Attention-deficit/Hyperactivity Disorder: Associations

with Overeating and Obesity

Caroline Davis
Published online: 15 July 2010
# Springer Science+Business Media, LLC 2010
Abstract In the past decade, we have become increasingly
aware of strong associations between overweight/obesity
and symptoms of attention-deficit/hyperactivity disorder
(ADHD) in children, adolescents, and adults. This review
addresses the prevalence of the comorbidity and discusses
some of the mechanisms that could account for their
relationship. It is suggested that the inattentive and
impulsive behaviors that characterize ADHD could con-
tribute to overeating in our current food environment, with
its emphasis on fast food consumption and its many food
temptations. It is also proposedbased on the compelling
evidence that foods high in fat, sugar, and salt are as
addictive as some drugs of abusethat excessive food
consumption could be a form of self-medication. This view
conforms with the well-established evidence that drug use
and abuse are substantially higher among those with
ADHD than among the general population.
Keywords ADHD
.
Obesity
.
Addiction
.
Impulsivity
Introduction
Attention-deficit/hyperactivity disorder (ADHD) was origi-
nally seen as a neuropsychological disturbance of childhood
because the developmentally inappropriate signs of distract-
ibility, impulsiveness, and inattention that characterize
this condition typically appear before the age of 7 years.
Eventually, however, it became evident that for many
individuals, these symptoms did not remit and persisted into
adulthood in a significantly debilitating way [1]. This
recognition has since prompted the reconceptualization of
ADHD as a life span disorder. Although its etiology is not
fully understood, there is general agreement that a biological
component of the disorder relates to (dys)functioning of the
prefrontal cortex, processes typically known as executive
functions because they subserve reasoning, planning, inhi-
bition, and decision making [2]. Considerably less is known
about environmental and development factors (including in
utero events) that may contribute to ADHD symptoms, or
about geneenvironment effects that could influence the
disorders onset.
It is very well-established, however, that ADHD coexists
with a host of other clinical disorders. For example, major
depression, bipolar disorder, and generalized anxiety are
highly prevalent in those with ADHD [3], and in some
cases, the disorder is associated with antisocial behavior
and criminality [4]. A wealth of evidence also links ADHD
to addiction disorders such as drug abuse and alcoholism
comorbidities that are robust and bidirectional [5, 6].
Indeed, a recent familial risk analysis indicated that ADHD
and drug dependence share a common vulnerability profile
rather than present with independent modes of transmission
[7]. As both disorders have strong links to mesocortico-
limbic pathways, Biederman and colleagues [7] proposed
the conjoint involvement of brain dopamine activation and
its regulation of arousal, attention, and reinforcement.
In recent years, we have become increasingly aware of
strong links between ADHD and obesity [8, 9]. The first
studies to draw attention to this association were published
in 2002 [9, 10]. Both found a substantially higher than
expected prevalence of ADHD in adults receiving treatment
for obesity and an even greater occurrence (close to 50%
C. Davis (*)
York University,
343 Bethune College, 4700 Keele Street,
Toronto, Ontario M3J 1P3, Canada
e-mail: cdavis@yorku.ca
Curr Psychiatry Rep (2010) 12:389395
DOI 10.1007/s11920-010-0133-7
of the sample) in those with class III obesity (body mass
index >40 km/m
2
). The comorbid group also had more
clinic visits and longer treatment duration than their non-
ADHD counterparts [9]. Recent data from a large,
nationally representative sample of adults in the United
States also found that adult ADHD was associated with
a 1.6 OR of being overweight and a 1.8 OR of being
obese [11].
Since then, other studies have assessed the obesity
association in children and adolescents with ADHD. In
one study, the prevalence of overweight and obesity was
significantly greater in the ADHD sample compared with
age-matched population norms [12]. At first glance, these
results are rather counterintuitive, as a preeminent charac-
teristic of ADHD in children is physical restlessness and
hyperactivity. Moreover, only 14% of the Holtkamp et al.
