Attention-deficit/hyperactivity disorder and impairment in executive functions: A barrier to weight loss in individuals with obesity?
An increasing body of research points to a significant association of obesity to Attention-Deficit/Hyperactivity Disorder (ADHD) and deficits in executive functions. There is also preliminary evidence suggesting that children with ADHD may be at risk of obesity in adulthood DISCUSSION: In this article, we discuss the evidence showing that ADHD and/or deficits in executive functions are a barrier to a successful weight control in individuals enrolled in weight loss programs. Impairing symptoms of ADHD or deficits in executive functions may foster dysregulated eating behaviors, such as binge eating, emotionally-induced eating or eating in the absence of hunger, which, in turn, may contribute to unsuccessful weight loss. ADHD-related behaviors or neurocognitive impairment may also hamper a regular and structured physical activity. There is initial research showing that treatment of comorbid ADHD and executive functions training significantly improve the outcome of obesity in individuals with comorbid ADHD or impairment in executive functions. Preliminary evidence suggests that comorbid ADHD and deficits in executive functions are a barrier to a successful weight loss in individuals involved in obesity treatment programs. If further methodologically sound evidence confirms this relationship, screening and effectively managing comorbid ADHD and/or executive functions deficits in individuals with obesity might have the potential to reduce not only the burden of ADHD but also the obesity epidemics.
D E B A T E Open Access
Attention-deficit/hyperactivity disorder and
impairment in executive functions: a barrier to
weight loss in individuals with obesity?
, Erika Comencini
, Brenda Vincenzi
, Mario Speranza
and Marco Angriman
Background: An increasing body of research points to a significant association of obesity to Attention-Deficit/
Hyperactivity Disorder (ADHD) and deficits in executive functions. There is also preliminary evidence suggesting that
children with ADHD may be at risk of obesity in adulthood.
Discussion: In this article, we discuss the evidence showing that ADHD and/or deficits in executive functions are a
barrier to a successful weight control in individuals enrolled in weight loss programs. Impairing symptoms of ADHD
or deficits in executive functions may foster dysregulated eating behaviors, such as binge eating, emotionally-
induced eating or eating in the absence of hunger, which, in turn, may contribute to unsuccessful weight loss.
ADHD-related behaviors or neurocognitive impairment may also hamper a regular and structured physical activity.
There is initial research showing that treatment of comorbid ADHD and executive functions training significantly
improve the outcome of obesity in individuals with comorbid ADHD or impairment in executive functions.
Summary: Preliminary evidence suggests that comorbid ADHD and deficits in executive functions are a barrier to a
successful weight loss in individuals involved in obesity treatment programs. If further methodologically sound
evidence confirms this relationship, screening and effectively managing comorbid ADHD and/or executive
functions deficits in individuals with obesity might have the potential to reduce not only the burden of ADHD but
also the obesity epidemics.
Keywords: ADHD, Executive functions, Obesity, Treatment resistance
Attention-Deficit/Hyperactivity Disorder (ADHD) is
defined by persistent, age inappropriate and impairing
levels of inattention and/or hyperactivity-impulsivity
. The Diagnostic and Statistical Manual of Mental
edition, Text Revision, IV-TR  defines
four types of ADHD: “predominantly inattentive”,“pre-
otherwise specified”. Although outside the scope of this
article, since the final text is not yet available, we note that
the core structure of the diagnostic criteria is largely
unchanged in the forthcoming fifth edition of the diagnos-
ADHD is one of the most frequent childhood-onset
psychiatric conditions, with an estimated worldwide-
pooled prevalence exceeding 5% in school-age children
. Impairing symptoms of ADHD persist into adult-
hood in up to 65% of childhood-onset cases  and the
pooled prevalence of ADHD in adults has been esti-
mated at ~2.5% .
