Current Obesity Reports

, Volume 1, Issue 2, pp 80–86 | Cite as

Attention Deficit/Hyperactivity Disorder and the Clinical Management of Obesity

  • Sherry Pagoto
  • Carol Curtin
  • Bradley M. Appelhans
  • Miguel Alonso-Alonso
Obesity Treatment (AM Sharma, Section Editor)

Abstract

Attention deficit/hyperactivity disorder (ADHD) has been associated with increased risk for obesity and obesity treatment failure. The present paper discusses how features of ADHD, including inattention, reward sensitivity, and impulsivity, may impact obesity risk and have implications for the management of obesity. In addition, we review emerging research on how obesity may contribute to brain changes that are associated with ADHD-like symptoms. Finally, suggestions for improving the clinical management of obesity in patients with ADHD are discussed, including pharmacological treatment, exercise, and cognitive behavior therapy. ADHD is a barrier to the clinical management of obesity and more research is needed to further understand the link between ADHD and obesity. Effective treatment approaches are needed given the significant difficulty patients with ADHD encounter in their attempts to regulate their weight in the context of an obesogenic environment.

Keywords

ADHD Attention deficit/hyperactivity disorder Obesity Impulsivity Treatment 

Introduction

Attention deficit/hyperactivity disorder (ADHD) is a neurobehavioral disorder, essential features of which include a persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than typically observed in individuals at a comparable level of development. The Diagnostic and Statistical Manual 4 th edition (DSM-IV) [1] 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. The DSM-IV describes three subtypes of ADHD: 1) inattentive type; 2) hyperactive-impulsive type; and 3) combined type. ADHD has been shown to persist into adulthood in half of children with ADHD [2] and affects over 9 million US adults [3]. An association between ADHD and obesity is well documented both in population [4, 5•, 6, 7, 8] and clinical samples [9, 10, 11].

In addition to ADHD being linked to greater risk for obesity, evidence is also emerging that ADHD may pose a significant barrier to the management of obesity [10, 12]. In the present paper we discuss the neurocognitive features of ADHD that may lead to obesogenic behavior and affect the patient’s ability to engage in the self-management skills that are instrumental to weight control. Treatment strategies for patients with comorbid ADHD and obesity are discussed as well as future directions for research on the clinical management of obesity in the patient with ADHD.

Inattention, Reward Sensitivity, and Impulsivity May Lead to Obesogenic Behavior

Some research has explored neurocognitive features of ADHD, including inattention, reward sensitivity, and impulsivity, to determine the extent to which these problems are associated with obesity and/or interfere with the ability to lose weight. Inattention, a hallmark of ADHD, refers to distractibility, reduced ability to sustain attention, and susceptibility to interference [13]. Inattention may adversely impact the individual’s capacity to execute goal-directed dietary and physical activity behaviors and the ability to regulate one’s weight resulting in irregular eating habits and poor adherence. Inattention might also affect awareness of internal hunger and satiety cues, especially when the individual is engaged in other activities [14, 15]. This could result in externally cued eating, which tends to be associated with overeating. Inattention may also interfere with other behaviors critical to successful weight loss, such as meal planning, implementation of specific behavioral skills (eg, consistently keeping a diet diary), following through with planned exercise, and the ability to detect changes in food portion sizes [16]. In some studies, the inattentive type of ADHD has been found to be more prevalent than the hyperactive/impulsive type in obese samples [12, 17, 18]. Additional research is needed to further describe specifically how inattention affects one’s ability to regulate their weight, as well as interventions that could be helpful in this contest (eg, cues/reminders, frequent feedback, etc.).

Reward sensitivity is a biologically based personality trait originally described by Gray [19] that may stem from hypo- or hyper-reactivity to reward at the neurobiological level. High “reward sensitivity” describes individuals who are especially sensitive to rewards in their environment, while diminished reward sensitivity describes individuals who are especially insensitive to rewards in their environment. Recent evidence has emerged that individuals with ADHD, particularly those with the inattentive type, are highly reward sensitive [20]. Reward sensitivity is implicated in appetitive motivation, such that it may mediate responses to appetitive stimuli, including drugs, food, and sex [21]. Mesolimbic dopaminergic (DA) processes are central to reward sensitivity [22, 23], with greater sensitivity to reward at the behavioral level being associated with either a hyper- or hyporesponsive mesolimbic DA system [24, 25, 26]. Because palatable foods enhance dopamine activation, eating might serve a “self-medicating” function for some individuals with ADHD [27]. Given that ADHD is generally characterized by reward sensitivity, obese adults with ADHD may be more sensitive to rewards relative to their obese counterparts without ADHD, which might manifest in eating pathology. For example, Davis et al. [28•] found that individuals with ADHD were more likely to meet criteria for “food addiction” than those without ADHD. Similarly, binge eating disorder has been shown to play a mediating role in the relationship between ADHD and obesity [10].