[12] sample were receiving pharmacologic treatment for
ADHD at the time of assessment, and the remainder were
medication naive. Medication status is clearly an important
consideration, as weight loss and decreased appetite are
among the adverse effects of the common psychomotor
stimulants (e.g., methylphenidate) used to treat individuals
with ADHD. Therefore, when investigating the ADHD
obesity links, it is important to consider possible moderator
effects of pharmacologic treatment. Of relevance to this
issue, a large US study found that unmedicated children and
adolescents with ADHD had about 1.5 times the odds of
being overweight, while their medicated counterparts had
similar odds of being underweight [13]. These results
were partially confirmed by Ptacek et al. [14], who found
that the nonmedicated children with ADHD had a higher
percentage of body fat compared with the methylphenidate-
medicated boys and with population norms, although there
were no significant height or weight group differences.
What is unclear about these correlational findings in
children and adolescents is whether treatment status reflects
an appetite suppression effect of the medication or an
improvement in behavioral regulation and therefore health-
ier eating habits. Another possible explanation is that the
greater cognitive effort required to execute standard mental
tasks by those with untreated ADHD may foster hyperpha-
gia. This interpretation is based on evidence that mental
work substantially increases ad libitum food intake [15].
In summary, almost a decade of research has established
sound links between ADHD and obesity in adults, children,
and adolescents. It also appears that this relationship is not
attributable to sociodemographic factors that influence
peoples dietary patterns and opportunity for physical
activity [16]. However, one impediment to our understand-
ing of the ADHDobesity relationship has been the focus
on studies that have included only cases of ADHD that
meet full diagnostic criteria for the disorder. Such an
approach has the potential for confound due to the higher
likelihood of comorbidities in cases compared with con-
trols. There is also the greater possibility of medication
effects (as we have seen in the studies described previously).
One strategy that avoids the potential confounds of clinical
research is to examine associations among ADHD symptoms,
aspects of overeating, and body weight in healthy participants
from the general population. This approach is predicated on
the assumption that personality factors and symptoms of
disorder are best conceptualized dimensionally and occur with
normal variation in the general population [17].
Mechanisms of Association
During the past few years, research has moved from an
emphasis on comorbidity prevalence rates to attempts at
identifying the mechanisms whereby obesity and ADHD
present as overlapping conditions. In a current reviewand
as a way of explaining why the ADHDobesity connection
only appeared in the literature in 2002Cortese et al.
[18] claim that the association was simply overlooked
in the past. In my opinion, there is no evidence of neglect or
oversight in the obesity or ADHD areas of research. Indeed,
a more plausible explanation is that the association only
emerged in the past decade with sufficient frequency for it
to be recognized as a clinically relevant phenomenon. In
other words, current conditions have given rise to a
comorbidity that was less visible (or nonexistent) in earlier
decades because the environmental risk for its development
was largely absent. For example, we have seen an
increasingly high prevalence of obesity since the 1980s
[19] that is in stark contrast to earlier time periods. There
have also been dramatic changes in our food environment
during the past generation that have had a profound effect
on population weight gain [20]. An added factor is the
groundswell of scientific research and clinical interest in
identifying the causes of obesity in recent years. Of
particular relevance are the strong links that have been
established among impulsivity, the purchase of high-calorie
foods, overeating, and obesity [21]. These relationships
almost certainly have guided scientific investigations in the
direction of syndromes such as ADHD, a disorder in which
impulse control is a key diagnostic facet.
For several reasons, I would argue that the ADHD
obesity association is essentially a modern variant of the
ADHDdrug abuse comorbidity that has been recognized
and documented for many years [6]. In the following
sections, I offer support for the premise that ADHD and
obesity are interconnected by virtue of their respective
associations with addiction disorders, the former displaying
a proneness to and the latter occurring as a consequence of
addiction. Expressed slightly differently, their comorbidity
is the function of a shared diathesis whereby a predisposi-
390 Curr Psychiatry Rep (2010) 12:389395
tion to impulsive responding collides with a toxic food
environment that exploits this vulnerability. The outcome is
an increased probability of overeating and chronic weight
gain in those with symptoms of ADHD.
Binge Eating and Food Addiction
Nowhere in nature is there food as high in fat, sugar, and
salt (HFSS)and sometimes caffeineas we find in most
of the processed foods we consume on a daily basis. Such
palatable foods have the facility to activate the mesocorti-
colimbic pathways in the brain in a manner similar to other
addictive substances, and much more potently than would
occur for natural sources of energy [22]. Compelling
evidence indicates, based largely on well-controlled animal
research, that HFSS foods have the potential for abuse and
can lead to dependence in the manner of other condensed
and concentrated substances such as cocaine and heroin
[23, 24]. Like drugs of abuse, they have the ability to
alter brain mechanisms in ways that contribute to their
increasingly compulsive use [25, 26]. Their excessive
ingestion also seems to foster binge eating episodes,
symptoms of tolerance and withdrawal, and craving-like
behaviors [22, 27].