Executive functions are defined as a set of neurocog-
nitive skills that are necessary to plan, monitor and exe-
cute a sequence of goal-directed complex actions and
include inhibition, working memory, planning, and sus-
tained attention . Besides the behavioural core symp-
toms of inattention, hyperactivity, and impulsivity, deficits
in executive functions are commonly, although not univer-
sally, associated with ADHD . Indeed, executive dys-
function is not required for the diagnosis of ADHD, which
* Correspondence: email@example.com
Child Neuropsychiatry Unit, G. B. Rossi Hospital, Department of Life Science
and Reproduction, Verona University, Verona, Italy
Phyllis Green and Randolph Cowen Institute for Pediatric Neuroscience,
Child Study Center of the NYU Langone Medical Center, New York, NY, USA
Full list of author information is available at the end of the article
© 2013 Cortese et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Cortese et al. BMC Psychiatry 2013, 13:286
is defined at the behavioral, rather than neuropsychological,
level. Additionally, ADHD is usually comorbid with other
neurodevelopmental and/or psychiatric conditions, such as
learning disorders, oppositional defiant/conduct disorder,
mood and anxiety disorders, substance use disorders, and
sleep disturbances [7,8].
Currently, the mainstay of treatment, at least for severe
cases, is pharmacologic, with psychostimulant medications
(methylphenidate and amphetamines) as the first line,
and non-stimulants as secondary option [6,9]. Non-
pharmacological treatments, such as behavioural ther-
apies, diet regimens, cognitive training, and neurofeedback,
are also available. Although the empirical evidence for
their efficacy for ADHD core symptoms is so far weak
, such treatments may effectively address related be-
havioural or neuropsychological dysfunctions.
disorders/conditions, ADHD entails an enormous burden
on society in terms of psychological dysfunction, adverse
vocational outcomes, stress on families, and societal finan-
cial costs. The U.S. annual incremental costs of ADHD
have been recently estimated at $143-$266 billion  and
high costs have been reported in other countries as well
Whereas the comorbidity between ADHD and psychi-
atric disorders has been extensively explored , the asso-
ciation with general medical conditions has received much
less attention. However, among medical disorders, there is
increasing evidence pointing to a significant association
between overweight/obesity and ADHD in children
[13,14] as well as in adults [15-17]. In particular, as de-
tailed in a previous systematic review  and outlined in
Table 1, all currently available studies show significantly
higher rates of ADHD in individuals with obesity treated
in specialized centres compared to normal weight controls
or population rates of ADHD. (Studies listed in Table 1
were retrieved searching Pubmed, Ovid, EMBASE, and
Web of Knowledge, from their inception to March 15
2013, using the following keywords, in multiple com-
bination combination: obesity, BMI, weight, body mass,
ADHD, Attention-Deficit/Hyperactivity Disorder, Attention
Deficit Disorder, Hyperkinetic Disorder; details of the
search strategy and syntax, adapted for each database, as
well as of the specific results from each database search,
are available from the corresponding author). Given the
cross-sectional design of such studies, they cannot allow
to infer the causal relationship between obesity and
ADHD. Theoretically, it is possible that: 1) ADHD con-
tributes to weight gain; 2) Obesity early in life fosters
symptoms of ADHD; 3) Both conditions are the expres-
sion of underlying neurobiological and psychopathological
dysfunctions. Recent studies have shaded light on the
causal relationship between ADHD and obesity, sup-
porting in part the notion that ADHD in childhood may
contribute to weight gain later on in life. Cortese et al. 
assessed body mass index (BMI) and obesity rates in a sam-
ple of 111 U.S. adults with childhood problems consistent
with DSM-IV(-TR) ADHD, combined type, followed up for
Table 1 Studies assessing the rates of Attention-Deficit/Hyperactivity Disorder (ADHD) in clinical samples of
treatment-seeking individuals with obesity
First author (year) [ref] Sample characteristics Key findings
Altfas (2004) 215 patients with obesity treated in a specialized
obesity clinic (Males: 22; mean age: 43.4 ± 10.9 years)
Prevalence of ADHD in the whole sample: 27.4%.
