Curr Obes RepDOI 10.1007/s13679-012-0012-0
OBESITY TREATMENT (AM SHARMA, SECTION EDITOR)
Attention Deficit/Hyperactivity Disorder and the ClinicalManagement of Obesity
Sherry Pagoto & Carol Curtin & Bradley M. Appelhans &Miguel Alonso-Alonso
# Springer Science+Business Media, LLC 2012
Abstract Attention deficit/hyperactivity disorder (ADHD)
pharmacological treatment, exercise, and cognitive behavior
has been associated with increased risk for obesity and
therapy. ADHD is a barrier to the clinical management of
obesity treatment failure. The present paper discusses how
obesity and more research is needed to further understand
features of ADHD, including inattention, reward sensitivity,
the link between ADHD and obesity. Effective treatment
and impulsivity, may impact obesity risk and have implica-
approaches are needed given the significant difficulty
tions for the management of obesity. In addition, we review
patients with ADHD encounter in their attempts to regulate
emerging research on how obesity may contribute to brain
their weight in the context of an obesogenic environment.
changes that are associated with ADHD-like symptoms.
Finally, suggestions for improving the clinical management
Keywords ADHD . Attention deficit/hyperactivity
of obesity in patients with ADHD are discussed, including
disorder . Obesity . Impulsivity . Treatment
Division of Preventive and Behavioral Medicine,Department of Medicine,University of Massachusetts Medical School, 55 Lake Avenue
Attention deficit/hyperactivity disorder (ADHD) is a neuro-
behavioral disorder, essential features of which include a
persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than typically
C. CurtinEunice Kennedy Shriver Center, Department Family Medicine
observed in individuals at a comparable level of develop-
& Community Health, University of Massachusetts
ment. The Diagnostic and Statistical Manual 4th edition
Medical School, 200 Trapelo Road, Waltham, MA 02452, USA
(DSM-IV)  specifies that these symptoms must have
persisted for at least 6 months, originated before the age of
7 years, and impairment is present in two or more settings.
Preventive Medicine, Rush Medical College, 1700 W. Van Buren,
The DSM-IV describes three subtypes of ADHD: 1) inat-
tentive type; 2) hyperactive-impulsive type; and 3) com-
bined type. ADHD has been shown to persist into
adulthood in half of children with ADHD and affects
Neurology, Harvard Medical School, Boston, USA
over 9 million US adults [An association between
ADHD and obesity is well documented both in population
Berenson-Allen Center for Noninvasive Brain Stimulation,
In addition to ADHD being linked to greater risk for
obesity, evidence is also emerging that ADHD may pose asignificant barrier to the management of obesity [In
the present paper we discuss the neurocognitive features of
Division of Cognitive Neurology, Beth Israel Deaconess MedicalCenter, 330 Brookline Avenue, Ks-158, Boston, MA 02215, USA
ADHD that may lead to obesogenic behavior and affect the
patient’s ability to engage in the self-management skills that
eating might serve a “self-medicating” function for
are instrumental to weight control. Treatment strategies for
some individuals with ADHD [Given that ADHD
patients with comorbid ADHD and obesity are discussed as
is generally characterized by reward sensitivity, obese
well as future directions for research on the clinical man-
adults with ADHD may be more sensitive to rewards relative
agement of obesity in the patient with ADHD.
to their obese counterparts without ADHD, which mightmanifest in eating pathology. For example, Davis et al.