These findings, in addition to a host of testimonials from
those who suffer from compulsive overeating, have prompted
the claims that some cases of obesity may be the consequence
of a food addiction [27, 28]. For some individuals,
overeating is mostly a passive event that occurs without
much awareness and takes place in the form of frequent
snacking, eating calorie-dense meals, and selecting large
portion sizes. For others, however, it can be an excessively
driven activity. We have recently argued that binge eating
disorder (BED) is a particular pattern of overeating with the
strongest parallels to other addiction disorders and therefore
is the quintessential food addiction phenotype [27]. We
also believe that sound clinical and scientific evidence
supports this viewpoint. For example, Cassin and von
Ranson [29] found that 94% of their adult BED sample
described themselves as food addicts or compulsive
overeaters and met criteria for substance-dependence
disorder when the term substance referred to binge eating.
In the general population, binge eating has strong
connections with symptoms of ADHD, similar to the
longstanding associations of ADHD with addictive drug
use/abuse [30]. Clinical research also has demonstrated that
binge eating behaviors, such as those seen in BED or
bulimia nervosa, occur in patients with ADHD [31]. In
addition, BED seems to mediate the relationship between
ADHD and overweight/obesity [11]. Various causal mech-
anisms could link binge eating and ADHD. The symptoms
and hypodopaminergic functioning that characterize ADHD
seem to be ameliorated by dopamine-elevating behaviors
(hence the treatment success of psychomotor stimulants) and
may explain why some individuals succumb to illicit and/or
recreational drug taking. It is therefore plausible that
comfort foods could serve as a form of self-medication
in those with ADHD given their dopamine-activating
properties. If we accept that BED is appropriately concep-
tualized as a food addiction, then excessive HFSS food
consumption can be seen as just another form of drug abuse.
In other words, ADHD is a disorder defined by various
maladaptive traits, and drug use is just one of the behavioral
manifestations of the deficits associated with this condition.
Another possible causal mechanism is based on the well-
established evidence that cross-sensitization occurs from
one drug of abuse to anotherand that cross-sensitization
also occurs between intermittent sugar intake and addictive
drugs [22]. It may therefore be that stimulant treatment
(eg, Ritalin; Novartis, Basel, Switzerland) in early life
predisposes these individuals to the reinforcing properties
of sugar as they mature, thereby increasing their proneness
to obesity. Currently, I am unaware of any research that has
prospectively assessed whether those with childhood
ADHD and previously treated with stimulants are more
likely to be obese as adults compared with their nontreated
counterparts. Such a possibility provides an intriguing area
for future research.
Self-regulation Deficits
Among the impairing traits associated with obesity and
ADHDand another unifying thread in their comorbidity
is the centrality of high impulsivity in both conditions. This
term is used to describe a multidimensional and relatively
stable human personality trait that is characterized by 1) the
diminished ability to exhibit restraint when this is the most
advantageous and socially appropriate response in a particular
situation, 2) an enhanced tendency to approach and engage in
rewarding and pleasurable stimuli, and 3) impetuous respond-
ing without an appropriately adaptive concern for the future
consequences of ones actions.
We have learned that brain dopamine pathways play an
important regulatory role in the expression of this endo-
phenotype, which varies greatly in the general population
[32, 33]. A high level of impulsivity has been associated
with a wide range of psychological problems and dis-
turbances. For instance, it correlates positively and consis-
tently with drug use and abuse [34], binge eating [35],
and ADHD, for which it serves as one of the diagnostic
criteria for this disorder. In a recent and relevant prospec-
tive study, it was also found that low impulsivity predicted
decreases in body mass index percentile rank in children
from fifth to eighth grade. In other words, the self-controlled
(nonimpulsive) children seemed to be protected from weight
gain in their transition to adolescence [36].
Curr Psychiatry Rep (2010) 12:389395 391
The impulsivity that characterizes ADHD is almost
certainly a key factor mediating the relationship between
this disorder and obesity. However, the mechanisms by
which impulsivity contributes to weight gain are less clear.
