEBQ-SE in the ASD sample) were
computed (Table 2), and ordinary least squares regression
analyses controlling for gender and age were used to
explore the unique contributions of cognitive/behavioral
rigidity and oral texture/smell sensitivity (Table 3). We
did not control for parental education because these data
were missing for large subsets of participants from two of
the four samples. In the three non-ASD samples,
a variable assessing non-oral texture sensitivity was also
included.
To compare magnitude of effect sizes for predictors
across the four samples, standard errors of the standar-
dized regression coefficients were used to test for sig-
nificance of group differences in the magnitude of
significant predictors; although we did not use formal
guidelines to assess the magnitude of standardized
betas, they are interpreted in units of standard devia-
tion increases in the dependent variable, SE, for a 1-SD
increase in the predictor variables. Non-significant pre-
dictors were not included in the standardized models.
Differences in the magnitude of standardized coeffi-
cients that were greater than ±2 SE were considered
significant. This procedure was used to address specific
aim 2, whether the two non-clinical samples differed in
the overall magnitude of predictors of SE (see
Figure 1). To address age-related differences in the
level of SE, independent-samples t-tests were used to
compare mean score on the NIAS-PE between the
unselected child sample and young adult sample, and
Representative Sample Undergraduate Sample ASD Sample
NIAS-PE NIAS-PE CEBQ-SE
−.10 −.04 −.03
.003 −.04 .08
.24*** .23*** .32***
.33*** .27*** .19**
.15* .04 .10
.20** .16*** –
Table 3. Selective eating regressed onto age, gender, rigidity, and sensory processing.
Anxiety/OC Spectrum Clinic Sample Representative Sample Undergraduate Sample ASD Sample
F(6,172) = 8.95, R2 =.21 F(6,243) = 8.01, R2 =.14 F(6,502) = 10.27, R2 =.10 F(5,179) = 6.02, R2 =.15
B (β) CI (B) t(1) p B (β) CI (B) t(1) p B (β) CI (B) t(1) p B (β) CI (B) t(1) p
Intercept 5.07 [2.39, 7.75] 3.74 <.001 5.58 [2.49, 8.08] 5.67 <.001 3.36 [0.49, 6.22] 2.30 .02 1.24 [0.17, 2.30] 2.29 .02
Age −0.12 (−.08) [−0.31, 0.07] −1.22 .23 −0.08 (−0.07) [−0.22, 0.06] −1.19 .24 −0.06 (−0.04) [−0.21, 0.07] −0.93 .30 0.03 (0.09) [−0.02, 0.08] 1.21 .23
Gender −0.06 (−.01) [−1.36, 1.23] −0.10 .92 −0.16 (−0.02) [−1.22, 0.90] −029 .77 −0.24 (−0.03) [−0.86, 0.50] −0.93 .59 0.19 (0.08) [−0.14, 0.52] 1.12 .26
Rigidity 0.51 (0.20) [0.16, 0.86] 2.87 .005 0.49 (.21) [0.22, 0.77] 3.53 <.001 0.34 (0.19) [0.18, 0.49] 4.31 <.001 0.04 (0.32) [0.02, 0.06] 4.54 <.001
Oral texture 14.07 (0.38) [8.09, 20.05] 4.64 <.001 5.29 (0.25) [2.49, 8.07] 3.27 <.001 3.91 (0.26) [2.30, 5.51] 4.79 <.001 0.22 (0.26) [0.04, 0.40] 2.46 .02
Smell 1.21 (.06) [−1.44, 3.85] 0.90 .37 0.52 (.04) [−1.03, 2.08] 0.66 .51 0.46 (0.02) [−1.23, 2.15] 0.53 .60 −0.12 (−0.14) [−0.31, 0.06] 1.32 .19
Non-oral texture 1.25 (0.02) [−6.16, 8.65] 0.33 .74 1.04 (0.10) [−0.28, 2.37] 1.55 .12 −1.3 (0.05) [−4.19, 1.59] −0.88 .38 –
In three non-ASD samples, sensory scores range = 0–1, rigidity scores range = 0–10; in ASD sample, sensory scores range = 1–5, rigidity scores range = 0–81.
Standardized betas used in Figure 1 were from trimmed models including only rigidity and oral texture sensitivity as predictors of SE.
In all samples, male = 1, female = 0.
RIGIDITY AND SENSORY SENSITIVITY
7
8 H. F. ZICKGRAF ET AL.

