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Research Article
Eating Problems and Overlap with ADHD and
Autism Spectrum Disorders in a Nationwide Twin Study of
9- and 12-Year-Old Children
Maria Råstam,1Jakob Täljemark,1Armin Tajnia,2Sebastian Lundström,2,3,4
Peik Gustafsson,1Paul Lichtenstein,5Christopher Gillberg,4
Henrik Anckarsäter,2and Nóra Kerekes2,3
1Department of Clinical Sciences, Lund, Child and Adolescent Psychiatry, Lund University, Soav¨
agen 2D, SE-22241 Lund, Sweden
2Centre for Ethics, Law and Mental Health (CELAM), University of Gothenburg, Wallinsgatan 8, SE-43141 M¨
olndal, Sweden
3SwedishPrisonandProbationService,R&DUnit,Gothenburg,Wallinsgatan8,SE-43141M
¨
olndal, Sweden
4Gillberg Neuropsychiatry Centre, Institution of Neuroscience and Physiology, University of Gothenburg, Kungsgatan 12,
SE-41119 G¨
oteborg, Sweden
5Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Nobels V¨
ag 17, SE-17165 Solna, Sweden
Correspondence should be addressed to Maria R˚
astam; maria.rastam@med.lu.se
Received February ; Accepted March
Academic Editors: C. M. Beasley, C. C. Chiu, and C. Gonz´
alez-Blanch
Copyright © Maria R˚
astam et al. is is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Aim. To establish the prevalence of restrictive eating problems, the overlap and association with attention-decit/hyperactivity
disorder (ADHD), and autism spectrum disorders (ASD) and to estimate the heritability of eating problems in a general population
sample of twins aged and . Methods. Parents of all Swedish - and -year-old twin pairs born between and (𝑛=
12,) were interviewed regarding symptoms of ADHD, ASD, and eating problems (EAT-P). Intraclass correlations and structural
equation modelling were used for evaluating the inuence of genetic and environmental factors. Cross-twin, cross-trait correlations
were used to indicate a possible overlap between conditions. Results. e prevalence of eating problems was .% in the study
population and was signicantly higher in children with ADHD and/or ASD. Among children with eating problems, % were
screened positive for ADHD and/or ASD. Social interaction problems were strongly associated with EAT-P in girls, and impulsivity
and activity problems with EAT-P in boys. e cross-twin, cross-trait correlations suggested low correlations between EAT-P and
ADHD or EAT-P and ASD. Genetic eects accounted for % of the variation in liability for eating problems. Conclusions.Inthe
group with eating problems, there was a clear overrepresentation of individuals with ADHD and/or ASD symptoms.
1. Introduction
In typically developing younger children, the prevalence of
theclinicaleatingdisordersislow[,], with one large-scale
study reporting a prevalence of .% for DSM-IV eating
disorders in - to -year olds []. However, some degree of
milder eating problems is relatively common, aecting from
to percent of children []. Selective eating or picky
or faddy eating is a transient problem in over % of all
toddlers []. A recent surveillance study []basedonclose
to Canadian paediatricians’ reports on “any disordered
eating behavior sucient to cause a disruption, weight gain,
or actual loss of weight” found children from to years
of age. e highest incidence, . cases per person-
years,wasfoundingirlsagedfromtoyears(.forboys).
Dieting as a general, non-specic risk factor increases
the risk of developing an eating disorder by about ve
times []. It has been suggested that subclinical variants
of eating disorders start at an earlier age now than was
the case in the twentieth century and that the prevalence
of early dieting/restrictive eating is increasing []. While
eating problems in childhood may be a risk factor for the
development of eating disorders in adolescence and young
adulthood [–], a comprehensive review on risk factors for
eating disorders stressed a need for larger-scale studies [].
e Scientic World Journal
Children with early symptomatic neuropsychiatric disor-
ders have been found to have high frequencies of feeding/
eating problems [,] compared to children without such
disorders, but there have been few, if any, large-scale studies
in the general population investigating this problem [].
As far as we are aware, there are few studies on heritability
in prepubertal eating problems/eating disorders. In one
study of over twins aged from to years, parent-
reported food neophobia was highly heritable explaining
% of the variance while % was explained by nonshared
environmental factors [].
e present paper assesses the rate of eating problems in
a large young cohort of twins from the general population.