Impulsivity is another common feature of ADHD that has implications for obesogenic behavior and possibly risk for obesity. Although it is a multifaceted construct, impulsivity can simply be characterized as action without foresight [29]. Some evidence suggests that people high in impulsivity are prone to overeating, weight gain [30, 31, 32], and obesity [33]. Among 228 adolescent girls with ADHD, impulsivity was a much stronger predictor of eating pathology than inattention, although both inattentive and impulsive ADHD subtypes were equally likely to be obese [34]. This suggests that impulsivity might be instrumental in the observed association between ADHD and binge eating disorder [5•, 35, 36]. Greater impulsivity could also lead to greater difficulty inhibiting the consumption of high energy–dense palatable foods, especially in response to stress and other cues, as described by Lowe et al. [37]. Cognitive models of ADHD emphasize the role of inhibitory control as a critical requirement for other executive functions that subserve self-regulation and goal-directed behavior [38]. Consuming a healthy diet in an obesogenic environment or restricting intake to lose weight can be thought of as goal-oriented behavior, thus any impairment in inhibitory control could hijack their optimal execution. The increasingly obesogenic environment may be particularly challenging for people high in impulsivity (ie, low inhibitory control), given the omnipresence of food cues. Supporting this contention is a study showing that impulsivity was associated with greater food consumption in an environment characterized by high food variety, but not in one characterized by monotonous foods [39]. This impulsivity-by-environment interaction suggests that persons with ADHD might be disproportionately vulnerable to obesogenic environments.

Impulsive individuals also appear to have less inhibitory control during hunger, as evidenced in a study that found that impulsive individuals consumed more food when exposed to highly palatable food than their less impulsive counterparts under conditions of hunger, but not under conditions of satiety [40]. These findings suggest that restrictive diets in the context of an obesogenic environment might be especially challenging for people with ADHD. Accordingly, Nederkoorn et al. [41] reported that impulsivity predicted less weight loss following treatment in children.

One particular manifestation of impulsivity, delay discounting, seems particularly relevant to understanding the association between ADHD and obesity. Delay discounting reflects the degree to which an individual undervalues rewards with increasing delays [42]. For both humans and animals, immediate rewards have a disproportionately strong influence on our decisions and actions. Less valuable immediate rewards (eg, $200 today) can often be preferred to more valuable future rewards (ie, $240 in 3 months). A number of studies have found steeper delay discounting among children and adults with ADHD relative to controls [43, 44]. These effects appear to be more robust among those with the hyperactive/impulsive or combined subtypes [44, 45, 46], which is consistent with the conceptualization of delay discounting as a facet of impulsivity. The tendency to discount delayed rewards steeply is associated with several conditions in which impulsivity and hyper-responsivity to appetitive cues are thought to play an etiological role, such as compulsive gambling, tobacco use, and drug addiction [47, 48, 49].

Recently, delay discounting has also been linked to eating behavior and obesity [50•, 51]. For example, obese women show steeper discounting of delayed rewards than normal weight women [52], and greater delay discounting has been associated with higher intake of palatable food among lean, overweight, and obese subjects who are most sensitive to the rewarding properties of food [53, 54]. It has been hypothesized that a greater predisposition for delay discounting would likely manifest as heightened sensitivity to the immediate reward from palatable food and decreased valuation of the long-term rewards associated with a healthy diet and weight maintenance, which in combination would contribute to obesity [55, 56]. The neurobiological mechanisms underlying individual differences in delay discounting have also been linked to the neurocognitive deficits in ADHD and the brain regulation of eating behavior. Specifically, alterations in mesolimbic dopamine function have been associated with a stronger preference for immediate rewards in the context of delay discounting tasks, palatable food intake, and ADHD [20, 57, 58, 59, 60]. In contrast, “executive” brain regions found to be altered in ADHD, particularly the lateral prefrontal cortex, appear to play a critical role in inhibiting impulsive behaviors and pursuing long-term goals, including sustained weight loss [50•, 61, 62, 63, 64, 65]. Thus, heightened delay discounting appears to stem from a neurocognitive profile implicated in both ADHD and obesity. Developing a regular pattern of eating and the removal of food cues in the home environment may be helpful for the impulsive individual, in addition to assistance in setting shorter-term goals. Additional research is needed to identify effective weight loss strategies for individuals who are high in impulsivity.

Chicken or the Egg? Obesity May Produce ADHD-Like Symptoms

Aside from common underlying mechanisms between ADHD and obesity and the impact that ADHD may have on weight gain and obesity, there is some, albeit limited, evidence for the possibility that obesity contributes to the development of ADHD-like symptoms. For example, short-term experimental overfeeding in lean humans has been shown to lead to brain changes including an increase in the activation of the default mode network (DMN), a set of areas that are active typically at rest and seem to be involved in self-referential cognition and introspection [66]. This effect goes in the direction of ADHD-like brain changes, characterized by DMN overactivation and difficulty in suppressing this network during effortful tasks [67, 68]. Additional evidence comes from a study showing improvements in attention/executive functioning in obese subjects following weight loss [69]. Animal studies provide more direct evidence in support of this association. Diet-induced obesity in a swine model leads to changes in brain perfusion that are selectively located in areas implicated in ADHD, such as the dorsolateral prefrontal cortex, and the amount of weight gain negatively correlates with perfusion in these locations [70]. Lastly, a brain effect of obesity is supported by biological plausibility, as obesity-related changes can affect neuroplasticity and cognitive function through different mechanisms (eg, the release of proinflammatory substances to the systemic circulation) [71]. Altogether, the evidence suggests that obesity may worsen ADHD symptomatology or facilitate the development of ADHD-like symptoms via brain changes; however, direct evidence for this association in humans is not available yet and future studies are warranted. To the extent that obesity-induced brain changes impair weight control, patients with long-standing obesity and more severe obesity may be the most treatment resistant. Research is needed to determine whether these brain changes are reversible via weight loss and/or lifestyle changes (eg, caloric restriction, exercise).