Nowadays, in the face of an overabundance of high-calorie
snacks and meals, effortful control of food intakewhat is
colloquially called willpoweris essential for the mainte-
nance of a healthy body weight. Historically, however, such
self-regulated restraint would have been rather antithetical
to the strong appetitive drives that fostered optimal fitness
during most of our evolution. In the world of ready-made
meals and cafeteria dining, healthy food choices are clearly
not the easiest option. They typically require forethought
and planning, extended time for preparation, and the ability
to show steadfast control when faced with tempting and
quicker alternatives. A better understanding of the natural
human variation in self-regulated behaviors is clearly a way
forward in explaining why some individuals are prone
to chronic overeating while others, living in the same
environment, can eat moderately and maintain a healthy
body weight [37].
Impulsivity has been a difficult construct to study
because it involves at least two identifiable cognitive/
emotional processes: reward-driven behaviors on the one
hand and those characterized by poor inhibition on the
other. It has also generated many measures and assessment
devices that are not always highly correlated [38]. Inhibitory
control deficits, seen as impulsive responding and inatten-
tion, are largely regulated by the prefrontal cortex, which
undergoes major developmental changes from childhood to
adolescence [39]. Impairment in these processes is typical of
those with ADHD. Verbeken et al. [40] also found that
overweight children showed less efficient executive inhibi-
tory control and more reward-directed behavior as assessed
by performance-based tasks. In addition, in a recent study,
we demonstrated poor decision making and diminished
ability to delay gratification in two groups of obese adults
those with and those without BED [37]. Although the two
obese groups did not differ from each other, they were both
significantly impaired compared with an age- and gender-
matched group of normal weight adults.
To our knowledge, only two studies have assessed
whether impulsivity predicts success in a weight reduction
program [41, 42]. In the more recent and larger study, high
impulsivity predicted greater weight loss in adolescents, but
not in children. Not only is this finding rather counterin-
tuitive, but it is in direct contrast with the former study,
which showed, as one would expect, that low-impulsive
children lost more weightfindings that also mesh with
adult research obtained from patients at a bariatric treatment
center [9]. At this point, however, we must conclude that
the role of impulsivity in weight loss and weight loss
maintenance is still inconclusive given the very few
systematic treatment studies that have been published.
Future replication studies and more detailed investigations
with stratified analyses based on age, gender, and other
relevant covariates are needed before firm conclusions can
be drawn.
Environmental Influences
Twin and adoption studies indicate that genetic factors
make a large contribution to the etiology of ADHD, with
estimates of heritability ranging from 60% to 91% [43]. It is
also generally agreed that complex mental disorders such as
ADHD are the result of a reciprocity between genetic
factors and environmental influences (G E). To date,
however, the manner in which susceptibility genes interact
with environmental risk factors is not clearly understood.
Essentially, there are two broad possibilities to describe
how a G E interplay could come about. On the one hand,
environmental factors only lead to an adverse outcome in
the presence of a specific genetic makeup; on the other
hand, an individual with a susceptible genetic makeup will
only develop the adverse outcome if additional environ-
mental pathogens are present [44]. In the case of the
ADHDobesity links, the latter seems the more probable
causal route in that the association only emerged when the
food environment changed dramatically during the past
generation or so. That the exponential increase in the
prevalence of obesity has also occurred in a relatively short
period of time highlights the importance of the interaction
between the ADHD genotype and the toxic food culture in
which it began to find itself. Those with the greatest genetic
vulnerability are those who are likely to show the greatest
weight gain, whereas those with genetic resistance tend to
remain relatively weight stable [44].
Prenatal Drug Use
ADHD and its subsequent developmental course, which
shows both continuity and change, are influenced by
various pre- and perinatal, biological, and psychosocial
environmental risk factors. Some that have stood the test of
replication include the deleterious influence of maternal
smoking and alcohol consumption during pregnancy, as
well as low infant birth weight/prematurity [45]. Fetal
alcohol syndrome was first identified in 1973 as a condition
with severe birth defects, including facial disfiguration and
mental retardation, and was associated with heavy maternal
alcohol use during pregnancy. However, it was not until the
1980s that the US Surgeon General issued an advisory
recommending that women abstain from drinking alcohol
during pregnancy, and almost a decade later before health
warning labels were added to alcoholic beverage containers
392 Curr Psychiatry Rep (2010) 12:389395
[46]. During the late-1980s, it was estimated that about
30% of American women were still drinking alcohol during
pregnancy despite these warnings, so one can only assume
the rates were considerably higher before that time,
especially with the growing visibility of female alcoholism
in the decades following World War II [47].