Prevalence of ADHD in individuals with BMI ≥40 kg/m
42.6%. Mean BMI loss among patients with ADHD: 2.6 BMI
)vs. 4.0 for non-ADHD (p < 0.002)
Erermis (2004) 30 adolescents with obesity (Males: 14; mean age: 13.8 ±
1.2 years) seeking treatment in a paediatric endocrinology
Prevalence of ADHD: 13.3%
Agranat-Meged (2005) 26 adolescents in a tertiary referral centre for obesity
(Males: 13; mean age: 13.04 ±2.8 years ), all with
morbid obesity (BMI > 95 percentile)
57.7% of the subjects presented with ADHD diagnosed with
Fleming (2005) 75 women with severe obesity (BMI ≥35 kg/m
(mean age: 40.4 ± 7.25 years) referred for non surgical
treatment of obesity
26.7% of women reported impairing symptoms of ADHD in
both childhood and adulthood
Alfonsson (2012) 187 individuals (Males: 50; mean age: 44.28 ± 6.02 years)
with obesity, candidate for bariatric surgery
10% of the subjects presented with ADHD. ADHD
symptoms significantly correlated with anxiety, depression,
and disordered eating (“lack of control over eating”,“eating
alone because embarrassed”,“eating until feeling
uncomfortable”, and “feeling guilty after overeating”)
Gruss (2012) 116 patients (Males: 31; mean age: 44.28 ± 6.02 years)
candidate for bariatric surgery
12% of the patients screened positive for ADHD. Rates of
Binge Eating disorder did not differ between patients with
and without ADHD
Nazar (2012) 150 women (mean age: 38.9 ± years) Prevalence of ADHD: 28.3%. ADHD was significantly
correlated with more severe binge eating, bulimic
behaviors, and depressive symptoms severity
Cortese et al. BMC Psychiatry 2013, 13:286 Page 2 of 7
33 years, and matched comparisons (N = 111) without
childhood ADHD. They found that BMI and obesity rates
were significantly higher in individuals with childhood
ADHD vs. non ADHD comparisons (41.4% vs. 21.6%, re-
spectively), even after controlling for possible confounders
such as socio-economic status (SES) and comorbid psychi-
atric disorders associated with obesity, i.e., mood, anxiety,
and substance use disorders. However, anthropometric
data were not collected in childhood, which prevented the
authors from determining whether the association be-
tween childhood ADHD and weight status at follow-up in
adulthood was attributable to weight status in childhood
or whether it developed later. Using a dimensional ap-
proach (i.e., considering the intensity of each ADHD
symptom) rather than a categorical approach based on
the DSM-IV-TR nosography, Fuemmelar et al. 
found a significant linear relationship between the num-
ber of retrospectively reported symptoms of inattention
or hyperactivity/impulsivity in childhood and adulthood
BMI in a population based sample of 15,197 individuals
(National Longitudinal Study of Adolescent Health).
Extending such evidence, Cortese et al.  analyzed a
sample of 34,653 U.S. adults from the National Epide-
miologic Survey on Alcohol and Related Conditions and
found a significant association between the number of
symptoms of inattention, hyperactivity, or impulsivity
(retrospectively reported) in childhood and obesity in
adulthood. However, after controlling for SES and an
extensive set of psychiatric disorders, the association
held only in women, thus calling for future studies taking
into account possible gender differences. The retrospective
report of ADHD symptoms is a limitation of this study.
