Attention-deficit/Hyperactivity Disorder: Associationswith Overeating and Obesity

Caroline Davis

Published online: 15 July 2010# Springer Science+Business Media, LLC 2010

Abstract In the past decade, we have become increasinglyaware of strong associations between overweight/obesityand symptoms of attention-deficit/hyperactivity disorder(ADHD) in children, adolescents, and adults. This reviewaddresses the prevalence of the comorbidity and discussessome of the mechanisms that could account for theirrelationship. It is suggested that the inattentive andimpulsive behaviors that characterize ADHD could con-tribute to overeating in our current food environment, withits emphasis on fast food consumption and its many foodtemptations. It is also proposed—based on the compellingevidence that foods high in fat, sugar, and salt are asaddictive as some drugs of abuse—that excessive foodconsumption could be a form of self-medication. This viewconforms with the well-established evidence that drug useand abuse are substantially higher among those withADHD 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 childhoodbecause the developmentally inappropriate signs of distract-ibility, impulsiveness, and inattention that characterizethis condition typically appear before the age of 7 years.

Eventually, however, it became evident that for manyindividuals, these symptoms did not remit and persisted intoadulthood in a significantly debilitating way [1]. Thisrecognition has since prompted the reconceptualization ofADHD as a “life span disorder.” Although its etiology is notfully understood, there is general agreement that a biologicalcomponent of the disorder relates to (dys)functioning of theprefrontal cortex, processes typically known as “executivefunctions” because they subserve reasoning, planning, inhi-bition, and decision making [2]. Considerably less is knownabout environmental and development factors (including inutero events) that may contribute to ADHD symptoms, orabout gene–environment effects that could influence thedisorder’s onset.

It is very well-established, however, that ADHD coexistswith a host of other clinical disorders. For example, majordepression, bipolar disorder, and generalized anxiety arehighly prevalent in those with ADHD [3], and in somecases, the disorder is associated with antisocial behaviorand criminality [4]. A wealth of evidence also links ADHDto addiction disorders such as drug abuse and alcoholism—comorbidities that are robust and bidirectional [5, 6].Indeed, a recent familial risk analysis indicated that ADHDand drug dependence share a common vulnerability profilerather than present with independent modes of transmission[7]. As both disorders have strong links to mesocortico-limbic pathways, Biederman and colleagues [7] proposedthe conjoint involvement of brain dopamine activation andits regulation of arousal, attention, and reinforcement.

In recent years, we have become increasingly aware ofstrong links between ADHD and obesity [8, 9]. The firststudies to draw attention to this association were publishedin 2002 [9, 10]. Both found a substantially higher thanexpected prevalence of ADHD in adults receiving treatmentfor obesity and an even greater occurrence (close to 50%

C. Davis (*)York University,343 Bethune College, 4700 Keele Street,Toronto, Ontario M3J 1P3, Canadae-mail: cdavis@yorku.ca

Curr Psychiatry Rep (2010) 12:389–395DOI 10.1007/s11920-010-0133-7

of the sample) in those with class III obesity (body massindex >40 km/m2). The comorbid group also had moreclinic visits and longer treatment duration than their non-ADHD counterparts [9]. Recent data from a large,nationally representative sample of adults in the UnitedStates also found that adult ADHD was associated witha 1.6 OR of being overweight and a 1.8 OR of beingobese [11••].

Since then, other studies have assessed the obesityassociation in children and adolescents with ADHD. Inone study, the prevalence of overweight and obesity wassignificantly greater in the ADHD sample compared withage-matched population norms [12]. At first glance, theseresults are rather counterintuitive, as a preeminent charac-teristic of ADHD in children is physical restlessness andhyperactivity. Moreover, only 14% of the Holtkamp et al.[12] sample were receiving pharmacologic treatment forADHD at the time of assessment, and the remainder weremedication naive. Medication status is clearly an importantconsideration, as weight loss and decreased appetite areamong the adverse effects of the common psychomotorstimulants (e.g., methylphenidate) used to treat individualswith ADHD. Therefore, when investigating the ADHD–obesity links, it is important to consider possible moderatoreffects of pharmacologic treatment. Of relevance to thisissue, a large US study found that unmedicated children andadolescents with ADHD had about 1.5 times the odds ofbeing overweight, while their medicated counterparts hadsimilar odds of being underweight [13••]. These resultswere partially confirmed by Ptacek et al. [14], who foundthat the nonmedicated children with ADHD had a higherpercentage of body fat compared with the methylphenidate-medicated boys and with population norms, although therewere no significant height or weight group differences.What is unclear about these correlational findings inchildren and adolescents is whether treatment status reflectsan appetite suppression effect of the medication or animprovement in behavioral regulation and therefore health-ier eating habits. Another possible explanation is that thegreater cognitive effort required to execute standard mentaltasks by those with untreated ADHD may foster hyperpha-gia. This interpretation is based on evidence that mentalwork substantially increases ad libitum food intake [15].