The neurobehavioral deficits found in children with
prenatal exposure to alcoholwhat are now called fetal
alcohol spectrum disorders (FASDs) or alcohol-related
neurodevelopmental disorderinclude symptoms of
inattention, restlessness, impulsivity, antisocial behavior,
and a diminished ability to anticipate future consequences.
Clearly, these deficits vary in severity, and in cases of mild
symptomatology, there may not be any formal diagnosis at
all. To some extent, the severity of symptoms may be a
dose-dependent consequence of the extent and timing of the
mothers alcohol intake. It is now generally agreed that
even relatively small amounts of alcohol can cause fetal
impairments in some cases.
What is instantly evident is the remarkable similarity of
FASD symptoms to those of ADHD. Indeed, a substantially
high proportion of children with prenatal alcohol exposure
as many as 70%are also diagnosed with ADHD[48]. Some
recent studies have compared FASD and ADHD and
reported certain qualitative differences in their respective
types of attention problems [49]. However, such studies are
problematic and inconclusive because of the high dual
diagnosis between FASD and ADHD and therefore the
inability to compare pure groups of each condition.
Moreover, few if any studies of ADHD take account of
those with and without prenatal alcohol exposure. It is
entirely possible that maternal alcohol use, which was not
significantly curtailed until a decade or so ago, is one
environmental causal contributor to this disorder and not
merely a condition with pronounced symptom similarities.
Prenatal exposure may have a sensitizing drug influence on
the developing fetus and may also account for the higher
than expected drug use and abuse in those with ADHD.
Prenatal Dietary Factors
Using data collected from three affluent Scandinavian
societies, a prospective study showed for the first time that
maternal overweight and obesity increased the risk of
having a child with ADHD symptoms compared with
mothers who were normal weight at the time they became
pregnant [50]. Interestingly, these findings persisted after
controlling for babys birth weight, maternal age, and
mothers smoking status in the statistical analyses. However,
the authors speculated that perhaps the relationship occurred
because a genetic predisposition accounted for both the
mothers weight status and the subsequent ADHD symptoms
in the child.
To test this prediction and to ascertain whether the
previous associations would exist independent of other
potential causal risk factors (eg, parental ADHD symptoms),
a large replication and extension study was carried out of
prepregnancy obesity and offspring symptoms of ADHD.
Again it was found that children of obese mothers had a
twofold increase in teacher-rated inattention scores com-
pared with children of normal weight mothers [51]. These
inattentive children also displayed significantly greater
negative emotionality. Arguments against the possibility
that a common genetic predisposition linked maternal
weight and child ADHD symptoms rest on the fact that
the associations remained statistically significant after
controlling for ADHD symptoms in both parents. The
author concluded that maternal prepregnancy obesity is not
merely an artifact of other influences that may coexist with
mothers weight status.
While Rodriguez [51] proposed certain mechanisms
that could account for the associations observed in her
study, in my view, one possibility of considerable relevance
to the ADHDobesity link was overlooked. Excess body
weight is in large part the result of high fat consumption,
whereas high sugar intake seems to be responsible for
producing addictive-like behaviors such as cravings, with-
drawal, and compulsive intake [24]. In our current food
environment, with its superfluity of highly palatable foods,
mothers who are overweight and obese are likely to
consume larger and more frequent quantities of HFSS
foods than normal weight mothers. As noted previously,
good evidence indicates that these foods can cause brain
neurochemical responses similar to those caused by other
drugs of abuse. Therefore, highly processed and calorie-
dense food consumed in abundance during pregnancy could
produce deleterious outcomes in the unborn child in the
same way that we see in the offspring of mothers who
smoke and/or drink alcohol during pregnancy. In other
words, the excessive ingestion of HFSS foods could
produce what I will loosely call a fetal sugar spectrum
disorder, with consequences that are not dissimilar to those
seen in the offspring of mothers who drank alcohol and
smoked nicotine during pregnancy.