With regards to executive dysfunctions, there is an
emerging literature indicating their possible associ-
ation with overweigh/obesity. In a recent systematic
review  including 31 papers limited to children and
adolescents, Reinert and colleagues concluded that
inhibitory control, assessed with several neuropsycho-
logical tests, was the most consistently impaired execu-
tive function across studies. About 77% of the retained
studies in children and 73% of the papers relative to
adolescents with obesity reported a significant impair-
ment in this executive function. Additionally, scores
on neuropsychological tests assessing inhibitory con-
trol were significantly lower (p < 0.01) in children with
obesity than in normal weight comparisons, when
pooling data across studies. Another recent systematic
review  considering individuals across the lifespan
and using a different approach in the selection of the
papers, showed that decision making, planning and
problem solving were the most compromised domains,
although the authors note the high heterogeneity
across studies in the methodology and in the selection
of the neuropsychological tests.
Summarizing, there is increasing evidence that both
ADHD, at least considering samples of treatment-seeking
individuals, and deficits in executive functions, even in the
absence of a formal diagnosis of ADHD, may be associated
with obesity. Additionally, there is preliminary evidence
that ADHD may causally contribute to obesity/overweight.
However, an important aspect to note is that the impact of
ADHD or executive dysfunction on obesity outcome is
still underexplored. In the next section, we discuss the
preliminary evidence showing that ADHD or executive
dysfunction may represent an important barrier to suc-
cessful weight loss in patients with obesity during weight
loss programs. We also point out the clinical implications
of these findings, as well as possible future research direc-
tions in this emerging area of investigation.
Several possible dysfunctional behavioural pathways
associated with either ADHD (as a categorical diagno-
sis) or related neuropsychological deficits in executive
functions lead to hypothesize that impairing symptoms
of impulsivity, inattention or hyperactivity (the behavioural
core symptoms of ADHD) and/or related neurocognitive
impairment may be a barrier to successful weight loss
during treatment interventions for individuals with
First, it is possible that impulsivity and deficient neuro-
cognitive inhibitory control foster impulsive and dysregu-
lated eating behaviors, which, in turn, would hamper the
success of dietetic regimen. These abnormal eating behav-
iors include binge eating, “external eating”(i.e., eating in
response to food-related stimuli, regardless of the internal
state of hunger or satiety) and “emotionally-induced
eating”(i.e., excessive eating as a response to emotional
states), all of which have been related to obesity and
Second, another dysfunction related to impulsivity and
deficits in inhibitory control, namely altered reward sensi-
tivity, may also contribute to dysregulated eating behav-
iors. Indeed, a subset of individuals with ADHD present
with a preference for small immediate over larger delayed
rewards [29,32]. This could therefore hamper dietetic ef-
forts when considering eating-related rewards deriving
from appetizing foods.
Third, it has been noted that attention and related ex-
ecutive functions such as planning and organizational
skills are important for a successful adhesion to dietetic
regimen and regular physical exercise , both of which
underpin effective and sustained weight control.
The previous hypotheses of a correlation between
ADHD symptoms and/or executive function deficits
and abnormal eating start being supported by empirical
evidence. With regards to ADHD symptoms, Cortese
et al.  found a significant correlation between
Cortese et al. BMC Psychiatry 2013, 13:286 Page 3 of 7
inattentive and impulsive ADHD symptoms and binge
eating behaviors, even after controlling for comorbid
depression and anxiety, in a study of 99 consecutively
referred severe obese adolescents (12-17 years). By
means of structural equation modelling, Davis et al. 
found a significant correlation between ADHD symptoms
and abnormal eating behaviors (including binge eating
and emotionally-induced eating) in a sample of healthy
adult women (25-46 years). Using the same modelling,
Strimas et al.  confirmed these results also in a sample
of 145 non-clinical adult males.
There is also evidence that deficit in executive dysfunc-
tions are related to abnormal eating behaviors, although
causal relationship has not been tested. For example, in a
study of 55 women reporting weekly binge eating in the
absence of regular compensatory behaviors, Kelly et al.
 found a significant correlation between frequency of
binge eating behaviors and deficit in executive functions
such as flexibility in thinking and shifting attention. By
means of path analyses, Dempsey et al.  confirmed a
significant correlation between deficit in executive func-
tions and overeating behaviors in a sample of 135 individ-
uals from the community. This evidence has been
extended to young children. Pieper and Laugero  re-
cently reported a significant correlation between executive
function deficits, measured by means of child-completed
tasks and parental as well as teacher reports, and eating
in the absence of hunger in a sample of 29 preschool
children (3-6 years).