In summary, almost a decade of research has establishedsound links between ADHD and obesity in adults, children,and adolescents. It also appears that this relationship is notattributable to sociodemographic factors that influencepeople’s dietary patterns and opportunity for physicalactivity [16]. However, one impediment to our understand-ing of the ADHD–obesity relationship has been the focuson studies that have included only cases of ADHD thatmeet full diagnostic criteria for the disorder. Such anapproach 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 medicationeffects (as we have seen in the studies described previously).One strategy that avoids the potential confounds of clinicalresearch is to examine associations among ADHD symptoms,aspects of overeating, and body weight in healthy participantsfrom the general population. This approach is predicated onthe assumption that personality factors and symptoms ofdisorder are best conceptualized dimensionally and occur withnormal variation in the general population [17].

Mechanisms of Association

During the past few years, research has moved from anemphasis on comorbidity prevalence rates to attempts atidentifying the mechanisms whereby obesity and ADHDpresent as overlapping conditions. In a current review—andas a way of explaining why the ADHD–obesity connectiononly appeared in the literature in 2002—Cortese et al.[18••] claim that the association was simply “overlooked”in the past. In my opinion, there is no evidence of neglect oroversight in the obesity or ADHD areas of research. Indeed,a more plausible explanation is that the association onlyemerged in the past decade with sufficient frequency for itto be recognized as a clinically relevant phenomenon. Inother words, current conditions have given rise to acomorbidity that was less visible (or nonexistent) in earlierdecades because the environmental risk for its developmentwas largely absent. For example, we have seen anincreasingly high prevalence of obesity since the 1980s[19] that is in stark contrast to earlier time periods. Therehave also been dramatic changes in our food environmentduring the past generation that have had a profound effecton population weight gain [20]. An added factor is thegroundswell of scientific research and clinical interest inidentifying the causes of obesity in recent years. Ofparticular relevance are the strong links that have beenestablished among impulsivity, the purchase of high-caloriefoods, overeating, and obesity [21]. These relationshipsalmost certainly have guided scientific investigations in thedirection of syndromes such as ADHD, a disorder in whichimpulse control is a key diagnostic facet.

For several reasons, I would argue that the ADHD–obesity association is essentially a modern variant of theADHD–drug abuse comorbidity that has been recognizedand documented for many years [6]. In the followingsections, I offer support for the premise that ADHD andobesity are interconnected by virtue of their respectiveassociations with addiction disorders, the former displayinga proneness to and the latter occurring as a consequence ofaddiction. Expressed slightly differently, their comorbidityis the function of a shared diathesis whereby a predisposi-

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tion to impulsive responding collides with a toxic foodenvironment that exploits this vulnerability. The outcome isan increased probability of overeating and chronic weightgain in those with symptoms of ADHD.

Binge Eating and Food Addiction

Nowhere in nature is there food as high in fat, sugar, andsalt (HFSS)—and sometimes caffeine—as we find in mostof the processed foods we consume on a daily basis. Suchpalatable foods have the facility to activate the mesocorti-colimbic pathways in the brain in a manner similar to otheraddictive substances, and much more potently than wouldoccur for natural sources of energy [22••]. Compellingevidence indicates, based largely on well-controlled animalresearch, that HFSS foods have the potential for abuse andcan lead to dependence in the manner of other condensedand concentrated substances such as cocaine and heroin[23, 24]. Like drugs of abuse, they have the ability toalter brain mechanisms in ways that contribute to theirincreasingly compulsive use [25, 26]. Their excessiveingestion also seems to foster binge eating episodes,symptoms of tolerance and withdrawal, and craving-likebehaviors [22••, 27••].