Conclusions
I am aware of only one study that has examined the effects
of treating ADHD symptoms in obese individuals who are
attempting to lose weight. Levy and colleagues [52]
recently reported the results of a longitudinal investigation
in which they observed obese patients with newly diag-
nosed ADHD for more than a year following pharmaco-
logic treatment for the disorder. Significant weight loss was
noted in these patients compared with an untreated control
Curr Psychiatry Rep (2010) 12:389395 393
group, who actually gained weight during the same time
period. The authors also found that treating symptoms of
ADHD with medication improved the mental and physical
health and the quality of life of those who were obese.
Although the appetite-suppressing effects of the medication
appeared to diminish after a few months, patients continued
to lose weight and reported improvements in self-
directedness and an increased capacity for persistence.
They also reported that they no longer used food for self-
medication purposesthat is, to restore energy or to focus
attention. Importantly, binge eating diminished very sub-
stantially or stopped altogether in these patients.
This study was the first to target ADHD in the treatment
protocol and therefore has important implications for the
management of obesity and its adverse health consequences.
Although surgical procedures such as laparoscopic banding
and gastric bypass are increasingly popular options for
handling refractory obesity, their success depends on adhering
to strict postoperative dietary instructions following the
treatment.
Based on clinical observation, Levy and colleagues
[52] claim that obese patients with comorbid ADHD are
less able to comply with postsurgical recommendations
than others; therefore, careful screening of obese patients
seeking surgical treatment is strongly advised.
Disclosure No potential conflict of interest relevant to this article
was reported.
References
Papers of particular interest, published recently, have been
highlighted as:
Of importance
Of major importance
1. Barkley RA, Fischer M, Smallish L, et al.: The persistence of
attention-deficit/hyperactivity disorder into young adulthood as a
function of reporting source and definition of disorder. J Abnorm
Psychol 2002, 111:279289.
2. Walshaw PD, Alloy LB, Sabb FW: Executive function in pediatric
bipolar disorder and attention-deficit hyperactivity disorder: in
search of distinct phenotypic profiles. Neuropsychol Rev 2010,
20:103120.
3. Faraone SV: The scientific foundation for understanding attention-
deficit/hyperactivity disorder as a valid psychiatric disorder. Eur
Child Adolesc Psychiatry 2005, 14:110.
4. Thapar A, Langley K, ODonovan M, et al.: Refining the attention
deficit hyperactivity disorder phenotype for molecular genetic
studies. Mol Psychiatry 2006, 11:714720.
5. Fuemmeler BF, Kollins SH, McClernon FJ: Attention deficit
hyperactivity disorder symptoms predict nicotine dependence and
progression to regular smoking from adolescence to young
adulthood. J Pediatr Psychol 2007, 32:12031213.
6. Golden SM: Does childhood use of stimulant medication as a
treatment for ADHD affect the likelihood of future drug abuse and
dependence? A literature review. J Child Adolesc Subst Abuse
2009, 18:243258.
7. Biederman J, Petty CR, Wilens TE, et al.:. Familial risk analyses
of attention deficit hyperactivity disorder and substance use
disorders. Am J Psychiatry 2008, 165:107115.
8. Agranat-Meged AN, Deitcher C, Goldzweig G, et al.: Childhood
obesity and attention deficit/hyperactivity disorder: a newly
described comorbidity in obese hospitalized children. Int J Eat
Disord 2005, 37:357359.
9. Altfas JR: Prevalence of attention deficit/hyperactivity disorder
among adults in obesity treatment. BMC Psychiatry 2002, 2:18.
10. Fleming J, Levy L: Eating disorders in women with AD/HD. In
Gender Issues and AD/HD: Research, Diagnosis, and Treatment.
Edited by Quinn PO, Nadeau KG. Silver Springs, MD: Advantage
Books; 2002:411426.
11. Pagoto SL, Curtin C, Lemon SC, et al.: Association between
adult attention deficit/hyperactivity disorder and obesity in the US
population. Obesity 2009, 17:539544. Data from a large sample
of US residents indicated that adult ADHD was associated with
about a 1.5 OR of being overweight and a 1.8 OR of being obese.
This was the first population-based study to examine these
relationships.
12. Holtkamp K, Konrad K, Muller B, et al.: Overweight and obesity
in children with attention-deficit/hyperactivity disorder. Int J Obes
2004, 28:685689.
13. Waring ME, Lapane KL: Overweight in children and
adolescents in relations to attention-deficit/hyperactivity disorder:
results from a national sample. Pediatrics 2008, 122:e1e6. Data
from a large, nationally representative sample in the United States
found that among unmedicated children and adolescents with
ADHD, there was a 1.5 times the odds risk of being overweight.