Results are broken down by gender, genetic background
factors, and by validated screening diagnoses of ADHD and
ASD. In addition, we examined which facets of ADHD and
ASD that had the strongest associations with eating problems.
2. Methods
2.1. Subjects. e Child and Adolescent Twin Study in Swe-
den (CATSS) is an ongoing longitudinal twin study targeting
alltwinsborninSwedensinceJuly,.Since,parents
of twins are interviewed regarding their children’s somatic
and mental health and social environments in connection
with the children’s th or th birthdays (CATSS-/), with
an overall response rate of % of all families contacted [].
Parental information on , children from the birth
cohorts between and of CATSS was used for
analysis. In the present study, individuals were excluded
becausetheyhadknownseverebraindamageorknown
chromosomal aberrations, leaving data on , individuals
(boysandgirls).Inafurthercasesthere
were missing items on key variables. erefore in analyses
including all key variables , children ( boys and
girls aged and boys and girls aged ) were
included.
2.2. Measures
2.2.1. e A-TAC Inventory. All twins participating in the
study were screened for possible neurodevelopmental prob-
lems using a specially developed inventory, the Autism-
Tics, ADHD, and other Comorbidities (A-TAC) inventory,
including a previously used algorithm for eating problems
and validated algorithms for ADHD and ASD [].
e A-TAC inventory includes questions to investigate
child psychiatric problems based on criteria stated in the
Diagnostic and Statistical Manual of Mental Disorders, th
edition []. e A-TAC was designed for use in large-scale
epidemiological research as an easy-to-administer, dimen-
sional, and comprehensive parental interview that can be
carried out by lay interviewers over the phone [,]. e
instrument is freely available as additional web material
to the second validation study []. Items are organized
into modules (e.g., Concentration/Attention and Impulsive-
ness/Activity form the ADHD domain, and Language, Social
interaction, and Flexibility form the ASD domain). Modules
are assessed without diagnostic hierarchies or exclusion
criteria.
2.2.2. Questions and Scoring. In two validation studies [,]
lower cutos for screening purpose and higher cutos for
use as clinical proxies have been dened for both the ADHD
andtheASDscales.Inthepresentstudywehaveusedthe
lower cutos for identifying children screening positive for
ADHD (scores ≥; sensitivity, .; specicity, .) and/or
ASD (scores ≥.; sensitivity, .; specicity, .) [].
Modules used in the present study were Concentration
and Attention, Impulsiveness and Activity, Language, Social
interaction, Flexibility, and Feeding/Eating. Each module
starts with a reminder that the questions refer to a lifetime
perspective, in comparison to peers, and that the questions
addressing specic symptoms or characteristics may be
answered by the response categories “no” (score ), “yes, to
some extent” (score .), and “yes” (score .). As alternatives,
“donotknow”or“donotwishtoanswer”aregiven,bothof
which are coded as “missing.”
e Eating module screens for restrictive eating prob-
lems. Eating problems “(EAT-P)” was dened here as scoring
≥. on the collapsed score for the two key questions of the
Eating module []. ese questions are () has s/he ever failed
to gain enough weight for more than a year? () Has s/he
seemed fearful of gaining weight or growing fat?
2.3. Statistical Analyses
2.3.1. Association Analyses. To investigate the association
between the dierent facets of ADHD: () Concentration/
Attention and () Hyperactivity/Impulsiveness, and ASD:
() Language, () Social interaction, and () Flexibility- and
EAT-Pweusedabinarylogisticregressionresponsemodel
with data on , children. To account for the dependency
within twin pairs a generalized estimation equation (GEE)
modelwasttedtothedata.Allvariableswereinsertedas
continuous covariates, except age. In a rst step all factors
wereassessedinaunivariatemodel,and,inasecondstep,a
multivariate model was created that only included signicant
associations from the univariate model.
2.3.2. Twin Statistics. Twin methodology is based on the
comparison of monozygotic and dizygotic twin pairs.