] found that individuals with ADHD were more
Inattention, Reward Sensitivity, and Impulsivity May
likely to meet criteria for “food addiction” than those
without ADHD. Similarly, binge eating disorder has beenshown to play a mediating role in the relationship between
Some research has explored neurocognitive features of
ADHD, including inattention, reward sensitivity, and impul-
Impulsivity is another common feature of ADHD that has
sivity, to determine the extent to which these problems are
implications for obesogenic behavior and possibly risk for
associated with obesity and/or interfere with the ability to
obesity. Although it is a multifaceted construct, impulsivity
lose weight. Inattention, a hallmark of ADHD, refers to
can simply be characterized as action without foresight [
distractibility, reduced ability to sustain attention, and sus-
Some evidence suggests that people high in impulsivity are
ceptibility to interference ]. Inattention may adversely
prone to overeating, weight gain –and obesity [
impact the individual’s capacity to execute goal-directed
Among 228 adolescent girls with ADHD, impulsivity was a
dietary and physical activity behaviors and the ability to
much stronger predictor of eating pathology than inatten-
regulate one’s weight resulting in irregular eating habits
tion, although both inattentive and impulsive ADHD sub-
and poor adherence. Inattention might also affect awareness
types were equally likely to be obese ]. This suggests that
of internal hunger and satiety cues, especially when the
impulsivity might be instrumental in the observed associa-
individual is engaged in other activities , This could
tion between ADHD and binge eating disorder ,
result in externally cued eating, which tends to be associated
Greater impulsivity could also lead to greater difficulty
with overeating. Inattention may also interfere with other
inhibiting the consumption of high energy–dense palatable
behaviors critical to successful weight loss, such as meal
foods, especially in response to stress and other cues, as
planning, implementation of specific behavioral skills (eg,
described by Lowe et al. [Cognitive models of ADHD
consistently keeping a diet diary), following through with
emphasize the role of inhibitory control as a critical require-
planned exercise, and the ability to detect changes in food
ment for other executive functions that subserve self-
portion sizes ]. In some studies, the inattentive type of
regulation and goal-directed behavior [. Consuming a
ADHD has been found to be more prevalent than the hy-
healthy diet in an obesogenic environment or restricting intake
peractive/impulsive type in obese samples
to lose weight can be thought of as goal-oriented behavior,
Additional research is needed to further describe specifically
thus any impairment in inhibitory control could hijack their
how inattention affects one’s ability to regulate their weight,
optimal execution. The increasingly obesogenic environment
as well as interventions that could be helpful in this contest
may be particularly challenging for people high in impulsivity
(eg, cues/reminders, frequent feedback, etc.).
(ie, low inhibitory control), given the omnipresence of food
Reward sensitivity is a biologically based personality
cues. Supporting this contention is a study showing that
trait originally described by Gray ] that may stem from
impulsivity was associated with greater food consumption in
hypo- or hyper-reactivity to reward at the neurobiological
an environment characterized by high food variety, but not
level. High “reward sensitivity” describes individuals who
in one characterized by monotonous foods . This
are especially sensitive to rewards in their environment,
impulsivity-by-environment interaction suggests that persons
while diminished reward sensitivity describes individuals
with ADHD might be disproportionately vulnerable to obeso-
who are especially insensitive to rewards in their environ-
ment. Recent evidence has emerged that individuals with
Impulsive individuals also appear to have less inhibitory
ADHD, particularly those with the inattentive type, are
control during hunger, as evidenced in a study that found
highly reward sensitive ]. Reward sensitivity is implicat-
that impulsive individuals consumed more food when ex-
ed in appetitive motivation, such that it may mediate
posed to highly palatable food than their less impulsive
responses to appetitive stimuli, including drugs, food, and
counterparts under conditions of hunger, but not under con-
sex . Mesolimbic dopaminergic (DA) processes are
ditions of satiety [These findings suggest that restrictive
central to reward sensitivity , ], with greater sensitivity
diets in the context of an obesogenic environment might be
to reward at the behavioral level being associated with either
especially challenging for people with ADHD. Accordingly,
a hyper- or hyporesponsive mesolimbic DA system .
Nederkoorn et al. reported that impulsivity predicted less
Because palatable foods enhance dopamine activation,
weight loss following treatment in children.
One particular manifestation of impulsivity, delay
Chicken or the Egg? Obesity May Produce ADHD-Like
discounting, seems particularly relevant to understanding
the association between ADHD and obesity. Delay dis-counting reflects the degree to which an individual
Aside from common underlying mechanisms between
undervalues rewards with increasing delays [For
ADHD and obesity and the impact that ADHD may have
both humans and animals, immediate rewards have a
on weight gain and obesity, there is some, albeit limited,
disproportionately strong influence on our decisions
evidence for the possibility that obesity contributes to the
and actions. Less valuable immediate rewards (eg, $200
development of ADHD-like symptoms. For example, short-
today) can often be preferred to more valuable future
term experimental overfeeding in lean humans has been
rewards (ie, $240 in 3 months). A number of studies