While the correlation of impulsivity and inattention
domains to abnormal eating behaviors associated with
obesity may be intuitive, one could think that the hyper-
active component of ADHD is not involved at all and,
actually, it may favour weight loss rather than weight
gain. However, it is well known that the motor hyper-
activity of ADHD is not constant. Actigraphic measures
have shown that motor hyperactivity is modulated by
situational variables and may be indistinguishable from
normal when there is sufficient stimulation. For ex-
ample, no significant differences in hyperactivity levels
between children with ADHD and healthy comparisons
have been detected while watching television, whereas
children with ADHD show significantly more hyper-
activity during classes at school ; it is important to
note that children with ADHD have also been shown to
watch more television than non ADHD children. Inter-
estingly, psychostimulant medications induce an in-
crease, rather than a decrease, and a normalization of
motor activity during physical education, where move-
ment is appropriate and expected . It is also possible
that excessive motor activity in the morning during
breakfast hampers a correct consumption of breakfast;
in turn, skipping breakfast has been shown as a risk
factor for weight gain and obesity . Additionally,
restlessness during lunch and dinner may decrease
regular food consumption during these structured mo-
ments, with inappropriate and excessive compensatory
calories intake outside meals. Therefore, we hypothesize
that the balance between the tendency to overeat in an
irregular way following irregular breakfast and meals,
from one side, and the inconstant energy expenditure
associated with motor hyperactivity in ADHD, on the
other side, may explain why ADHD hyperactivity con-
tributes to increase the risk of obesity.
So, if ADHD or related executive functions deficits
foster abnormal eating behaviors contributing to obesity,
is there evidence supporting that ADHD and executive
dysfunction also represent a barrier to effective and lasting
weight loss in individuals with obesity? This starts being
reported in the literature, although further and more
methodologically sound evidence is needed.
In an observational study of 215 adults with obesity in a
specialized clinics, Altfas  was the first to note that
those without comorbid ADHD achieved nearly twice the
BMI loss compared to patients with comorbid ADHD,
despite the fact that the latter engaged in more visits, thus
suggesting a pattern of “taking more time to accomplish
less”associated with ADHD. Afterwards, in a study of
adults involved in a behavioral weight loss program,
Pagoto et al.  confirmed that participants with ADHD
reported more previous weight loss attempts and lost less
weight than those who did not screen positive for ADHD.
Another recent study showed that patients presenting for
bariatric surgery (BS) with comorbid ADHD had signifi-
cantly more difficulties in following visits after BS than
those without comorbid ADHD .
Indirect support to the hypothesis that executive func-
tion deficit is a barrier to effective weight control is also
provided by a longitudinal prospective study by Speranza
et al.  who found that alexithymia was a significant
predictor of treatment outcome at 3-year follow-up in a
sample of youths with eating disorder. Indeed, alexithymia
is related to executive function deficits, as summarized
Given this preliminary literature, a crucial question is
whether treatment of ADHD and/or improvement in ex-
ecutive functions are also effective in decreasing/pre-
venting obesity in children with both conditions. There
is initial evidence indicating that the answer may be
In a study  of 242 individuals with a lengthy history
of weight loss failure consecutively referred for refractory
obesity, 78 patients (32.2%) screened positive for ADHD.