Monozygotic twins share all their genes, while dizygotic
twins, on average, share % of their segregating alleles. is
makesitpossibletodisentanglegeneticfromenvironmental
components of a trait or condition. In twin methodology,
etiological factors are partitioned into genetic (A) factors,
shared environmental (C) factors (factors that make the twins
more similar), and nonshared environmental factors (E)
(factors that make twins dissimilar). Intraclass correlations
and standard continuous univariate heritability models were
calculated in Mx [].Wedidnotattempttoreducethemod-
elssincethatcanleadtobiasesintheobservedestimates[].
Cross-twin, cross-trait correlations (the continuous score of
trait in twin is correlated with the continuous score of trait
intwin)werecalculatedusingthePROCCORRprocedure
in SAS .. Cross-twin, cross-trait correlations are used to
indicate if common genetic and environmental eects over
two traits existed. If the correlation is higher for monozygotic
e Scientic World Journal
T : Prevalence of EAT-P.
Groups
Total study g roupa
𝑛
(boys + girls)
EAT-P
𝑛
(boys + girls)
% within the group
(boys + girls)
ADHD only .
( + ) ( + ) (. + .)
ASD only .
( + ) ( + ) (. + .)
ADHD + ASD .
( + ) ( + ) (. + .)
Comparison (no
ADHD, no ASD)
.
( + ) ( + ) (. + .)
Study population
(boys + girls)
a .
( + ) ( + ) (. + .)
aExcluding individuals for whom items were missing on the response variables yielded , individuals for prevalence analyses.
EAT-P: eating problems; ADHD: attention decit hyperactivity disorder; ASD: autism spectrum disorder.
twins than for dizygotic twins, then common genetic eects
inuencing both traits are implicated. As the cross-twin cross
traits correlations were quite similar for monozygotic and
dizygotictwins,wedidnotgoontoattemptbivariatemodel
tting.
Zygositywasdeterminedinover%ofthetwinswith
a panel of single nucleotide polymorphisms or, for those
twins where DNA samples were missing, with the help of
validated algorithms [].
3. Results
3.1. Prevalence of EAT-P, ADHD, and ASD. Of the ,
children included in the present study, were screened
positive for ADHD only (scoring ≥. in the ADHD and
<. in the ASD blocks), were screen positive for ASD
only (scoring ≥. in the ASD and < in the ADHD blocks),
and children were screened positive for both ASD and
ADHD. e rest of the children (𝑛=11,) constituted the
comparison group.
e prevalence of EAT-P was low (𝑛=72; .%) of the
total population of , children aged and , with a close-
to-equal distribution between ages, and a predominance of
girls ( boys and girls). In the comparison group of ,
children with no ADHD/ASD, there were children with
EAT-P (.%; boys .%, girls .%) (Tab l e ). In the group of
children with ADHD and/or ASD (𝑛 = 1280) there were
children with EAT-P (%; boys %, girls %). e prevalence
of EAT-P was signicantly higher in the group of children
with ADHD and/or ASD compared to the group of children
with no ADHD and no ASD (𝑃 < 0.001). e highest
prevalence of EAT-P was seen in children scoring positive for
both ADHD and ASD (.%; boys .%, girls .%).
3.2. Prevalence of ADHD and ASD in Children with and
without EAT-P. Fortypercentofallchildrenwhowere
reported to have EAT-P and % of those without EAT-P were
screen positive for ADHD and/or ASD, as shown in Figure .
60%
(𝑛=43)
17%
(𝑛=12)
1%
(𝑛=1)
22%
(𝑛=16)
Eating problems (𝑛=72)
No ADHD, no ASD
+ADHD
+ASD
+ADHD+ASD
F : Prevalence of ADHD and/or ASD in the children with
EAT-P. EAT-P: eating problems; ADHD: attention decit hyperac-
tivitydisorder;ASD:autismspectrumdisorder.
3.3. Associations with Subdomains of ADHD and ASD.
Table summarizes the association in measures of odds
ratios (ORs) between EAT-P and age and between modules
of ADHD and ASD, separately for both genders. Both
ADHD modules (Concentration/Attention, and Impulsive-
ness/Activity)andallthreeASDmodules(Language,Social
interaction, and Flexibility) were signicantly associated with
EAT-P in both genders in the univariate models. For example,
for each new Concentration/Attention symptom the risk of
eating problems increased with % in boys and with % in
girls (OR = 1.36/.; CI =.–./.–., resp.). When
tting all the signicant variables of EAT-P into a multivariate
model, only three variables were signicantly associated with
EAT-P. ese were Social interaction problems (OR = 1.95,
𝑃 < 0.005) for girls, and for boys Impulsiveness/Activity
e Scientic World Journal
T : Measuring associations between EAT-P and subdomains of ADHD and ASD, for boys and girls separately by GEE models.