shown to lead to brain changes including an increase in
have found steeper delay discounting among children
the activation of the default mode network (DMN), a set
and adults with ADHD relative to controls
of areas that are active typically at rest and seem to be
These effects appear to be more robust among those with
involved in self-referential cognition and introspection
the hyperactive/impulsive or combined subtypes ,
]. This effect goes in the direction of ADHD-like brain
which is consistent with the conceptualization of delay
changes, characterized by DMN overactivation and difficul-
discounting as a facet of impulsivity. The tendency to dis-
ty in suppressing this network during effortful tasks [
count delayed rewards steeply is associated with several con-
Additional evidence comes from a study showing
ditions in which impulsivity and hyper-responsivity to
improvements in attention/executive functioning in obese
appetitive cues are thought to play an etiological role, such
subjects following weight loss ]. Animal studies provide
as compulsive gambling, tobacco use, and drug addiction
more direct evidence in support of this association. Diet-
induced obesity in a swine model leads to changes in brain
Recently, delay discounting has also been linked to
perfusion that are selectively located in areas implicated in
eating behavior and obesity [•, For example, obese
ADHD, such as the dorsolateral prefrontal cortex, and the
women show steeper discounting of delayed rewards than
amount of weight gain negatively correlates with perfusion
normal weight women , and greater delay discounting
in these locations [Lastly, a brain effect of obesity is
has been associated with higher intake of palatable food
supported by biological plausibility, as obesity-related
among lean, overweight, and obese subjects who are
changes can affect neuroplasticity and cognitive function
most sensitive to the rewarding properties of food [
through different mechanisms (eg, the release of proinflam-
It has been hypothesized that a greater predisposi-
matory substances to the systemic circulation) Alto-
tion for delay discounting would likely manifest as
gether, the evidence suggests that obesity may worsen
heightened sensitivity to the immediate reward from
ADHD symptomatology or facilitate the development of
palatable food and decreased valuation of the long-
ADHD-like symptoms via brain changes; however, direct
term rewards associated with a healthy diet and weight
evidence for this association in humans is not available yet
maintenance, which in combination would contribute to
and future studies are warranted. To the extent that obesity-
obesity [, The neurobiological mechanisms un-
induced brain changes impair weight control, patients with
derlying individual differences in delay discounting have
long-standing obesity and more severe obesity may be the
also been linked to the neurocognitive deficits in ADHD
most treatment resistant. Research is needed to determine
and the brain regulation of eating behavior. Specifically,
whether these brain changes are reversible via weight loss
alterations in mesolimbic dopamine function have been
and/or lifestyle changes (eg, caloric restriction, exercise).
associated with a stronger preference for immediaterewards in the context of delay discounting tasks, palat-able food intake, and ADHD ]. In contrast, “exec-
Obesity Management in the Patient with ADHD
utive” brain regions found to be altered in ADHD, particularlythe lateral prefrontal cortex, appear to play a critical role in
Because the association between ADHD and obesity has
inhibiting impulsive behaviors and pursuing long-term goals,
only recently been observed, specialized interventions have
including sustained weight loss [•, –]. Thus, height-
not been developed; however, some evidence suggests that
ened delay discounting appears to stem from a neurocognitive
individuals with ADHD are less responsive to standard
profile implicated in both ADHD and obesity. Developing a
behavioral interventions for obesity. Only two studies have
regular pattern of eating and the removal of food cues in the
examined weight loss treatment outcomes in individuals
home environment may be helpful for the impulsive individ-
with ADHD and both found that these patients lost less
ual, in addition to assistance in setting shorter-term goals.
weight in a behavioral weight loss program than their coun-
Additional research is needed to identify effective weight loss
terparts without ADHD , Altfas [conducted a
strategies for individuals who are high in impulsivity.
retrospective chart review for 215 weight loss clinic patients
and observed that patients who met diagnostic criteria for
underwent pharmacological treatment (primarily stimulants)
ADHD achieved only 65% of the weight loss of patients
for ADHD for a mean of 466 days. Patients who stayed on
without ADHD (2.6 vs 4.0 kg, respectively). In spite of
the medication (83%) lost a mean of 15.05 kg (12.36%),
poorer weight loss outcomes, patients with ADHD had a
while patients who went off the medication gained 3.26 kg
greater number of visits than their non-ADHD counterparts
(2.78%). Although not a randomized controlled trial, this
(mean, 56.6 vs 39.4 visits), and although not statistically
amount of weight loss among individuals with ADHD is far
significant, longer treatment duration (38.7 vs 28.6 months).
higher than observed in other studies that did not utilize
Pagoto et al. [also documented weight loss in 63 patients
medication (eg, [, ]). Although concerns had been
of an outpatient behavioral weight loss program. Similar to
raised about the cardiovascular side effects of stimulant
Altfas [patients screening positive for ADHD lost only
medications, a large population-based study recently
60% of the weight of their counterparts who screened neg-
showed no impact of stimulants on cardiovascular events
ative (mean weight loss, 3.72 vs 6.17 kg, respectively).