Rigidity: Standardized regression

coefficients ±2*SE
0.6
0.5
0.4
0.3
0.2
0.1
0
Anxiety/OCD Representative Undergraduate ASD
Spectrum

Oral texture: Standardized

regression coefficients ±2*SE
0.6

0.5

0.4

0.3

0.2

0.1

0
Anxiety/OCD Representative Undergraduate ASD
-0.1 Spectrum

Figure 1. Statistical comparison of the magnitude of standardized beta coefficients from trimmed models, including only the two
significant independent variables shown in Table 3.

between the anxiety clinic sample and the unselected
child sample. The magnitude of group differences was
assessed using Cohen’s d effect sizes, with effect sizes of
.20 considered small, .50 medium, and .80 large
(Cohen, 1992).
Results
In all four samples, rigidity and oral texture sensitivity
showed significant zero-order correlations with selec-
tive eating (Table 2). In the three non-ASD samples
non-oral texture sensitivity was also correlated with
selective eating, although more modestly than oral
texture sensitivity in each sample. The two primary
predictor variables showed modest intercorrelations.
In all three non-ASD samples, AQ set shifting was
correlated with non-oral texture sensitivity (rs = .33,
.17, and .24 in the anxiety/OC spectrum clinic, repre-
sentative, and undergraduate samples, respectively),
whereas oral texture sensitivity was only significantly
correlated with AQ set shifting (p < .01) in the
undergraduate samples (rs = .09, .11, and .21). In the
ASD sample, oral texture sensitivity was not signifi-
cantly correlated with rigidity measured on the
Flexibility scale (r = .12). Smell sensitivity was not
significantly correlated with rigidity in any sample (rs
in the three non-ASD samples were −.06, .05, and .05;
in the ASD sample, r = – .11).
Across the four samples, VIF was <2.0 for each
predictor, supporting the assumption of non-
multicollinearity. Across all four samples, both flexibil-
ity and oral texture sensitivity emerged as significant,
independent predictors of SE. Sensitivity to smell and
non-oral texture was not independently associated with
SE in the three samples in which it was explored.
Overall model R2 and standardized beta coefficients for
the predictors were examined across the four samples to
explore the relative magnitude of relationships between
sensory sensitivity/cognitive flexibility and SE. There were
sample differences in the amount of overall SE variance
explained by the predictors, with R2 of .21 in the anxiety
clinic sample, .15 in the ASD sample, .14 in the