Factors/covariates Crude measures Univariate model Multivariate modela
𝑛Min–max 𝑀SD OR % CI OR % CI
Boys EAT-P (Prevalence .%)
Age — — — .∗.–. .∗.–.
Age (reference group) — — — — —
Concentration/attention problems – . . .∗∗∗ .–. . .–.
Impulsiveness/activity problems – . . .∗∗∗ .–. .∗∗∗ .–.
Language problems – . . .∗∗∗ .–. . .–.
Social interaction problems – . . .∗∗∗ .–. . .–.
Flexibility problems – . . .∗∗∗ .–. . .–.
Girls EAT-P (prevalence .%)
Age — — — . .–. —
Age (reference group) — — — — —
Concentration/attention problems – . . .∗∗∗ .–. . .–.
Impulsiveness/activity problems – . . .∗∗∗ .–. . .–.
Language problems – . . .∗∗∗ .–. . .–.
Social interaction problems – . . .∗∗∗ .–. .∗∗ .–.
Flexibility problems – . . .∗∗∗ .–. . .–.
𝑁=,, boys 𝑛 = 6331,Girls𝑛 = 5996; EAT-P: eating problems; awith signicant variables of the univariate models; ∗𝑃 < 0.05;∗∗𝑃 = 0.005;∗∗∗𝑃<
0.001.
problems (OR = 1.41,𝑃 < 0.001), and age years compared
to years (OR = 0.37,𝑃 < 0.05).
3.4. Heritability. Intraclass correlations were at least twice
as strong in monozygotic pairs as in dizygotic same-sex
pairs, both generally and in each gender separately (Tab l e ).
Genetic eects (heritability) accounted for % of the vari-
ance in EAT-P. ere was no indication of shared environ-
mental eects. e remaining variance was due to nonshared
environmental eects. e phenotypic correlations did not
exceed ., and the cross twin, cross trait correlations sug-
gested low correlations (<.) between EAT-P and ADHD
or EAT-P and ASD, which did not dier substantially between
monozygotic and dizygotic twins.
4. Discussion
EAT-P in the present study was dened by parent-reported
weight stop/loss combined with fear of gaining weight in the
child, and the main ndings were as follows.
(i) eprevalenceofEAT-Pwaslow(underonepercent)
in these cohorts of - and -year olds.
(ii) e prevalence of EAT-P was signicantly higher
in children who also screened positive for ADHD
and/or ASD, with the highest prevalence of EAT-P,
almost ten percent, reported for girls who screened
positive for both ADHD and ASD.
(iii) Social interaction problems were strongly associated
with EAT-P in girls, and impulsivity and activity
problems were strongly associated with EAT-P in
boys.
(iv) In childhood, eating problems seemed to be in equal
parts accounted for by genetic and nonshared envi-
ronmental background factors.
Based on earlier published reports, the low prevalence of
restrictive eating in the age cohorts in the present study was
to be expected [,]. However, as far as we are aware there
have been few studies on the general population of to
-year olds. Furthermore, few existing reports have looked
specically at the critical prepubertal years, critical if the
purpose is to examine early onset of restrictive eating [].
e expected overrepresentation of girls could be expected
from all previous epidemiological studies. In boys there
was a signicant increase in EAT-P with age. However,
earlier literature also gives the expectation of an increasing
prevalenceofrestrictiveeatingin-yearoldgirlscompared
to -year olds []whichwasnotsubstantiatedinthisstudy.
e prevalence of EAT-P, at least as dened in this
study, was relatively low compared to other developmental
problems []. Similar to some previous studies [,],
in the present study children screening positive for ADHD
and/or ASD had an increased risk of eating problems causing
weight loss. In the children with such eating problems
there was a clear overrepresentation of individuals with
ADHD and/or ASD. Concerning this nding there are few
studies except a study in UK of a nonclinical sample of
schoolchildren with similar results []. Eating disorders are
now considered to be neurodevelopmental disorders [],
andalinkwithchildhoodobsessive-compulsivepersonality
traits [], and even with ASD, has been suggested [,].
e neurodevelopmental disorders should be considered in
children with eating disorders, especially in girls where mild
formsofADHDandASDtendtobeoverlooked[].
e Scientic World Journal
T : Intraclass correlations, heritability estimates, and cross-twin cross-trait correlations for the collapsed sample and by gender.