Obesity Management in the Patient with ADHD

Because the association between ADHD and obesity has only recently been observed, specialized interventions have not been developed; however, some evidence suggests that individuals with ADHD are less responsive to standard behavioral interventions for obesity. Only two studies have examined weight loss treatment outcomes in individuals with ADHD and both found that these patients lost less weight in a behavioral weight loss program than their counterparts without ADHD [10, 12]. Altfas [12] conducted a retrospective chart review for 215 weight loss clinic patients and observed that patients who met diagnostic criteria for ADHD achieved only 65% of the weight loss of patients without ADHD (2.6 vs 4.0 kg, respectively). In spite of poorer weight loss outcomes, patients with ADHD had a greater number of visits than their non-ADHD counterparts (mean, 56.6 vs 39.4 visits), and although not statistically significant, longer treatment duration (38.7 vs 28.6 months). Pagoto et al. [10] also documented weight loss in 63 patients of an outpatient behavioral weight loss program. Similar to Altfas [12], patients screening positive for ADHD lost only 60% of the weight of their counterparts who screened negative (mean weight loss, 3.72 vs 6.17 kg, respectively). Participants with ADHD symptoms reported significantly more short-lived (< 3 days) weight loss attempts than those who denied such symptoms. They had significantly more frequent fast food consumption, higher emotional eating scores, rated weight loss skills as more difficult, and reported lower self-efficacy to control their eating. Although more research is needed comparing weight loss outcomes among patients with and without ADHD, these studies suggest that patients with ADHD lose significantly less weight than their counterparts and may have more difficulty managing their intake.

Improving Clinical Management of Obesity in Patients with ADHD

Given that symptoms of ADHD appear to be associated with obesogenic behavior and greater difficulty losing weight, obesity treatment approaches that offset these symptoms are needed. Research supports the potential for psychopharmacology, physical activity, and cognitive behaviorial therapy (CBT) to assist in the clinical management of obesity in this population.

Psychopharmacology

Psychopharmacology, including psychostimulants, some antidepressants, and norepinephrine reuptake inhibitors, is considered the first-line treatment in ADHD for both children and adults [72, 73]. These agents have been shown to improve clinical and core symptoms of ADHD, including vigilance, divided attention, focused attention, and cognitive flexibility in adults [74]. Medications appear to have an impact on risk for obesity among children with ADHD. Two observational studies of children showed that ADHD was associated with obesity only in children who were not using medication for their ADHD, but not in children who were medicated [6, 75]. Other research suggests that medications for ADHD may cause weight loss. For example, an observational study by Levy et al. [76] followed a sample of 78 obese adult patients diagnosed with ADHD who underwent pharmacological treatment (primarily stimulants) for ADHD for a mean of 466 days. Patients who stayed on the medication (83%) lost a mean of 15.05 kg (12.36%), while patients who went off the medication gained 3.26 kg (2.78%). Although not a randomized controlled trial, this amount of weight loss among individuals with ADHD is far higher than observed in other studies that did not utilize medication (eg, [10, 12]). Although concerns had been raised about the cardiovascular side effects of stimulant medications, a large population-based study recently showed no impact of stimulants on cardiovascular events in young and middle-aged adults [77].

Others studies have shown a weight loss effect of medications that are often used to treat ADHD in obese patients who do not have ADHD. Anderson et al. [78] conducted a double-blind, placebo-controlled, randomized trial of obese adults who were assigned to placebo, bupropion sustained-release 300 or 400 mg/d. All participants received behavioral weight loss counseling and meal replacements. Results indicated that bupropion yielded statistically and clinically significant net weight losses relative to placebo. A second study by Gadde et al. [79] randomized 30 obese women to atomoxetine, a norepinephrine reuptake inhibitor, or placebo with both conditions receiving a behavioral weight loss program. Patients in the atomoxetine group lost significantly more weight than did controls (-3.6 [1.0] vs 0.1 [0.4] kg, respectively). Three other studies have shown that methylphenidate acutely suppressed appetite and energy intake [80, 81, 82]. Although only 25% of adults with ADHD are estimated take medication to control their symptoms [3], stimulants and other ADHD medications may be a particularly important treatment option to consider for adults with comorbid ADHD and obesity.