Participants with ADHD symptoms reported significantly
Others studies have shown a weight loss effect of medi-
more short-lived (< 3 days) weight loss attempts than those
cations that are often used to treat ADHD in obese patients
who denied such symptoms. They had significantly more
who do not have ADHD. Anderson et al. ] conducted a
frequent fast food consumption, higher emotional eating
double-blind, placebo-controlled, randomized trial of obese
scores, rated weight loss skills as more difficult, and
adults who were assigned to placebo, bupropion sustained-
reported lower self-efficacy to control their eating. Although
release 300 or 400 mg/d. All participants received behav-
more research is needed comparing weight loss outcomes
ioral weight loss counseling and meal replacements. Results
among patients with and without ADHD, these studies
indicated that bupropion yielded statistically and clinically
suggest that patients with ADHD lose significantly less
significant net weight losses relative to placebo. A second
weight than their counterparts and may have more difficulty
study by Gadde et al. [randomized 30 obese women to
atomoxetine, a norepinephrine reuptake inhibitor, or placebowith both conditions receiving a behavioral weight lossprogram. Patients in the atomoxetine group lost significantly
Improving Clinical Management of Obesity in Patients
more weight than did controls (-3.6 [1.0] vs 0.1 [0.4] kg,
respectively). Three other studies have shown that methyl-phenidate acutely suppressed appetite and energy intake
Given that symptoms of ADHD appear to be associated with
–]. Although only 25% of adults with ADHD are
obesogenic behavior and greater difficulty losing weight,
estimated take medication to control their symptoms
obesity treatment approaches that offset these symptoms
stimulants and other ADHD medications may be a particu-
are needed. Research supports the potential for psychophar-
larly important treatment option to consider for adults with
macology, physical activity, and cognitive behaviorial ther-
apy (CBT) to assist in the clinical management of obesity inthis population.
Exercise may be especially beneficial for patients withcomorbid ADHD and obesity. Both human and animal
Psychopharmacology, including psychostimulants, some
studies strongly support the impact of exercise on improved
antidepressants, and norepinephrine reuptake inhibitors, is
cognitive function ]. Exercise has been found to improve
considered the first-line treatment in ADHD for both chil-
executive function and increase prefrontal activation during
dren and adults . These agents have been shown to
executive function tasks in children •], and some initial
improve clinical and core symptoms of ADHD, including
work has documented that exercise in children with ADHD
vigilance, divided attention, focused attention, and cognitive
has yielded improvements in overall behavior, sustained
flexibility in adults . Medications appear to have an
attention, vigilance, and impulsivity . Exercise
impact on risk for obesity among children with ADHD.
increases brain-derived neurotrophic factor, a molecule in-
Two observational studies of children showed that ADHD
volved in synaptic plasticity, learning, and memory, which
was associated with obesity only in children who were not
may be particularly important for individuals with ADHD
using medication for their ADHD, but not in children who
]. Additionally, Gapin et al. ] reported some prelim-
were medicated ]. Other research suggests that medi-
inary, albeit indirect, evidence that exercise increases dopa-
cations for ADHD may cause weight loss. For example, an
mine levels in children with ADHD ]. Exercise might be
observational study by Levy et al. ] followed a sample
a first step in treatment for patients with comorbid obesity
of 78 obese adult patients diagnosed with ADHD who
and ADHD given that its cognitive benefits might also result
in improved self-regulation, which could facilitate adher-
pathology, poor adherence to structured attempts to lose
ence to other weight loss strategies .
weight, and increased vulnerability to obesogenic environ-ments. When ADHD is suspected in an obese patient, refer-
ral for assessment and treatment is highly recommended.
The clinician should note that people with ADHD may
A version of CBT ] has been developed specifically for
experience greater than average difficulty with organization,
adults with ADHD to reduce ADHD symptoms and im-
self-monitoring, planning, follow through on goals, resisting
prove overall functioning. Because ADHD symptoms inter-
food temptations, and consistency. These symptoms should
fere with the execution of weight loss skills, CBT for
not be confused with poor motivation or irresponsibility in
ADHD might be a useful adjunct to obesity treatment
the patient who is unsuccessful at controlling his/her weight.
among adults with ADHD. CBT provides patients with the
It should also be considered that even in the absence of an
opportunity to learn the functional skills that do not come
ADHD diagnosis, obesity may be associated with brain
naturally to them (eg, time/task management, organizational
changes that produce symptoms that mimic ADHD. Patients
skills, and task analysis), resulting in new skills that can
with comorbid obesity and ADHD likely require extra sup-
enhance functioning and effectiveness in occupational,
port and more intensive weight loss intervention to over-
scholastic, and interpersonal domains. CBT also incorpo-
come these challenges. In addition to pharmacological
rates cognitive modification strategies that assist the patient
treatment, exercise and CBT are two potentially helpful
in identifying automatic thoughts, recognizing the ensuing
adjuncts to weight loss treatment for those with ADHD.
feelings and behaviors that lead to maladaptive responses,
Further research is needed to understand the association
and in reframing and problem solving to devise and imple-
between obesity and ADHD and/or ADHD-like symptoms.
ment more adaptive behaviors. Several studies have shownthe efficacy of CBT in improving ADHD symptoms [–],organizational skills ], depression and anxiety [inpatients with ADHD. Research is needed to determine wheth-
No potential conflicts of interest relevant to this article
er the incorporation of CBT strategies for ADHD into abehavioral weight loss program would improve both ADHDsymptoms and weight loss.