These findings, in addition to a host of testimonials fromthose who suffer from compulsive overeating, have promptedthe claims that some cases of obesity may be the consequenceof a “food addiction” [27••, 28]. For some individuals,overeating is mostly a passive event that occurs withoutmuch awareness and takes place in the form of frequentsnacking, eating calorie-dense meals, and selecting largeportion sizes. For others, however, it can be an excessivelydriven activity. We have recently argued that binge eatingdisorder (BED) is a particular pattern of overeating with thestrongest parallels to other addiction disorders and thereforeis the quintessential food addiction phenotype [27••]. Wealso believe that sound clinical and scientific evidencesupports this viewpoint. For example, Cassin and vonRanson [29] found that 94% of their adult BED sampledescribed themselves as “food addicts” or “compulsiveovereaters” and met criteria for substance-dependencedisorder when the term substance referred to “binge eating.”

In the general population, binge eating has strongconnections with symptoms of ADHD, similar to thelongstanding associations of ADHD with addictive druguse/abuse [30]. Clinical research also has demonstrated thatbinge eating behaviors, such as those seen in BED orbulimia nervosa, occur in patients with ADHD [31]. Inaddition, BED seems to mediate the relationship betweenADHD and overweight/obesity [11••]. Various causal mech-anisms could link binge eating and ADHD. The symptomsand hypodopaminergic functioning that characterize ADHDseem to be ameliorated by dopamine-elevating behaviors

(hence the treatment success of psychomotor stimulants) andmay explain why some individuals succumb to illicit and/orrecreational drug taking. It is therefore plausible that“comfort foods” could serve as a form of self-medicationin those with ADHD given their dopamine-activatingproperties. If we accept that BED is appropriately concep-tualized as a food addiction, then excessive HFSS foodconsumption can be seen as just another form of drug abuse.In other words, ADHD is a disorder defined by variousmaladaptive traits, and drug use is just one of the behavioralmanifestations of the deficits associated with this condition.

Another possible causal mechanism is based on the well-established evidence that cross-sensitization occurs fromone drug of abuse to another—and that cross-sensitizationalso occurs between intermittent sugar intake and addictivedrugs [22••]. It may therefore be that stimulant treatment(eg, Ritalin; Novartis, Basel, Switzerland) in early lifepredisposes these individuals to the reinforcing propertiesof sugar as they mature, thereby increasing their pronenessto obesity. Currently, I am unaware of any research that hasprospectively assessed whether those with childhoodADHD and previously treated with stimulants are morelikely to be obese as adults compared with their nontreatedcounterparts. Such a possibility provides an intriguing areafor future research.

Self-regulation Deficits

Among the impairing traits associated with obesity andADHD—and another unifying thread in their comorbidity—is the centrality of high impulsivity in both conditions. Thisterm is used to describe a multidimensional and relativelystable human personality trait that is characterized by 1) thediminished ability to exhibit restraint when this is the mostadvantageous and socially appropriate response in a particularsituation, 2) an enhanced tendency to approach and engage inrewarding and pleasurable stimuli, and 3) impetuous respond-ing without an appropriately adaptive concern for the futureconsequences of one’s actions.

We have learned that brain dopamine pathways play animportant 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 associatedwith 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 diagnosticcriteria for this disorder. In a recent and relevant prospec-tive study, it was also found that low impulsivity predicteddecreases in body mass index percentile rank in childrenfrom fifth to eighth grade. In other words, the self-controlled(nonimpulsive) children seemed to be protected from weightgain in their transition to adolescence [36].

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The impulsivity that characterizes ADHD is almostcertainly a key factor mediating the relationship betweenthis disorder and obesity. However, the mechanisms bywhich impulsivity contributes to weight gain are less clear.Nowadays, in the face of an overabundance of high-caloriesnacks and meals, effortful control of food intake—what iscolloquially called willpower—is essential for the mainte-nance of a healthy body weight. Historically, however, suchself-regulated restraint would have been rather antitheticalto the strong appetitive drives that fostered optimal fitnessduring most of our evolution. In the world of ready-mademeals and cafeteria dining, healthy food choices are clearlynot the easiest option. They typically require forethoughtand planning, extended time for preparation, and the abilityto show steadfast control when faced with tempting andquicker alternatives. A better understanding of the naturalhuman variation in self-regulated behaviors is clearly a wayforward in explaining why some individuals are proneto chronic overeating while others, living in the sameenvironment, can eat moderately and maintain a healthybody weight [37•].