Intraclass correlations (% CI:s) Heritability estimates (% CI:s) Cross-twin, cross-trait correlations (% CI:s) Phenotypic correlations (% CI:s)
EAT-P MZ DZ ss A C E ADHD ASD ADHD ASD
MZ DZ ss MZ DZ ss
ALL . . . . . . . . . . .
(.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.)
Boys . . . . . . . . . . .
(.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.)
Girls . . . . . . . . . . .
(–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.) (.–.)
EAT-P: eating problems, MZ: monozygotic, DZ-ss: dizygotic same sex, CI:s: condence intervals.
A: genetic factors, C: shared environmental factors, and E: nonshared environmental factors.
Pairs where information was eligible from both twins were included in the analyses, giving a total of MZ boys, ; DZ girls, DZ-ss boys , and DZ-ss girls.
e Scientic World Journal
Gender specic dierences could be seen concern-
ing neurodevelopmental problems associated with EAT-P.
Hyperactivity and impaired social interaction showed strong
and signicant association to EAT-P for both genders. As
farasweknowitisanewndingforprepubertaleating
symptoms,butitwouldseemtobeinagreementwithearlier
literature on adolescent onset eating disorders [–]. How-
ever, in the multivariate analysis, the strongest association
of EAT-P for girls was problems with social interaction, and
in boys the strongest association was with hyperactivity and
impulsivity. ese gender dierences seem to be in agreement
with some reports of excessive exercise as more common in
male than in female eating disorders [].
Eating problems in to -year olds appear, similar to
later in adolescence [,], to have an equally large genetic
and non-shared environmental background. However, the
scant literature of boys and men with eating problems/eating
disorders does not allow any comparing with earlier ndings.
e very similar cross-twin cross-trait correlations together
with the low phenotypic correlation suggested that the small
part of variance that is shared between the conditions is
mainly due to shared environmental factors. Future studies
should investigate if this association is similar above the
diagnostic threshold. A review [] stressed the complexity of
inuences on eating behaviours and weight as parents provide
both the genetic predispositions and the environment (the
food and the attitudes to food) in which these predispositions
are expressed. Maternal food intake strongly correlates with
child food intake []. e clinical implications of the
interplay between environmental and genetic risk factors for
eating disorders have been comprehensively described in a
recent review [].
e strengths and limitations of the study should be taken
into account in interpreting ndings. e population-based
nature of the study sample is an important strength. An obvi-
ous limitation is that the information regarding symptoms
and behaviour consisted of parent ratings in a telephone
interview. e A-TAC inventory has a proven excellent ability
to distinguish children with neurodevelopmental problems
from children with no such problems [], but it has not
been validated for the assessment of eating problems which
suggests that the results should be interpreted with caution.
e focus of this study is on restrictive eating, and questions
on bingeing and obesity have not been included in the
analyses in the present study. e study was cross-sectional
and could not say anything about causality.
e clinical implication of this study is that neurode-
velopmental disorders should be considered in children
with disordered eating, and, conversely, that eating prob-
lems/disorders should be considered in children with ADHD
and/or ASD. Interventions must be matched to the patient,
and only if neurodevelopmental aspects are considered in
each individual case, one can expect results.
Ethical Approval
e CATSS-/ study has ethical approval from the Karolin-
ska Institute Ethical Review Board: Dnr - and /-
/.
Acknowledgments
e CATSS-/-study is supported by the Swedish Council
for Working Life and Social Research and the Swedish
Research Council (Medicine). e authors have no conict
of interests including nancial interests and relationships
and aliations relevant to the subject of this paper. e
participants gave informed written consent.
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