Exercise

Exercise may be especially beneficial for patients with comorbid ADHD and obesity. Both human and animal studies strongly support the impact of exercise on improved cognitive function [83]. Exercise has been found to improve executive function and increase prefrontal activation during executive function tasks in children [84•], and some initial work has documented that exercise in children with ADHD has yielded improvements in overall behavior, sustained attention, vigilance, and impulsivity [85, 86]. Exercise increases brain-derived neurotrophic factor, a molecule involved in synaptic plasticity, learning, and memory, which may be particularly important for individuals with ADHD [83]. Additionally, Gapin et al. [87] reported some preliminary, albeit indirect, evidence that exercise increases dopamine levels in children with ADHD [87]. Exercise might be a first step in treatment for patients with comorbid obesity and ADHD given that its cognitive benefits might also result in improved self-regulation, which could facilitate adherence to other weight loss strategies [88].

Cognitive Behavioral Therapy

A version of CBT [89] has been developed specifically for adults with ADHD to reduce ADHD symptoms and improve overall functioning. Because ADHD symptoms interfere with the execution of weight loss skills, CBT for ADHD might be a useful adjunct to obesity treatment among adults with ADHD. CBT provides patients with the opportunity to learn the functional skills that do not come naturally to them (eg, time/task management, organizational skills, and task analysis), resulting in new skills that can enhance functioning and effectiveness in occupational, scholastic, and interpersonal domains. CBT also incorporates cognitive modification strategies that assist the patient in identifying automatic thoughts, recognizing the ensuing feelings and behaviors that lead to maladaptive responses, and in reframing and problem solving to devise and implement more adaptive behaviors. Several studies have shown the efficacy of CBT in improving ADHD symptoms [89, 90, 91, 92], organizational skills [91], depression and anxiety [89] in patients with ADHD. Research is needed to determine whether the incorporation of CBT strategies for ADHD into a behavioral weight loss program would improve both ADHD symptoms and weight loss.

Bariatric Surgery

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 ADHD may experience the same difficulties with weight control following bariatric surgery, and therefore may be at higher-than-average risk for regain. Assessment for ADHD symptoms should be included in the pre-surgery screening process and extra support provided for these patients post surgery. The Adult ADHD Self-Report Scale is a brief, validated measure that is feasible for clinical settings [93]. We are aware of no studies that have evaluated bariatric surgery outcomes among individuals with ADHD; such research is needed. Research on whether bariatric surgery impacts executive function, inhibitory control, and other symptoms of ADHD would also broaden our understanding of how obesity and weight loss affect these symptoms.

Conclusions

ADHD is a risk factor for both obesity and obesity treatment failure. Inattention, reward sensitivity, and impulsivity are features of ADHD that may contribute to overeating, eating pathology, poor adherence to structured attempts to lose weight, and increased vulnerability to obesogenic environments. When ADHD is suspected in an obese patient, referral for assessment and treatment is highly recommended. The clinician should note that people with ADHD may experience greater than average difficulty with organization, self-monitoring, planning, follow through on goals, resisting food temptations, and consistency. These symptoms should not be confused with poor motivation or irresponsibility in the patient who is unsuccessful at controlling his/her weight. It should also be considered that even in the absence of an ADHD diagnosis, obesity may be associated with brain changes that produce symptoms that mimic ADHD. Patients with comorbid obesity and ADHD likely require extra support and more intensive weight loss intervention to overcome these challenges. In addition to pharmacological treatment, exercise and CBT are two potentially helpful adjuncts to weight loss treatment for those with ADHD. Further research is needed to understand the association between obesity and ADHD and/or ADHD-like symptoms.

Notes

Disclosure

No potential conflicts of interest relevant to this article were reported.

References

Papers of particular interest, published recently, have been highlighted as: • Of importance