Papers of particular interest, published recently, have been
Although bariatric surgery is often indicated for individuals
who have repeatedly failed to lose weight in structured
programs and/or on their own, individuals with ADHDmay experience the same difficulties with weight control
1. American Psychiatric Association, Diagnostic and statistical manual
of mental disorders. 4th ed. 1994, Washington, DC.
following bariatric surgery, and therefore may be at higher-
2. Lara C, et al. Childhood predictors of adult attention-deficit/hy-
than-average risk for regain. Assessment for ADHD symp-
peractivity disorder: Results from the World Health Organization
toms should be included in the pre-surgery screening pro-
World Mental Health Survey Initiative. Biol Psychol. 2009;65
cess and extra support provided for these patients post
3. Kessler RC, et al. The prevalence and correlates of adult ADHD in
surgery. The Adult ADHD Self-Report Scale is a brief,
the United States: Results from the National Comorbidity Survey
validated measure that is feasible for clinical settings ].
Replication. Am J Psychiatry. 2006;163(4):716–23.
We are aware of no studies that have evaluated bariatric
4. Lam LT, Yang L. Overweight/obesity and attention deficit and
surgery outcomes among individuals with ADHD; such
hyperactivity disorder tendency among adolescents in China. IntJ Obes (Lond). 2007;31(4):584–90.
research is needed. Research on whether bariatric surgery
5.• Pagoto SL, et al. Association between adult attention deficit/
impacts executive function, inhibitory control, and other
hyperactivity disorder and obesity in the US population. Obesity.
symptoms of ADHD would also broaden our understanding
2009;17(3):539–44. This is the first US population-based study
of how obesity and weight loss affect these symptoms.
demonstrating a link between ADHD and both obesity and bingeeating disorder.
6. Waring ME, Lapane KL. Overweight in children and adolescents
in relation to attention-deficit/hyperactivity disorder: Results from
a national sample. Pediatrics. 2008;122(1):e1–6.
7. Kim J, et al. Health behaviors and obesity among US children with
attention deficit hyperactivity disorder by gender and medication
ADHD is a risk factor for both obesity and obesity treatment
use. Prev Med. 2011;52(3–4):218–22.
failure. Inattention, reward sensitivity, and impulsivity are
8. Fuemmeler BF, et al. Association between attention-deficit/hyper-
features of ADHD that may contribute to overeating, eating
activity disorder symptoms and obesity and hypertension in early
adulthood: a population-based study. Int J Obes (Lond). 2011;35
29. Winstanley CA, Eagle DM, Robbins TW. Behavioral models of
impulsivity in relation to ADHD: Translation between clinical and
9. Cortese S, et al. Attention-deficit/hyperactivity disorder (ADHD)
preclinical studies. Clin Psychol Rev. 2006;26(4):379–95.
and obesity: A systematic review of the literature. Crit Rev Food
30. Nederkoorn C, et al. Effects of impulsivity on food purchase and
weight gain over time. Appetite. 2008;51:752.
10. Pagoto SL, et al. Weight loss following a clinic-based weight loss
31. Guerrieri R, Nederkoorn C, Jansen A. How impulsiveness and
program among adults with Attention Deficit/Hyperactivity Disor-
variety influence food intake in a sample of healthy women. Appetite.
der symptoms. Eat Weight Disord. 2010;15:e166–72.
11. Gruss, B., et al., Attention-deficit/Hyperactivity Disorder in a Pre-
32. Nederkoorn C, et al. Control yourself or just eat what you like?
bariatric Surgery Sample. Eur Eat Disord Rev, 2011.
Weight gain over a year is predicted by an interactive effect of
12. Altfas JR. Prevalence of attention deficit/hyperactivity disorder
response inhibition and implicit preference for snack foods. Health
among adults in obesity treatment. BMC Psychiatry. 2002;2:9.
13. Arnsten AF. Fundamentals of attention-deficit/hyperactivity disor-
33. Nederkoorn C, et al. Why obese children cannot resist food: The
der: Circuits and pathways. J Clin Psychiatry. 2006;67 Suppl 8:7–
role of impulsivity. Eat Behav. 2006;7(4):315–22.