Of these, 65 started pharmacotherapy for ADHD with
psychostimulants, in addition to standard management for
weight loss, and were followed up for an average of 466
days. Those who refused pharmacological treatment or
who did not tolerate it for adverse events (n = 13) were
Cortese et al. BMC Psychiatry 2013, 13:286 Page 4 of 7
also followed up, serving as comparisons, and received
standard care for weight loss management. At follow-up,
individuals who received treatment lost 12.36% of their
initial weight, whereas comparisons gained an average of
2.78% (p < 0.001). A putative confounder in interpreting
these results is the possible anorexigenic effect that may
be associated with psychostimulant treatment. However,
appetite reduction was evident in the first 4–6weeksof
treatment, but then it diminished and vanished in most of
the subjects within 2 months. Therefore, the authors of
the study concluded that it is unlikely that the anorexi-
genic effect of psychostimulants contributed to the weight
loss at follow-up, after more than one year from the start
of the treatment. A limitation of this study is its design: al-
though the study was controlled, it was not randomized.
Indeed, since the pharmacological treatment for ADHD is
effective and is recommended in several guidelines, [6,9],
for ethical reason it was not possible to randomize partici-
pants either to pharmacological treatment or placebo. As
such, this study cannot provide high-level evidence. Al-
though a randomized study testing the effects on weight
of psychostimulants for ADHD would be challenging,
interestingly, there is preliminary evidence from a ran-
domized trial  suggesting that the training of executive
functions is highly effective to improve the outcome of
obesity. In this trial, Verbeken and coworkers assessed the
effects of executive functions training with video games
aimed at improving inhibitory control and working mem-
ory. They randomized 44 children (8-14 years) who were
in the final part of a 10- month inpatients treatment pro-
gram in an obesity centre to either 6-week executive func-
tions training or to standard care for weight control. At 8
weeks after the training, children in the training group
showed significantly better weight loss maintenance than
those in the standard care group.
If further methodologically sound studies confirm that
ADHD and/or related executive functions deficits are a
barrier to effective weight loss, it would be worthy for the
clinicians and professionals involved in the management
of obesity to screen for ADHD and impairment in execu-
tive functions. We note that professionals involved in the
treatment of obesity usually do not have an appropriate
knowledge of ADHD and related disorders. A systematic
screening and appropriate treatment of ADHD and/or
executive functions deficits might not only reduce the bur-
den of ADHD, but also improve the outcome of patients
with a past history of weight loss failure. This is particu-
larly relevant in terms of decreasing the stigma associated
with obesity. Unfortunately, a common belief manifested
not only by the lay public but also by some professionals is
that individuals with obesity may fail to succeed at weight-
loss programs due to their “laziness”. Inattention and
related impaired executive functions, as well as impulsivity
that hamper the appropriate adherence to a regular diet
regimen, might be mistakenly attributed to laziness and
“character problems”. Therefore, awareness that unsuc-
cessful weight loss may be due, at least in part, to neu-
rocognitive impairment could contribute to decrease
Future research in the field
We believe that the relationship between ADHD/executive
functions and obesity, as well as the impact of neurocogni-
tive impairment on weight loss management, is still in a
developing phase. While the cross-sectional relationship
between ADHD and obesity starts being well character-
ized from a clinical descriptive standpoint, further longitu-
dinal studies are needed to better assess the causal
relationship. Studies aimed at elucidating common neuro-
biological and genetics underpinnings are still in their in-
fancy (e.g., ) and need further attention. Perhaps even
more important in terms of implementation science would
be to assess, by means of rigorous randomized controlled
trials, the effects of ADHD treatment or executive func-
tions training on weight outcome in individuals enrolled
in weight loss programs. In particular, it would be highly
relevant to establish if early management of ADHD in
young children leads to further better obesity outcome
later on. However, given the challenges, from an ethical
standpoint, of conducting long-term randomized con-
trolled trials where participants are assigned either to an
effective treatment for ADHD or to placebo, longitudinal
studies comparing the weight outcome of obese children
treated with ADHD medications vs those who opt for non
pharmacological approaches or no treatment, matched for
baseline BMI and socio economic status, could provide
useful data. This design will likely require multi-center
recruitment. Research in such area is worthy and could
contribute to decrease the worldwide obesity epidemics.