  1. 1.
    American Psychiatric Association, Diagnostic and statistical manual of mental disorders. 4th ed. 1994, Washington, DC.Google Scholar
  2. 2.
    Lara C, et al. Childhood predictors of adult attention-deficit/hyperactivity disorder: Results from the World Health Organization World Mental Health Survey Initiative. Biol Psychol. 2009;65(1):46–54.CrossRefGoogle Scholar
  3. 3.
    Kessler RC, et al. The prevalence and correlates of adult ADHD in the United States: Results from the National Comorbidity Survey Replication. Am J Psychiatry. 2006;163(4):716–23.PubMedCrossRefGoogle Scholar
  4. 4.
    Lam LT, Yang L. Overweight/obesity and attention deficit and hyperactivity disorder tendency among adolescents in China. Int J Obes (Lond). 2007;31(4):584–90.Google Scholar
  5. 5.•
    Pagoto SL, et al. Association between adult attention deficit/hyperactivity disorder and obesity in the US population. Obesity. 2009;17(3):539–44. This is the first US population-based study demonstrating a link between ADHD and both obesity and binge eating disorder.PubMedCrossRefGoogle Scholar
  6. 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.PubMedCrossRefGoogle Scholar
  7. 7.
    Kim J, et al. Health behaviors and obesity among US children with attention deficit hyperactivity disorder by gender and medication use. Prev Med. 2011;52(3–4):218–22.PubMedGoogle Scholar
  8. 8.
    Fuemmeler BF, et al. Association between attention-deficit/hyperactivity disorder symptoms and obesity and hypertension in early adulthood: a population-based study. Int J Obes (Lond). 2011;35(6):852–62.CrossRefGoogle Scholar
  9. 9.
    Cortese S, et al. Attention-deficit/hyperactivity disorder (ADHD) and obesity: A systematic review of the literature. Crit Rev Food Sci Nutr. 2008;48(6):524–37.PubMedCrossRefGoogle Scholar
  10. 10.
    Pagoto SL, et al. Weight loss following a clinic-based weight loss program among adults with Attention Deficit/Hyperactivity Disorder symptoms. Eat Weight Disord. 2010;15:e166–72.PubMedGoogle Scholar
  11. 11.
    Gruss, B., et al., Attention-deficit/Hyperactivity Disorder in a Prebariatric Surgery Sample. Eur Eat Disord Rev, 2011.Google Scholar
  12. 12.
    Altfas JR. Prevalence of attention deficit/hyperactivity disorder among adults in obesity treatment. BMC Psychiatry. 2002;2:9.PubMedCrossRefGoogle Scholar
  13. 13.
    Arnsten AF. Fundamentals of attention-deficit/hyperactivity disorder: Circuits and pathways. J Clin Psychiatry. 2006;67 Suppl 8:7–12.PubMedGoogle Scholar
  14. 14.
    Fleming, J. and L.D. Levy, Eating disorders in women with ADHD, in Gender Issues and ADHD: Research, Diagnosis and Treatment, P.O. Quinn and K.G. Nadeua, Editors. 2002, Advantage Books: Silver Spring, MD.Google Scholar
  15. 15.
    Schweickert LA, Strober M, Moskowitz A. Efficacy of methylphenidate in bulimia nervosa comorbid with attention-deficit hyperactivity disorder: A case report. Int J Eat Disord. 1997;21(3):299–301.PubMedCrossRefGoogle Scholar
  16. 16.
    Babiloni C, et al. Frontal attentional responses to food size are abnormal in obese subjects: an electroencephalographic study. Clin Neurophysiol. 2009;120(8):1441–8.PubMedCrossRefGoogle Scholar
  17. 17.
    Agranat-Meged A, et al. Childhood obesity and attention deficit/hyperactivity disorder: A newly described comorbidity in obese hospitalized children. Int J Eat Disord. 2005;37(4):357–9.PubMedCrossRefGoogle Scholar
  18. 18.
    Fleming JP, Levy LD, Levitan RD. Symptoms of attention deficit hyperactivity disorder in severely obese women. Eat Weight Disord. 2005;10(1):e10–3.PubMedGoogle Scholar
  19. 19.
    Gray JA. The neuropsychology of emotion and personality. In: Stahl SM, Iverson SD, Goodman EC, editors. Cognitive Neurochemistry. Oxford, UK: Oxford University Press; 1987. p. 171–90.Google Scholar
  20. 20.
    Volkow ND, et al. Evaluating dopamine reward pathway in ADHD: Clinical implications. JAMA. 2009;302(10):1084–91.PubMedCrossRefGoogle Scholar
  21. 21.
    Gray JA, McNaughton N. The neuropsychology of anxiety. Oxford, England: Oxford University Press; 2000.Google Scholar
  22. 22.
    Derryberry D, Tucker DM. The adaptive base of the neural hierarchy: Elementary motivational controls on network function. In: Dienstbier R, editor. Nebraska Symposium on Motivation: Vol 38 Perspectives on Motivation. Lincoln, NE: University of Nebraska Press; 1991. p. 289–342.Google Scholar
  23. 23.
    Reuter M, et al. Molecular genetics support Gray's personality theory: The interaction of COMT and DRD2 polymorphisms predicts the behavioural approach system. Int J Neuropsychopharmacol. 2006;9(2):155–66.PubMedCrossRefGoogle Scholar
  24. 24.
    Cohen MX, et al. Individual differences in extraversion and dopamine genetics predict neural reward responses. Brain Res Cogn Brain Res. 2005;25(3):851–61.PubMedCrossRefGoogle Scholar