34. Mikami AY, et al. Eating pathology among adolescent girls with
14. Fleming, J. and L.D. Levy, Eating disorders in women with
attention-deficit/hyperactivity disorder. J Abnorm Psychol. 2008;117
ADHD, in Gender Issues and ADHD: Research, Diagnosis and
Treatment, P.O. Quinn and K.G. Nadeua, Editors. 2002, Advantage
35. Biederman J, et al. Psychopathology in females with attention-
deficit/hyperactivity disorder: A controlled, five-year prospective
15. Schweickert LA, Strober M, Moskowitz A. Efficacy of methyl-
study. Biol Psychiatry. 2006;60(10):1098–105.
phenidate in bulimia nervosa comorbid with attention-deficit hy-
36. Ivan I, et al. Does binge eating mediate the relationship between
peractivity disorder: A case report. Int J Eat Disord. 1997;21
ADHD characteristics and obesity severity? Obesity. 2009;17
16. Babiloni C, et al. Frontal attentional responses to food size are
37. Lowe MR, et al. Neural correlates of individual differences related
abnormal in obese subjects: an electroencephalographic study. Clin
to appetite. Physiol Behav. 2009;97(5):561–71.
38. Barkley RA. Attention-deficit/hyperactivity disorder, self-regulation,
17. Agranat-Meged A, et al. Childhood obesity and attention deficit/
and time: toward a more comprehensive theory. J Dev Behav Pediatr.
hyperactivity disorder: A newly described comorbidity in obese
hospitalized children. Int J Eat Disord. 2005;37(4):357–9.
39. Guerrieri R, Nederkoorn C, Jansen A. The interaction between
18. Fleming JP, Levy LD, Levitan RD. Symptoms of attention deficit
impulsivity and a varied food environment: Its influence on food
hyperactivity disorder in severely obese women. Eat Weight Disord.
intake and overweight. Int J Obes (Lond). 2008;32(4):708–14.
40. Nederkoorn C, et al. The interactive effect of hunger and impul-
19. Gray JA. The neuropsychology of emotion and personality. In:
sivity on food intake and purchase in a virtual supermarket. Int J
Stahl SM, Iverson SD, Goodman EC, editors. Cognitive Neuro-
chemistry. Oxford, UK: Oxford University Press; 1987. p. 171–90.
41. Nederkoorn C, et al. Impulsivity predicts treatment outcome in
20. Volkow ND, et al. Evaluating dopamine reward pathway in
obese children. Behav Res Ther. 2007;45(5):1071–5.
ADHD: Clinical implications. JAMA. 2009;302(10):1084–91.
42. Odum AL. Delay Discounting: I'm a k, You're a k. J Exp Anal Behav.
21. Gray JA, McNaughton N. The neuropsychology of anxiety. Oxford,
England: Oxford University Press; 2000.
43. Marco R, et al. Delay and reward choice in ADHD: an experimen-
22. Derryberry D, Tucker DM. The adaptive base of the neural hier-
tal test of the role of delay aversion. Neuropsychology. 2009;23
archy: Elementary motivational controls on network function. In:
Dienstbier R, editor. Nebraska Symposium on Motivation: Vol 38
44. Wilson VB, et al. Delay discounting of reward in ADHD:
Perspectives on Motivation. Lincoln, NE: University of Nebraska
application in young children. J Child Psychol Psychiatry. 2011;52
23. Reuter M, et al. Molecular genetics support Gray's personality
45. Scheres A, Lee A, Sumiya M. Temporal reward discounting and
theory: The interaction of COMT and DRD2 polymorphisms pre-
ADHD: task and symptom specific effects. J Neural Transm.
dicts the behavioural approach system. Int J Neuropsychopharma-
46. Scheres A, et al. Temporal reward discounting in attention-deficit/
24. Cohen MX, et al. Individual differences in extraversion and dopa-
hyperactivity disorder: the contribution of symptom domains, re-
mine genetics predict neural reward responses. Brain Res Cogn
ward magnitude, and session length. Biol Psychiatry. 2010;67
25. Depue RA, Collins PF. Neurobiology of the structure of
47. Reynolds B. A review of delay-discounting research with humans:
personality: Dopamine, facilitation of incentive motivation,
relations to drug use and gambling. Behav Pharmacol. 2006;17
and extraversion. Behav Brain Sci. 1999;22(3):491–517. discussion
48. Petry NM. Pathological gamblers, with and without substance use
26. Evans AH, et al. Relationship between impulsive sensation seek-
disorders, discount delayed rewards at high rates. J Abnorm Psychol.
ing traits, smoking, alcohol and caffeine intake, and Parkinson's
disease. J Neurol Neurosurg Psychiatry. 2006;77(3):317–21.