Impulsivity has been a difficult construct to studybecause it involves at least two identifiable cognitive/emotional processes: reward-driven behaviors on the onehand and those characterized by poor inhibition on theother. It has also generated many measures and assessmentdevices that are not always highly correlated [38]. Inhibitorycontrol deficits, seen as impulsive responding and inatten-tion, are largely regulated by the prefrontal cortex, whichundergoes major developmental changes from childhood toadolescence [39]. Impairment in these processes is typical ofthose with ADHD. Verbeken et al. [40] also found thatoverweight children showed less efficient executive inhibi-tory control and more reward-directed behavior as assessedby performance-based tasks. In addition, in a recent study,we demonstrated poor decision making and diminishedability to delay gratification in two groups of obese adults—those with and those without BED [37•]. Although the twoobese groups did not differ from each other, they were bothsignificantly impaired compared with an age- and gender-matched group of normal weight adults.

To our knowledge, only two studies have assessedwhether impulsivity predicts success in a weight reductionprogram [41, 42]. In the more recent and larger study, highimpulsivity predicted greater weight loss in adolescents, butnot 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-impulsivechildren lost more weight—findings that also mesh withadult research obtained from patients at a bariatric treatmentcenter [9]. At this point, however, we must conclude thatthe role of impulsivity in weight loss and weight lossmaintenance is still inconclusive given the very few

systematic treatment studies that have been published.Future replication studies and more detailed investigationswith stratified analyses based on age, gender, and otherrelevant covariates are needed before firm conclusions canbe drawn.

Environmental Influences

Twin and adoption studies indicate that genetic factorsmake a large contribution to the etiology of ADHD, withestimates of heritability ranging from 60% to 91% [43]. It isalso generally agreed that complex mental disorders such asADHD are the result of a reciprocity between geneticfactors and environmental influences (G × E). To date,however, the manner in which susceptibility genes interactwith environmental risk factors is not clearly understood.Essentially, there are two broad possibilities to describehow a G × E interplay could come about. On the one hand,environmental factors only lead to an adverse outcome inthe presence of a specific genetic makeup; on the otherhand, an individual with a susceptible genetic makeup willonly develop the adverse outcome if additional environ-mental pathogens are present [44]. In the case of theADHD–obesity links, the latter seems the more probablecausal route in that the association only emerged when thefood environment changed dramatically during the pastgeneration or so. That the exponential increase in theprevalence of obesity has also occurred in a relatively shortperiod of time highlights the importance of the interactionbetween the ADHD genotype and the toxic food culture inwhich it began to find itself. Those with the greatest geneticvulnerability are those who are likely to show the greatestweight gain, whereas those with genetic resistance tend toremain relatively weight stable [44].

Prenatal Drug Use

ADHD and its subsequent developmental course, whichshows both continuity and change, are influenced byvarious pre- and perinatal, biological, and psychosocialenvironmental risk factors. Some that have stood the test ofreplication include the deleterious influence of maternalsmoking and alcohol consumption during pregnancy, aswell as low infant birth weight/prematurity [45]. Fetalalcohol syndrome was first identified in 1973 as a conditionwith severe birth defects, including facial disfiguration andmental retardation, and was associated with heavy maternalalcohol use during pregnancy. However, it was not until the1980s that the US Surgeon General issued an advisoryrecommending that women abstain from drinking alcoholduring pregnancy, and almost a decade later before healthwarning labels were added to alcoholic beverage containers

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[46]. During the late-1980s, it was estimated that about30% of American women were still drinking alcohol duringpregnancy despite these warnings, so one can only assumethe rates were considerably higher before that time,especially with the growing visibility of female alcoholismin the decades following World War II [47].

The neurobehavioral deficits found in children withprenatal exposure to alcohol—what are now called fetalalcohol spectrum disorders (FASDs) or alcohol-relatedneurodevelopmental disorder—include symptoms ofinattention, restlessness, impulsivity, antisocial behavior,and a diminished ability to anticipate future consequences.Clearly, these deficits vary in severity, and in cases of mildsymptomatology, there may not be any formal diagnosis atall. To some extent, the severity of symptoms may be adose-dependent consequence of the extent and timing of themother’s alcohol intake. It is now generally agreed thateven relatively small amounts of alcohol can cause fetalimpairments in some cases.