  25. 25.
    Depue RA, Collins PF. Neurobiology of the structure of personality: Dopamine, facilitation of incentive motivation, and extraversion. Behav Brain Sci. 1999;22(3):491–517. discussion 518-69.PubMedGoogle Scholar
  26. 26.
    Evans AH, et al. Relationship between impulsive sensation seeking traits, smoking, alcohol and caffeine intake, and Parkinson's disease. J Neurol Neurosurg Psychiatry. 2006;77(3):317–21.PubMedCrossRefGoogle Scholar
  27. 27.
    Bowirrat A, Oscar-Berman M. Relationship between dopaminergic neurotransmission, alcoholism, and reward deficiency. American Journal of Medical Genetics. 2005;132:29–37.Google Scholar
  28. 28.•
    Davis C, et al. Evidence that 'food addiction' is a valid phenotype of obesity. Appetite. 2011;57(3):711–7. This paper extends the validation of the Yale Food Addiction Scale and demonstrates elevated rates of food addiction among obese adults with binge eating disorder, depression, and ADHD.PubMedCrossRefGoogle Scholar
  29. 29.
    Winstanley CA, Eagle DM, Robbins TW. Behavioral models of impulsivity in relation to ADHD: Translation between clinical and preclinical studies. Clin Psychol Rev. 2006;26(4):379–95.PubMedCrossRefGoogle Scholar
  30. 30.
    Nederkoorn C, et al. Effects of impulsivity on food purchase and weight gain over time. Appetite. 2008;51:752.CrossRefGoogle Scholar
  31. 31.
    Guerrieri R, Nederkoorn C, Jansen A. How impulsiveness and variety influence food intake in a sample of healthy women. Appetite. 2007;48(1):119–22.PubMedCrossRefGoogle Scholar
  32. 32.
    Nederkoorn C, et al. Control yourself or just eat what you like? Weight gain over a year is predicted by an interactive effect of response inhibition and implicit preference for snack foods. Health Psychol. 2010;29(4):389–93.PubMedCrossRefGoogle Scholar
  33. 33.
    Nederkoorn C, et al. Why obese children cannot resist food: The role of impulsivity. Eat Behav. 2006;7(4):315–22.PubMedCrossRefGoogle Scholar
  34. 34.
    Mikami AY, et al. Eating pathology among adolescent girls with attention-deficit/hyperactivity disorder. J Abnorm Psychol. 2008;117(1):225–35.PubMedCrossRefGoogle Scholar
  35. 35.
    Biederman J, et al. Psychopathology in females with attention-deficit/hyperactivity disorder: A controlled, five-year prospective study. Biol Psychiatry. 2006;60(10):1098–105.PubMedCrossRefGoogle Scholar
  36. 36.
    Ivan I, et al. Does binge eating mediate the relationship between ADHD characteristics and obesity severity? Obesity. 2009;17 Suppl 2:S286.Google Scholar
  37. 37.
    Lowe MR, et al. Neural correlates of individual differences related to appetite. Physiol Behav. 2009;97(5):561–71.PubMedCrossRefGoogle Scholar
  38. 38.
    Barkley RA. Attention-deficit/hyperactivity disorder, self-regulation, and time: toward a more comprehensive theory. J Dev Behav Pediatr. 1997;18(4):271–9.PubMedCrossRefGoogle Scholar
  39. 39.
    Guerrieri R, Nederkoorn C, Jansen A. The interaction between impulsivity and a varied food environment: Its influence on food intake and overweight. Int J Obes (Lond). 2008;32(4):708–14.CrossRefGoogle Scholar
  40. 40.
    Nederkoorn C, et al. The interactive effect of hunger and impulsivity on food intake and purchase in a virtual supermarket. Int J Obes (Lond). 2009;33(8):905–12.CrossRefGoogle Scholar
  41. 41.
    Nederkoorn C, et al. Impulsivity predicts treatment outcome in obese children. Behav Res Ther. 2007;45(5):1071–5.PubMedCrossRefGoogle Scholar
  42. 42.
    Odum AL. Delay Discounting: I'm a k, You're a k. J Exp Anal Behav. 2011;96(3):427–39.PubMedGoogle Scholar
  43. 43.
    Marco R, et al. Delay and reward choice in ADHD: an experimental test of the role of delay aversion. Neuropsychology. 2009;23(3):367–80.PubMedCrossRefGoogle Scholar
  44. 44.
    Wilson VB, et al. Delay discounting of reward in ADHD: application in young children. J Child Psychol Psychiatry. 2011;52(3):256–64.PubMedCrossRefGoogle Scholar
  45. 45.
    Scheres A, Lee A, Sumiya M. Temporal reward discounting and ADHD: task and symptom specific effects. J Neural Transm. 2008;115(2):221–6.PubMedCrossRefGoogle Scholar
  46. 46.
    Scheres A, et al. Temporal reward discounting in attention-deficit/hyperactivity disorder: the contribution of symptom domains, reward magnitude, and session length. Biol Psychiatry. 2010;67(7):641–8.PubMedCrossRefGoogle Scholar
  47. 47.
    Reynolds B. A review of delay-discounting research with humans: relations to drug use and gambling. Behav Pharmacol. 2006;17(8):651–67.PubMedCrossRefGoogle Scholar
  48. 48.
    Petry NM. Pathological gamblers, with and without substance use disorders, discount delayed rewards at high rates. J Abnorm Psychol. 2001;110(3):482–7.PubMedCrossRefGoogle Scholar
  49. 49.