49. Heil SH, et al. Delay discounting in currently using and currently
27. Bowirrat A, Oscar-Berman M. Relationship between dopaminergic
abstinent cocaine-dependent outpatients and non-drug-using
neurotransmission, alcoholism, and reward deficiency. American
matched controls. Addict Behav. 2006;31(7):1290–4.
Journal of Medical Genetics. 2005;132:29–37.
50.• Appelhans BM. Neurobehavioral inhibition of reward-driven
28.• Davis C, et al. Evidence that 'food addiction' is a valid phenotype
feeding: Implications for dieting and obesity. Obesity (Silver
of obesity. Appetite. 2011;57(3):711–7. This paper extends the
Spring). 2009;17(4):640–7. This review paper summarizes the
validation of the Yale Food Addiction Scale and demonstrates
strengths and weaknesses of the appetitive model of eating be-
elevated rates of food addiction among obese adults with binge
havior and presents the literature linking control of hedonic feed-
eating disorder, depression, and ADHD.
ing to inhibitory processes localized in the prefrontal cortex, and
delineates a theoretical model in which hedonic feeding is viewed
73. Wilens TE, Biederman J, Spencer TJ. Attention deficit/hyperactiv-
as the product of an interaction between appetitive motivation and
ity disorder across the lifespan. Annu Rev Med. 2002;53:113–31.
74. Tucha O, et al. Methylphenidate-induced improvements of various
51. Epstein LH, et al. Food reinforcement, delay discounting and
measures of attention in adults with attention deficit hyperactivity
obesity. Physiol Behav. 2010;100(5):438–45.
disorder. J Neural Transm. 2006;113(10):1575–92.
52. Weller RE, et al. Obese women show greater delay discounting
75. Curtin C, et al. Prevalence of overweight in children and adoles-
than healthy-weight women. Appetite. 2008;51(3):563–9.
cents with attention deficit hyperactivity disorder and autism spec-
53. Rollins BY, Dearing KK, Epstein LH. Delay discounting moder-
trum disorders: A chart review. BMC Pediatr. 2005;5:48.
ates the effect of food reinforcement on energy intake among non-
76. Levy LD, Fleming JP, Klar D. Treatment of refractory obesity in
obese women. Appetite. 2010;55(3):420–5.
severely obese adults following management of newly diagnosed
54. Appelhans BM, et al. Inhibiting food reward: delay discounting,
attention deficit hyperactivity disorder. Int J Obes. 2009;33:326–
food reward sensitivity, and palatable food intake in overweight
and obese women. Obesity (Silver Spring). 2011;19(11):2175–82.
77. Habel, L.A., et al., ADHD Medications and Risk of Serious Car-
55. van den Bos R, de Ridder D. Evolved to satisfy our immediate
diovascular Events in Young and Middle-aged Adults. JAMA,
needs: self-control and the rewarding properties of food. Appetite.
78. Anderson JW, et al. Bupropion SR enhances weight loss: A 48-
56. Herman C, Polivy J. Dieting as an exercise in behavioral econom-
week double-blind, placebo- controlled trial. Obes Res. 2002;10
ics. In: Loewenstein G, Read D, Baumeister R, editors. Time and
Decision: Economic and Psychological Perspectives on Intertem-
79. Gadde KM, et al. Atomoxetine for weight reduction in obese
poral Choice. New York: Russell Sage; 2003. p. 459–89.
women: A preliminary randomised controlled trial. Int J Obes
57. Fulton S. Appetite and reward. Front Neuroendocrinol. 2010;31
80. Leddy JJ, et al. Influence of methylphenidate on eating in obese
58. Zheng H, et al. Appetite control and energy balance regulation in
the modern world: reward-driven brain overrides repletion signals.
81. Goldfield GS, Lorello C, Doucet E. Methylphenidate reduces
Int J Obes (Lond). 2009;33 Suppl 2:S8–S13.
energy intake and dietary fat intake in adults: a mechanism of
59. Paloyelis Y, et al. DAT1 and COMT effects on delay discounting
reduced reinforcing value of food? Am J Clin Nutr. 2007;86
and trait impulsivity in male adolescents with attention deficit/
hyperactivity disorder and healthy controls. Neuropsychopharma-
82. Davis, C., et al., The suppression of appetite and food consumption
by methylphenidate: the moderating effects of gender and weight
60. Berridge KC, et al. The tempted brain eats: pleasure and desire
status in healthy adults. Int J Neuropsychopharmacol, 2011: p. 1-7.
circuits in obesity and eating disorders. Brain Res. 2010;1350:43–
83. Archer, T. and R.M. Kostrzewa, Physical Exercise Alleviates
ADHD Symptoms: Regional Deficits and Development Trajectory.