Their medicated counterparts had 1.6 times the odds of being
underweight compared with aged-matched healthy controls.
14. Ptacek R, Kuzelova H, Pacit I, et al.: ADHD and growth:
anthropometric changes in medicated and non-medicated ADHD
boys. Med Sci Monit 2009, 15:CR595CR599.
15. Riverin M, Tremblay A: Obesity and ADHD. Int J Obes 2009,
33:945.
16. Chen AY, KimSE, Houtrow AJ, et al.: Prevalence of obesity among
children with chronic conditions. Obesity 2009, 18:210213.
17. Claridge G, Davis C: Personality and Psychological Disorders.
London: Arnold; 2003.
18. Cortese S, Angriman M, Maffeis C, et al.: Attention deficit/
hyperactivity disorder (ADHD) and obesity: a systematic review
of the literature. Crit Rev Food Sci Nutr 2008, 48:524537. This
paper provides an early review of the links between obesity and
ADHD and speculates on possible mechanisms to account for this
association. The review is limited to studies in which individuals
received a formal diagnosis of ADHD.
19. Bray GA, Nielsen SJ, Popkin BM: Consumption of high-fructose
corn syrup in beverages may play a role in the epidemic of
obesity. Am J Clin Nutr 2004, 79:537543.
20. Bray GA: Fructose: should we worry? Int J Obes 2008, 32:S127S131.
21. Nederkoorn C, Guerrieri R, Havermans RC, et al.: The interactive
effect of hunger and impulsivity on food intake and purchase in a
virtual supermarket. Int J Obes 2009, 33:905912.
22. Avena NM, Rada P, Hoebel BG: Evidence for sugar addiction:
behavioral and neurochemical effects of intermittent, excessive
sugar intake. Neursci Biobehav Rev 2008, 32:2039. This paper
presents compelling evidence from controlled laboratory animal
research for the argument that sugar is a potentially addictive
substance.
23. Ifland JR, Preuss HG, Marcus MT, et al.: Refined food addiction: a
classic substance use disorder. Med Hypotheses 2009, 72:518526.
24. Avena NM, Rada P, Hoebel BG: Sugar and fat bingeing have notable
differences in addictive-like behavior. J Nutr 2009, 139:623628.
394 Curr Psychiatry Rep (2010) 12:389395
25. Grigson PS: Like drugs for chocolate: separate rewards modulated
by common mechanisms. Physiol Behav 2002, 76:389395.
26. Spring B, Schneider K, Smith M, et al.: Abuse potential of
carbohydrates for overweight carbohydrate cravers. Psychophar-
macology 2008, 197:637647.
27. Davis C, Carter JC: Compulsive overeating as an addiction
disorder: a review of theory and evidence. Appetite 2009, 53:18.
This paper presents compelling evidence that some forms of
overeating (eg, binge eating) can be conceptualized as an
addiction disorder. This argument has significance for the well-
established links between obesity and ADHD.
28. Gearhardt AN, Corbin WR, Brownell KD: Food addiction. An
examination of the diagnostic criteria for dependence. J Addict
Med 2009, 3:17.
29. Cassin SE, von Ranson KM: Is binge eating experienced as an
addiction? Appetite 2007, 49:687690.
30. Davis C, Levitan RD, Smith M, et al.: Associations among
overeating, overweight, and attention deficit/hyperactivity disorder: a
structural equation modeling approach. Eat Behav 2006, 7:266274.
31. Cortese S, Bernardina BD, Mouren M-C: Attention-deficit/
hyperactivity disorder (ADHD) and binge eating. Nutr Rev
2007, 65:404411.
32. Limosin F, Romo L, Batel P, et al.: Association between dopamine
receptor D3 gene BalI polymorphism and cognitive impulsiveness
in alcohol-dependent men. Eur Psychiatry 2005, 20:304306.
33. Ondo WG, Lai DJ: Predictors of impulsivity and reward seeking
behavior with dopamine agonists. Parkinsonism Relat Disord
2008, 14:2832.
34. Verdejo-Garcia A, Bechara A, Recknor EC, et al.: Negative emotion-
driven impulsivity predicts substance dependence problems. Drug
Alcohol Depend 2007, 91:213219.