What is instantly evident is the remarkable similarity ofFASD symptoms to those of ADHD. Indeed, a substantiallyhigh proportion of children with prenatal alcohol exposure—as many as 70%—are also diagnosed with ADHD [48]. Somerecent studies have compared FASD and ADHD andreported certain qualitative differences in their respectivetypes of attention problems [49]. However, such studies areproblematic and inconclusive because of the high dualdiagnosis between FASD and ADHD and therefore theinability to compare “pure groups” of each condition.Moreover, few if any studies of ADHD take account ofthose with and without prenatal alcohol exposure. It isentirely possible that maternal alcohol use, which was notsignificantly curtailed until a decade or so ago, is oneenvironmental causal contributor to this disorder and notmerely a condition with pronounced symptom similarities.Prenatal exposure may have a sensitizing drug influence onthe developing fetus and may also account for the higherthan expected drug use and abuse in those with ADHD.

Prenatal Dietary Factors

Using data collected from three affluent Scandinaviansocieties, a prospective study showed for the first time thatmaternal overweight and obesity increased the risk ofhaving a child with ADHD symptoms compared withmothers who were normal weight at the time they becamepregnant [50]. Interestingly, these findings persisted aftercontrolling for baby’s birth weight, maternal age, andmother’s smoking status in the statistical analyses. However,the authors speculated that perhaps the relationship occurredbecause a genetic predisposition accounted for both themother’s weight status and the subsequent ADHD symptomsin the child.

To test this prediction and to ascertain whether theprevious associations would exist independent of otherpotential causal risk factors (eg, parental ADHD symptoms),a large replication and extension study was carried out ofprepregnancy obesity and offspring symptoms of ADHD.Again it was found that children of obese mothers had atwofold increase in teacher-rated inattention scores com-pared with children of normal weight mothers [51•]. Theseinattentive children also displayed significantly greaternegative emotionality. Arguments against the possibilitythat a common genetic predisposition linked maternalweight and child ADHD symptoms rest on the fact thatthe associations remained statistically significant aftercontrolling for ADHD symptoms in both parents. Theauthor concluded that maternal prepregnancy obesity is notmerely an artifact of other influences that may coexist withmother’s weight status.

While Rodriguez [51•] proposed certain mechanismsthat could account for the associations observed in herstudy, in my view, one possibility of considerable relevanceto the ADHD–obesity link was overlooked. Excess bodyweight is in large part the result of high fat consumption,whereas high sugar intake seems to be responsible forproducing addictive-like behaviors such as cravings, with-drawal, and compulsive intake [24]. In our current foodenvironment, with its superfluity of highly palatable foods,mothers who are overweight and obese are likely toconsume larger and more frequent quantities of HFSSfoods than normal weight mothers. As noted previously,good evidence indicates that these foods can cause brainneurochemical responses similar to those caused by otherdrugs of abuse. Therefore, highly processed and calorie-dense food consumed in abundance during pregnancy couldproduce deleterious outcomes in the unborn child in thesame way that we see in the offspring of mothers whosmoke and/or drink alcohol during pregnancy. In otherwords, the excessive ingestion of HFSS foods couldproduce what I will loosely call a fetal sugar spectrumdisorder, with consequences that are not dissimilar to thoseseen in the offspring of mothers who drank alcohol andsmoked nicotine during pregnancy.

Conclusions

I am aware of only one study that has examined the effectsof treating ADHD symptoms in obese individuals who areattempting to lose weight. Levy and colleagues [52••]recently reported the results of a longitudinal investigationin 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 wasnoted in these patients compared with an untreated control

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group, who actually gained weight during the same timeperiod. The authors also found that treating symptoms ofADHD with medication improved the mental and physicalhealth and the quality of life of those who were obese.Although the appetite-suppressing effects of the medicationappeared to diminish after a few months, patients continuedto 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 purposes—that is, to restore energy or to focusattention. Importantly, binge eating diminished very sub-stantially or stopped altogether in these patients.

This study was the first to target ADHD in the treatmentprotocol and therefore has important implications for themanagement of obesity and its adverse health consequences.Although surgical procedures such as laparoscopic bandingand gastric bypass are increasingly popular options forhandling refractory obesity, their success depends on adheringto strict postoperative dietary instructions following thetreatment.

Based on clinical observation, Levy and colleagues[52••] claim that obese patients with comorbid ADHD areless able to comply with postsurgical recommendationsthan others; therefore, careful screening of obese patientsseeking surgical treatment is strongly advised.

Disclosure No potential conflict of interest relevant to this articlewas reported.

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