representative child/adolescent sample, and .10 in the
undergraduate sample.
Differences in the effect sizes of the two significant SE
predictors, oral sensory sensitivity and cognitive rigidity,
and SE were explored by comparing standardized betas
and overall R2. We hypothesized that there would be no
significant difference between the strength of predictors
between the two non-clinical samples. Other compari-
sons were exploratory. Although there were some differ-
ences in apparent magnitude of effects in the untrimmed
models (Table 3; e.g., a standardized coefficient of 0.38
for oral texture sensitivity in the anxiety/OC-spectrum
clinic sample vs. standardized coefficients of .25, .26, and
.26 in the representative, undergraduate, and ASD sam-
ples, respectively), all effect sizes for both predictors were
within ±2 SE of one another (see Figure 1).
To explore age-related developmental differences in
the level of SE, an independent-samples t-test was used
to compare the mean NIAS-PE score between the
young adult sample and the non-clinical child/adoles-
cent sample. The difference in means (7.52 vs. 4.87,
standard deviations 4.62 vs. 2.07) was significant with
a moderate-large effect size: t(722) = 10.99, Cohen’s
d = 0.74, p < .001. The non-clinical child/adolescent
sample also had a significantly higher level of PE than
the anxiety clinic sample, although the difference was
associated with a small effect size: t(443) = 3.04,
Cohen’s d = 0.29, p < .001
Discussion
We found convergence across several (clinical and
non-clinical) populations using different measures
and different reporters (e.g., self- vs. parent-report)
in a study exploring two candidate transdiagnostic
mechanisms as independent contributors to symptoms
of SE. Whereas the role of sensory sensitivities in SE
has been relatively well studied (e.g., Nadon et al.,
2011; Zickgraf & Elkins, 2018), and explicitly linked
to the presentation of ARFID characterized by severe
SE (e.g., Thomas et al., 2017; Zickgraf et al., 2016),
this is the first study to identify the importance of
cognitive/behavioral rigidity as a predictor of SE in
neurotypical children and young adults, children with
anxiety/OC-spectrum disorders, and children with
ASD. Across populations (ASD diagnoses, anxiety/
OC spectrum diagnoses) and age groups (children
and adolescents 5–17, young adults 18–22) the
strength of the relationships between oral texture sen-
sitivity and rigidity and SE did not significantly differ:
standardized effect sizes for both oral texture sensitiv-
ity and rigidity were within ±2 standard errors of each
other. Within each sample, age was a non-significant
RIGIDITY AND SENSORY SENSITIVITY 9
predictor of SE despite the wide age ranges in the
three child samples. We had no hypotheses regarding
gender as a predictor of SE; there is little published
evidence for gender differences in levels of SE, and the
available evidence is somewhat mixed (Taylor et al.,
2015).
This study highlights the potential domain-specificity
of the sensory sensitivity/SE relationship. The current
results suggest that oral texture sensitivity is a more
specific predictor of SE across populations than smell
sensitivity despite both sensory modalities being
involved in the experience of eating and in sensory
exploration of new foods. Across samples, oral texture
sensitivity was a consistent predictor, with no significant
differences in effect size magnitude. Of note, although
the measures of sensory sensitivity to smell and oral
texture differed across samples, with a measure of gen-
eral sensory aversion used in the three neurotypical
samples (e.g., participants indicated whether or not
they/their child found various sensory experiences
unpleasant) and a measure of sensory-driven food avoid-
ance used in the ASD sample. These converging findings
suggest that oral texture aversions/distress and oral tex-
ture driven food avoidance appear to share the same
relationship with SE.
Future studies should address the interplay of these
two mechanisms in the development of SE behaviors. It
may be the case that neither sensory over-responsivity
nor rigidity alone is sufficient for the development of
SE. Instead, both might be necessary to set the stage for
the development of these eating challenges. Alternately,
either sensory sensitivity or rigidity alone, perhaps
above a certain severity threshold or in the context of
other variables not explored in this study (e.g., early
childhood exposure to food variety, parental feeding
practices), might be sufficient to cause SE.
Longitudinal studies are needed to identify the tem-
poral sequence and causal pathways to these relation-
ships and whether these pathways are modulated or
diverge across typical and atypical development (e.g.,
in ASD). Nevertheless, if this supposition is true, treat-
ments for SE and the related ARFID presentation
should target both mechanisms.
Interventions targeting sensory sensitivity should
involve repeated, gradual exposure to novel or non-
preferred foods. Research comparing the rate of habi-
tuation to fear vs. disgust in anxiety disorders suggests
that disgust is slower to habituate compared to fear.
Children’s neophobic reactions to novel foods involve
facial expressions of disgust, and sometimes gagging
and vomiting, and rarely appear to involve fear or
anxiety (Ventura & Worobey, 2013; Zickgraf, Murray,
et al., 2019). It is likely, therefore, that much of the
10 H. F. ZICKGRAF ET AL.
learning that takes place in any given exposure session
is likely to involve the use of coping skills or violation
of expectancies regarding the intensity of the sensory
aversion, or the patient’s hedonic reaction and ability to
cope with it.
If rigidity is a maintaining factor in SE, sensory
habituation alone is unlikely to be sufficient to substan-
tially expand an individual’s diet because the ability to
generalize sensory learning and habituation from one
food to other, seemingly similar foods, is likely
impaired in highly rigid individuals (e.g., Kashdan &
Rotterberg, 2010). The typical development of food
preferences, like other areas of cognitive development,
involves the assimilation and accommodation of food-
related schemas, with, for example, young children who
were experimentally exposed to the flavor of carrots in
utero or during breastfeeding more readily accepting,
and showing faster habituation to, pureed carrot baby
food despite its different appearance and texture
(Mennella et al., 2001).
Cognitive rigidity is associated with behavioral
inflexibility, including repetitive and compulsive beha-
vior. Rigidity in SE could, therefore, manifest itself in
the tendency to choose a repetitive diet, rigid food
rules, and black and white expectations about the sen-
sory/hedonic or affective experience of trying a new or
non-preferred food. A broader “insistence on same-
ness” is a characteristic feature of ASD with detrimental
impacts upon daily functioning and long-term out-
comes. Emerging evidence supports the effectiveness
of intervention programs that target cognitive inflex-
ibility, including Unstuck and On Target (Kenworthy
et al., 2014) that uses cognitive-behavioral approaches
with verbal children. While this school-based program
does not address food-related flexibility, a recently
developed intervention model, the Building Up Food
Flexibility and Exposure Treatment (BUFFET;
Kuschner et al., 2017), utilizes similar cognitive-
behavioral principles to address specifically the eating-
related rigidity and other associated challenges in chil-
dren with ASD. The current results suggest that similar
techniques emphasizing flexibility might be used to
address SE in typically developing individuals as well.
Limitations
This study had several strengths, including replication
across four samples, the use of multiple reporters (par-
ent report and self-report) and multiple measures of the
same constructs (e.g., different measures of SE, rigidity,
and sensory sensitivity in the ASD vs. neurotypical
samples), yet there are also several relevant limitations
to consider. The current study is a secondary analysis,
using data originally collected for other purposes by
different study authors; this is why the measures used
differed between the ASD sample and the other three
samples. Future studies by our group will be designed
to replicate and extend the current findings using con-
sistent measures across all samples. Although we feel
that the use of multiple measures of the constructs of
interest across samples was a strength, there is a need
for more published validity data supporting the ability
of existing measures, including the differing measures
of SE, rigidity, and sensory sensitivity used in the pre-
sent study, to tap the same construct in the same way
across samples differing in age, clinical status, and
other variables (Tyrell et al., 2019).
Demographic information beyond child age, gender/
sex, and race/ethnicity was not available. Including
indicators of socioeconomic status such as parental
education (which was not included in analyses because
it was only available for subsets of participants from
two of the four samples) and income, and information
about family composition (e.g., number of parents,
number of siblings) in the models might have explained
remaining variance in SE. For example, children from
lower-SES backgrounds have been found to demon-
strate higher levels of SE compared to peers (e.g.,
Dovey, et al., 2008), although it is unclear how SES
interacts with neurobehavioral predictors like sensory
sensitivity and cognitive rigidity. ASD diagnosis in the
ASD sample was based on parent-report of an existing
clinician provided diagnosis and meeting AQ-10
screening criteria, but was not confirmed by
a diagnostician; we also did not collect information
on intellectual or verbal functioning in this (or any)
sample. In addition, we did not have data on self- or
parent-reported ASD diagnoses in the two general/non-
clinical samples.
A related limitation was that we did not have
a measure of non-oral texture sensitivity in the ASD
sample. Based on the current results, it is not possible
to rule out overall texture sensitivity, a contributor to
SE in children with ASD. However, it seems unlikely
that non-oral texture sensitivity would have an inde-
pendent impact on SE after accounting for the correla-
tion between oral and non-oral texture sensitivity.
Relatedly, although oral texture sensitivity emerged as
the main predictor of SE in all samples, it is very likely
that taste sensitivity would also have emerged as an
important predictor. Future research should explore
the relative role of taste and texture sensitivity in pre-
dicting SE. It was not possible to explore taste sensitiv-
ity in the current study because existing measures of
sensory sensitivity conflate taste sensitivity with food
rejection (e.g., on the sensOR, taste sensitivity is