    Heil SH, et al. Delay discounting in currently using and currently abstinent cocaine-dependent outpatients and non-drug-using matched controls. Addict Behav. 2006;31(7):1290–4.PubMedCrossRefGoogle Scholar
  50. 50.•
    Appelhans BM. Neurobehavioral inhibition of reward-driven feeding: Implications for dieting and obesity. Obesity (Silver Spring). 2009;17(4):640–7. This review paper summarizes the strengths and weaknesses of the appetitive model of eating behavior and presents the literature linking control of hedonic feeding to inhibitory processes localized in the prefrontal cortex, and delineates a theoretical model in which hedonic feeding is viewed as the product of an interaction between appetitive motivation and inhibitory control.CrossRefGoogle Scholar
  51. 51.
    Epstein LH, et al. Food reinforcement, delay discounting and obesity. Physiol Behav. 2010;100(5):438–45.PubMedCrossRefGoogle Scholar
  52. 52.
    Weller RE, et al. Obese women show greater delay discounting than healthy-weight women. Appetite. 2008;51(3):563–9.PubMedCrossRefGoogle Scholar
  53. 53.
    Rollins BY, Dearing KK, Epstein LH. Delay discounting moderates the effect of food reinforcement on energy intake among non-obese women. Appetite. 2010;55(3):420–5.PubMedCrossRefGoogle Scholar
  54. 54.
    Appelhans BM, et al. Inhibiting food reward: delay discounting, food reward sensitivity, and palatable food intake in overweight and obese women. Obesity (Silver Spring). 2011;19(11):2175–82.CrossRefGoogle Scholar
  55. 55.
    van den Bos R, de Ridder D. Evolved to satisfy our immediate needs: self-control and the rewarding properties of food. Appetite. 2006;47(1):24–9.PubMedCrossRefGoogle Scholar
  56. 56.
    Herman C, Polivy J. Dieting as an exercise in behavioral economics. In: Loewenstein G, Read D, Baumeister R, editors. Time and Decision: Economic and Psychological Perspectives on Intertemporal Choice. New York: Russell Sage; 2003. p. 459–89.Google Scholar
  57. 57.
    Fulton S. Appetite and reward. Front Neuroendocrinol. 2010;31(1):85–103.PubMedCrossRefGoogle Scholar
  58. 58.
    Zheng H, et al. Appetite control and energy balance regulation in the modern world: reward-driven brain overrides repletion signals. Int J Obes (Lond). 2009;33 Suppl 2:S8–S13.CrossRefGoogle Scholar
  59. 59.
    Paloyelis Y, et al. DAT1 and COMT effects on delay discounting and trait impulsivity in male adolescents with attention deficit/hyperactivity disorder and healthy controls. Neuropsychopharmacology. 2010;35(12):2414–26.PubMedCrossRefGoogle Scholar
  60. 60.
    Berridge KC, et al. The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. Brain Res. 2010;1350:43–64.PubMedCrossRefGoogle Scholar
  61. 61.
    Alonso-Alonso M, Pascual-Leone A. The right brain hypothesis for obesity. Jama. 2007;297(16):1819–22.PubMedCrossRefGoogle Scholar
  62. 62.
    DelParigi A, et al. Successful dieters have increased neural activity in cortical areas involved in the control of behavior. Int J Obes (Lond). 2007;31(3):440–8.CrossRefGoogle Scholar
  63. 63.
    Le DS, et al. Less activation of the left dorsolateral prefrontal cortex in response to a meal: a feature of obesity. Am J Clin Nutr. 2006;84(4):725–31.PubMedGoogle Scholar
  64. 64.
    Le DS, et al. Less activation in the left dorsolateral prefrontal 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 Clin Nutr. 2007;86(3):573–9.PubMedGoogle Scholar
  65. 65.
    Kishinevsky, F., et al., fMRI reactivity on a delay discounting task predicts weight gain in obese women. Appetite, 2011. epub ahead of print.Google Scholar
  66. 66.
    Tregellas JR, et al. Altered default network activity in obesity. Obesity (Silver Spring). 2011;19(12):2316–21.CrossRefGoogle Scholar
  67. 67.
    Castellanos FX, et al. Cingulate-precuneus interactions: a new locus of dysfunction in adult attention-deficit/hyperactivity disorder. Biol Psychiatry. 2008;63(3):332–7.PubMedCrossRefGoogle Scholar
  68. 68.
    Fassbender C, et al. A lack of default network suppression is linked to increased distractibility in ADHD. Brain Res. 2009;1273:114–28.PubMedCrossRefGoogle Scholar
  69. 69.
    Siervo M, et al. Intentional weight loss in overweight and obese individuals and cognitive function: a systematic review and meta-analysis. Obes Rev. 2011;12(11):968–83.PubMedCrossRefGoogle Scholar
  70. 70.
    Val-Laillet D, et al. Changes in brain activity after a diet-induced obesity. Obesity (Silver Spring). 2011;19(4):749–56.CrossRefGoogle Scholar
  71. 71.
    Bruce-Keller AJ, Keller JN, Morrison CD. Obesity and vulnerability of the CNS. Biochim Biophys Acta. 2009;1792(5):395–400.PubMedGoogle Scholar
  72. 72.
    Spencer T, et al. A double-blind, crossover comparison of methylphenidate and placebo in adults with childhood-onset attention-deficit hyperactivity disorder. Arch Gen Psychiatry. 1995;52(6):434–43.PubMedCrossRefGoogle Scholar
  73. 73.