Preliminary evidence suggests that comorbid ADHD and
deficits in executive functions are a barrier to a successful
weight loss in individuals involved in obesity treatment
programs. If further methodologically sound evidence
confirms this relationship, screening and effectively man-
aging comorbid ADHD and/or executive functions deficits
in individuals with obesity might have the potential to re-
duce not only the burden of ADHD but also the obesity
ADHD: Attention-Deficit/Hyperactivity Disorder; BMI: Body mass index;
SES: Socioeconomic status.
Dr. Cortese has received financial support to attend medical meetings from
Eli Lilly & Company (2008) and Shire Pharmaceuticals (2009-2010), and has
Cortese et al. BMC Psychiatry 2013, 13:286 Page 5 of 7
been co-investigator in studies sponsored by GlaxoSmithKline (2007), Eli Lilly
& Company (2008), and Genopharm (2009). He has served as scientific
consultant for Shire Pharmaceuticals (2009-2010). Drs. Comencini, Vincenzi,
Speranza, and Angriman declare no competing conflict of interest.
Dr. Cortese conceived and drafter the manuscript and approved the final
version to be submitted; Drs. Comencini, Vincenzi, Speranza, and Angriman
critically revised the first draft, contributed to the literature search, and
approved the final version to be submitted. All authors read and approved
the final manuscript.
Dr. Cortese is a post doctoral fellow at the Institute for Pediatric
Neuroscience, New York University, New York, NY, USA and at the Child
Neuropsychiatry Unit, Verona University, Italy. His research interests focus on
ADHD, in particular on the neurobiology and on the evidence-based
treatment of ADHD. Dr. Comencini is a resident in child psychiatry at the
Child Neuropsychiatry Unit, Verona University, Italy. Her research focuses on
the psychopathology of children with obesity. Dr. Vincenzi is a research
fellow at the Massachusetts General Hospital, Schizophrenia Clinical and
Research Program, Boston, MA, USA. Her research focuses on eating
disorders and schizophrenia. Dr. Speranza is a consultant at the Child and
Adolescent Psychiatry, Versailles General Hospital. Le Chesnay, France and a
researcher at the University of Versailles Saint-Quentin-en-Yvelines, Versailles,
France. His research focuses on eating disorders, ADHD, and personality
disorders. Dr. Angriman is a consultant at the Child Neurology and
Neurorehabilitation Unit, Department of Pediatrics, Central Hospital of
Bolzano, Italy. His research focuses on ADHD, obesity, and sleep disorders.
Dr. Cortese was supported by a “Marie Curie”grant for Career Development,
International Outgoing Fellowship, PIOF-253103 from the European
Child Neuropsychiatry Unit, G. B. Rossi Hospital, Department of Life Science
and Reproduction, Verona University, Verona, Italy.
Phyllis Green and
Randolph Cowen Institute for Pediatric Neuroscience, Child Study Center of
the NYU Langone Medical Center, New York, NY, USA.
General Hospital, Schizophrenia Clinical and Research Program, Boston, MA,
EA4047, University of Versailles Saint-Quentin-en-Yvelines, Versailles,
Child and Adolescent Psychiatry, Versailles General Hospital, Le
Child Neurology and Neurorehabilitation Unit, Department
of Pediatrics, Central Hospital of Bolzano, Bolzano, Italy.
Unità Autonoma di
Neuropsichiatria Infantile, Ospedale G.B . Rossi, P.le L.A. Scuro, 12, Verona
Received: 31 March 2013 Accepted: 15 July 2013
Published: 7 November 2013
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Cite this article as: Cortese et al.:Attention-deficit/hyperactivity disorder
and impairment in executive functions: a barrier to weight loss in
individuals with obesity? BMC Psychiatry 2013 13:286.
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