assessed with questions about avoidance of, for exam-
ple, “sour foods” and “new foods” as opposed to “sour
tastes” and “unfamiliar tastes”).
Conclusions
The contribution of the two neurobehavioral
mechanisms to predicting SE was relatively consistent
over development from ages 5 to 22 and between
samples with anxiety/OC-spectrum, autism spectrum,
and no diagnoses. Because ARFID is a lifespan diag-
nosis, identifying mechanisms implicated in the
maintenance of SE at all ages is necessary for the
development of appropriate treatments. In order to
“outgrow” developmentally typical food neophobia,
children must generalize from their sensory experi-
ences with foods to other, similar foods. Cognitive
rigidity might impede this generalization by reducing
the flexibility and ease with which children can mod-
ify and expand their food schemas, or via behavioral
inflexibility (e.g., repetitive behavior, rigid expectan-
cies about their own sensory or emotional experi-
ences). This would likely result in reduced exposure
to foods via self-selection/food refusal. For exposure
to novel foods to result in acceptance of those foods,
or similar foods, in the future, the hedonic experi-
ence of eating these foods must be pleasant and
predictable, implicating sensory sensitivity in the
acquisition and development of food preferences.
Therefore, both sensory sensitivity and cognitive
rigidity might be maintenance mechanisms, involved
in the progression from age-appropriate SE and food
neophobia to impairing SE, in some cases leading to
ARFID.
Acknowledgments
We would like to thank the individuals and families who
participated in this research. GLW was funded through
a Pilot Project (WA00583863) from the Healthy Weight
Research Network. HFZ was funded through the
T32MH082761-10 NIH/NIMH, Midwestern Regional Eating
Disorders Training Grant.
Disclosure Statement
The authors have no conflicts of interest to report.
Funding
This work was supported by the National Institute of Health/
National Institute of Mental Health [T32MH082761-10];
Healthy Weight Research Network [WA00583863].
RIGIDITY AND SENSORY SENSITIVITY 11
ORCID
Hana F. Zickgraf http://orcid.org/0000-0002-9228-0139
Nancy L. Zucker http://orcid.org/0000-0003-2278-5008
Gregory L. Wallace http://orcid.org/0000-0003-0329-5054
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