    Wilens TE, Biederman J, Spencer TJ. Attention deficit/hyperactivity disorder across the lifespan. Annu Rev Med. 2002;53:113–31.PubMedCrossRefGoogle Scholar
  74. 74.
    Tucha O, et al. Methylphenidate-induced improvements of various measures of attention in adults with attention deficit hyperactivity disorder. J Neural Transm. 2006;113(10):1575–92.PubMedCrossRefGoogle Scholar
  75. 75.
    Curtin C, et al. Prevalence of overweight in children and adolescents with attention deficit hyperactivity disorder and autism spectrum disorders: A chart review. BMC Pediatr. 2005;5:48.PubMedCrossRefGoogle Scholar
  76. 76.
    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;33:326–34.CrossRefGoogle Scholar
  77. 77.
    Habel, L.A., et al., ADHD Medications and Risk of Serious Cardiovascular Events in Young and Middle-aged Adults. JAMA, 2011.Google Scholar
  78. 78.
    Anderson JW, et al. Bupropion SR enhances weight loss: A 48-week double-blind, placebo- controlled trial. Obes Res. 2002;10(7):633–41.PubMedCrossRefGoogle Scholar
  79. 79.
    Gadde KM, et al. Atomoxetine for weight reduction in obese women: A preliminary randomised controlled trial. Int J Obes (Lond). 2006;30(7):1138–42.CrossRefGoogle Scholar
  80. 80.
    Leddy JJ, et al. Influence of methylphenidate on eating in obese men. Obes Res. 2004;12(2):224–32.PubMedCrossRefGoogle Scholar
  81. 81.
    Goldfield GS, Lorello C, Doucet E. Methylphenidate reduces energy intake and dietary fat intake in adults: a mechanism of reduced reinforcing value of food? Am J Clin Nutr. 2007;86(2):308–15.PubMedGoogle Scholar
  82. 82.
    Davis, C., et al., The suppression of appetite and food consumption by methylphenidate: the moderating effects of gender and weight status in healthy adults. Int J Neuropsychopharmacol, 2011: p. 1-7.Google Scholar
  83. 83.
    Archer, T. and R.M. Kostrzewa, Physical Exercise Alleviates ADHD Symptoms: Regional Deficits and Development Trajectory. Neurotox Res, 2011.Google Scholar
  84. 84.•
    Davis C, et al. Exercise improves executive function and achievement and alters brain activation in overweight children: A randomized controlled trial. Heal Psychol. 2011;30(1):91–8. This randomized controlled trial is the first to show that benefits of exercise on executive function and achievement in overweight children.CrossRefGoogle Scholar
  85. 85.
    Gapin JI, Labban JD, Etnier JL. The effects of physical activity on attention deficit hyperactivity disorder symptoms: the evidence. Prev Med. 2011;52 Suppl 1:S70–4.PubMedCrossRefGoogle Scholar
  86. 86.
    Verret C, Gardiner P, Beliveau L. Fitness level and gross motor performance of children with attention-deficit hyperactivity disorder. Adapt Phys Activ Q. 2010;27(4):337–51.PubMedGoogle Scholar
  87. 87.
    Gapin J, Etnier JL. The relationship between physical activity and executive function performance in children with attention-deficit hyperactivity disorder. J Sport Exerc Psychol. 2010;32(6):753–63.PubMedGoogle Scholar
  88. 88.
    Joseph RJ, et al. The neurocognitive connection between physical activity and eating behaviour. Obes Rev. 2011;12(10):800–12.PubMedCrossRefGoogle Scholar
  89. 89.
    Safren SA, et al. Cognitive-behavioral therapy for ADHD in medication-treated adults with continued symptoms. Behav Res Ther. 2005;43(7):831–42.PubMedCrossRefGoogle Scholar
  90. 90.
    Safren SA. Cognitive-behavioral approaches to ADHD treatment in adulthood. J Clin Psychiatry. 2006;67 Suppl 8:46–50.PubMedGoogle Scholar
  91. 91.
    Stevenson CS, et al. A cognitive remediation programme for adults with attention deficit hyperactivity disorder. Aust N Z J Psychiatry. 2002;36(5):610–6.PubMedCrossRefGoogle Scholar
  92. 92.
    Hesslinger B, et al. Psychotherapy of attention deficit hyperactivity disorder in adults–a pilot study using a structured skills training program. Eur Arch Psychiatry Clin Neurosci. 2002;252(4):177–84.PubMedGoogle Scholar
  93. 93.
    Adler LA, et al. Validity of pilot Adult ADHD Self-Report Scale (ASRS) to rate adult ADHD symptoms. Ann Clin Psychiatry. 2006;18(3):145–8.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Sherry Pagoto
    • 1
  • Carol Curtin
    • 2
  • Bradley M. Appelhans
    • 3
  • Miguel Alonso-Alonso
    • 4
    • 5
    • 6
  1. 1.Division of Preventive and Behavioral Medicine, Department of MedicineUniversity of Massachusetts Medical SchoolWorcesterUSA
  2. 2.Eunice Kennedy Shriver Center, Department Family Medicine & Community HealthUniversity of Massachusetts Medical SchoolWalthamUSA
  3. 3.Preventive Medicine, Rush Medical CollegeChicagoUSA
  4. 4.Neurology, Harvard Medical SchoolBostonUSA
  5. 5.Berenson-Allen Center for Noninvasive Brain StimulationBostonUSA
  6. 6.Division of Cognitive NeurologyBeth Israel Deaconess Medical CenterBostonUSA

Personalised recommendations