61. Alonso-Alonso M, Pascual-Leone A. The right brain hypothesis
for obesity. Jama. 2007;297(16):1819–22.
84.• Davis C, et al. Exercise improves executive function and achieve-
62. DelParigi A, et al. Successful dieters have increased neural activity
ment and alters brain activation in overweight children: A ran-
in cortical areas involved in the control of behavior. Int J Obes
domized controlled trial. Heal Psychol. 2011;30(1):91–8. This
randomized controlled trial is the first to show that benefits of
63. Le DS, et al. Less activation of the left dorsolateral prefrontal
exercise on executive function and achievement in overweight
cortex in response to a meal: a feature of obesity. Am J Clin Nutr.
85. Gapin JI, Labban JD, Etnier JL. The effects of physical activity on
64. Le DS, et al. Less activation in the left dorsolateral prefrontal
attention deficit hyperactivity disorder symptoms: the evidence.
cortex in the reanalysis of the response to a meal in obese than in
lean women and its association with successful weight loss. Am J
86. Verret C, Gardiner P, Beliveau L. Fitness level and gross motor
performance of children with attention-deficit hyperactivity disor-
65. Kishinevsky, F., et al., fMRI reactivity on a delay discounting task
der. Adapt Phys Activ Q. 2010;27(4):337–51.
predicts weight gain in obese women. Appetite, 2011. epub ahead
87. Gapin J, Etnier JL. The relationship between physical activity
and executive function performance in children with attention-
66. Tregellas JR, et al. Altered default network activity in obesity.
deficit hyperactivity disorder. J Sport Exerc Psychol. 2010;32
Obesity (Silver Spring). 2011;19(12):2316–21.
67. Castellanos FX, et al. Cingulate-precuneus interactions: a new
88. Joseph RJ, et al. The neurocognitive connection between physical
locus of dysfunction in adult attention-deficit/hyperactivity disor-
activity and eating behaviour. Obes Rev. 2011;12(10):800–12.
der. Biol Psychiatry. 2008;63(3):332–7.
89. Safren SA, et al. Cognitive-behavioral therapy for ADHD in
68. Fassbender C, et al. A lack of default network suppression is linked
medication-treated adults with continued symptoms. Behav Res
to increased distractibility in ADHD. Brain Res. 2009;1273:114–
90. Safren SA. Cognitive-behavioral approaches to ADHD treatment
69. Siervo M, et al. Intentional weight loss in overweight and obese
in adulthood. J Clin Psychiatry. 2006;67 Suppl 8:46–50.
individuals and cognitive function: a systematic review and meta-
91. Stevenson CS, et al. A cognitive remediation programme for adults
analysis. Obes Rev. 2011;12(11):968–83.
with attention deficit hyperactivity disorder. Aust N Z J Psychiatry.
70. Val-Laillet D, et al. Changes in brain activity after a diet-induced
obesity. Obesity (Silver Spring). 2011;19(4):749–56.
92. Hesslinger B, et al. Psychotherapy of attention deficit hyperactivity
71. Bruce-Keller AJ, Keller JN, Morrison CD. Obesity and vulnera-
disorder in adults–a pilot study using a structured skills training
bility of the CNS. Biochim Biophys Acta. 2009;1792(5):395–400.
program. Eur Arch Psychiatry Clin Neurosci. 2002;252(4):177–
72. Spencer T, et al. A double-blind, crossover comparison of methyl-
phenidate and placebo in adults with childhood-onset attention-
93. Adler LA, et al. Validity of pilot Adult ADHD Self-Report Scale
deficit hyperactivity disorder. Arch Gen Psychiatry. 1995;52
(ASRS) to rate adult ADHD symptoms. Ann Clin Psychiatry.
Provincia di Pesaro e Urbino via Gramsci n.4 Pesaro Titolare di Posizione Organizzativa 5.5 “Sistema informativo del ’ente, telefonia, nodi tecnici, internet e rete telematica provinciale” • Principali mansioni e responsabilità Responsabile dei sistemi informativi e telefonici del ’ente, del a rete lan e del a rete wan. Progettazione e sviluppo dei progetti di e-goverment e del Cen
Determination of caffeine in tea by HPLC Preparation of standard solutions You will require standard solutions of Caffeine in Methanol: Concentration Caffeine µ g / ml Mobile Phase Preparation of tea sample 1. Grind approximately 7g of the tea sample. Carry out the rest of the procedure in duplicate. +/- 0.001g of the sample in duplicate into a 500 ml round bottomed flask. 3.