35. Davis C, Patte K, Levitan RD, et al.: A psychogenetic study of
associations between the symptoms of binge eating disorder and
those of attention deficit (hyperactivity) disorder. J Psychiatr Res
2009, 43:687696. This study demonstrated that symptoms of
ADHD were strongly associated with obesity in a nonclinical
community sample of adult men and women.
36. Duckworth AL, Tsukayama E, Geier AB: Self-controlled children
stay leaner in the transition to adolescence. Appetite 2010,
54:304308.
37. Davis C, Patte K, Curtis C, Reid C: Immediate pleasures and
future consequences: a neuropsychological study of binge eating
and obesity. Appetite 2010, 54:208213. Decision-making deficits
and a diminished ability to delay gratification were found in obese
womenwith and without BEDcompared with an age-matched
group of normal weight women.
38. Dawe S, Loxton, N: The role of impulsivity in the development of
substance use and eating disorders. Neurosci Biobehav Rev 2004,
28:343351.
39. Drechsler R, Rizzo P, Steinhausen HC: Decision-making on an
explicit risk-taking task in preadolescents with attention-deficit/
hyperactivity disorder. J Neural Transm 2008, 115:201209.
40. Verbeken S, Braet C, Claus L, et al.: Childhood obesity and
impulsivity: an investigation with performance-based measures.
Behav Change 2009, 26:153167.
41. Nederkoorn C, Jansen E, Mulkens S, et al.: Impulsivity predicts
treatment outcome in obese children. Behav Res Ther 2006,
45:10711075.
42. Pauli-Pott U, Albayrak O, Hebebrand J, et al.: Does inhibitory
control capacity in overweight and obese children and adolescents
predict success in a weight-reduction program? Eur Child Adolesc
Psychiatry 2010, 19:135141.
43. Thapar A, ODonovan M, Owen MJ: The genetics of attention deficit
hyperactivity disorder. Hum Mol Genet 2005, 14:R275R282.
44. Wermter A-K, Laucht M, Schimmelmann BG, et al.: From nature
versus nurture, via nature and nurture, to gene x environment
interaction in mental disorders. Eur Child Adolesc Psychiatry
2010, 19:199210.
45. Thapur A, Langley K, Asherson P, Gill M: Gene-environment
interplay in attention-deficit hyperactivity disorder and the
importance of a developmental perspective. Br J Psychiatry
2007, 190:13.
46. Grant TM, Huggins JE, Sampson PD, et al.: Alcohol use before
and during pregnancy in western Washington, 19892004:
implications for the prevention of fetal alcohol spectrum disorders.
Am J Obstet Gynecol 2009, 278:e1e8.
47. Golden J: An argument that goes back to the womb: the
demedicalization of fetal alcohol syndrome, 19731992. J Soc
Hist 1999, 33:269298.
48. Greenbaum RL, Stevens SA, Nash K, et al.: Social cognitive
and emotional processing abilities of children with fetal alcohol
spectrum disorders: a comparison with attention deficit hyper-
activity disorder. Alcohol Clin Exp Res 2009, 33:16561670.
49. Kooistra L, Crawford S, Gibbard B, et al.: Differentiating
attention deficits in children with fetal alcohol spectrum disorder
or attention-deficit-hyperactivity disorder. Dev Med Child Neurol
2010, 52:205211.
50. Rodriguez A, Miettunen J, Henrikson TB, et al.: Maternal
adiposity prior to pregnancy is associated with ADHD symptoms
offspring: evidence from three prospective pregnancy cohorts. Int
J Obes 2008, 32:550557.
51. Rodriguez A: Maternal pre-pregnancy obesity and risk for
inattention and negative emotionality in children. J Child Psychol
Psychiatry 2010, 51:134143. Prepregnancy overweight/obesity
was associated with a twofold increase in inattention symptoms in
kindergarten children even after controlling for parental ADHD
symptoms.
52. Levy LD, Fleming JP, Klar D: Treatment of refractory obesity
in severely obese adults following management of newly
diagnosed attention deficit hyperactivity disorder. Int J Obes
2009, 33:326334. This paper concludes that treatment of ADHD
with psychomotor stimulant medication is associated with
significant long-term weight loss in severely obese adults with a
lengthy history of weight loss failure.
Curr Psychiatry Rep (2010) 12:389395 395
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