developmental contributions to the obesity epidemic - cairn

DEVELOPMENTAL CONTRIBUTIONS TO THE OBESITY EPIDEMIC

Julie Carroll Lumeng, Elliott M. Blass

Presses Universitaires de France | « Enfance »

2008/3 Vol. 60 | pages 289 à 297 ISSN 0013-7545ISBN 9782130568322DOI 10.3917/enf.603.0289

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Developmental contributionsto the obesity epidemic

Julie C. Lumeng*, Elliott M. Blass**

SUMMARY

The obesity epidemic is a health crisis that is behavioral in origin. Weight statusand food preferences have their origins even prenatally. Obesity, once established evenin early childhood, tends to persist throughout the lifespan. Likewise, the window forestablishing food preferences and acceptances appears to close by about age 4 years.The ontogeny of weight status and food preferences begs a better understanding offactors which lead to the development of a dietary pattern that is obesigenic. Wereview briefly the epidemiological and neurobiological evidence for overeating and pre-ferences for sweets and fats being addictive behaviors, and obesity being an addictivedisorder. An innate or early-appearing preference for sweet, the soothing and opioid-like properties of sweet taste that reinforce its ingestion, and a simultaneous reluc-tance to sample unfamiliar foods make the early development of preferences for sweet,fat, and calorically-dense foods a very difficult behavior to change. The modern envi-ronment enables reduced energy expenditure, as well as increased energy consumptionthrough the relatively constant availability and promotion of energy-dense, palatablefoods. This environment compounds the risk incurred by the addictive properties offood. Public health interventions have successfully addressed other national and inter-national health crises of similar proportions, and a concerted, informed, careful andevidence-based approach may be similarly effective for obesity.

Key-words: Addiction, Food preferences, Child development.

RÉSUMÉ

Contributions développementales à l’épidémie de l’obésité

L’épidémie actuelle d’obésité est une crise sanitaire dont l’origine relève du com-portement. Le statut pondéral et les préférences alimentaires s’enracinent dans la

ENFANCE, no 3/2008, p. 289 à 297

* Center for Human Growth and Development, 300 North Ingalls, 10th Floor, Univer-sity of Michigan, Ann Arbor, Michigan, USA 48109-5406. E-mail : [email protected].

** Department of Psychology, Tobin 417, Amherst, Massachusetts, USA 01003. E-mail :[email protected].

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période prénatale. L’obésité, une fois établie durant l’enfance, tend à persister tout aulong de la vie. De la même façon, la formation des préférences et choix alimentairesapparaît largement acquise aux environs de 4 ans. L’ontogenèse du statut pondéral etdes préférences alimentaires requiert une meilleure compréhension des facteurs quicontribuent au développement d’un régime obésogène. Nous examinons brièvement lesdonnées épidémiologiques et neurobiologiques qui suggèrent que l’excès alimentaire etles préférences pour le sucré et le gras relèvent de comportements addictifs, et quel’obésité relève d’un trouble addictif. Une préférence innée ou précoce pour le sucré,les propriétés apaisantes et opioïdergiques du goût sucré qui favorisent son ingestion,et la réticence à essayer des aliments non familiers, rendent très difficile toute modifi-cation du développement précoce des préférences pour des aliments sucrés, gras etriches en calories. Par ailleurs, le mode de vie moderne favorise la réduction desdépenses énergétiques et l’accroissement de la consommation de calories à traversl’offre constante et la promotion de produits alimentaires caloriques et agréables augoût. Cet environnement aggrave les facteurs de risque liés aux propriétés addictivesdes aliments. Des mesures de santé publique ont fait face avec succès à d’autresurgences sanitaires nationales et internationales d’importance comparable, et uneapproche basée sur une connaissance concertée et précise des faits pourrait être toutaussi efficace pour circonvenir l’obésité.

Mots clés: Dépendance, Préférences alimentaires, Développement de l’enfant.

The obesity epidemic shows no sign of abating, rapidly spreading fromthe United States to all portions of the Western world, including Europe.Information concerning systematic causes of overeating will providedirection for combating the problem (Blass, 2008). In this essay, wediscuss the origin and persistence of food preferences and obesity fromearly childhood. We argue that overeating, specifically of sweets and fats,represents an addictive behavior. Finally, we describe how the addictiveproperties of food confer greatly increased obesity risk in the modernenvironment.

Concern about the development of healthy eating and food preferencesearly in life is warranted. First, childhood obesity, once established, tendsto persist (Freedman et al., 2005; Nader et al., 2006); an obese, comparedto a non-obese, 4-year-old is nearly 5 times as likely to be an obese adult(Whitaker et al., 1997). The etiology of this tracking of weight statusthrough the lifespan has not been identified, but is undoubtedly multi-fac-torial. Early childhood exercise, eating habits and food preferences maypersist. Alternatively, metabolism may be altered to favor the accumulationof adipose tissue, even in absence of drastic overeating. The intrauterineenvironment influences future weight status, suggesting that early metabolicinfluences might endure. Higher maternal pre-pregnancy and first trimesterweights predict higher birth weight, independent of potential confoundersincluding weight gain during pregnancy (Jensen et al., 2003). In turn,higher birth weight predicts overweight in childhood (Rugholm et al., 2005;Whitaker, 2004) and more rapid weight gain during the first year of life

290 JULIE C. LUMENG, ELLIOTT M. BLASS

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predicts future obesity even into adulthood (Baird et al., 2005; Dennisonet al., 2006; Ekelund et al., 2006; Stettler et al., 2002).

Secondly, new food acceptances are difficult to establish after 4 years ofage (Skinner et al., 2002), and once food preferences for unhealthy, calorie-dense foods (CDFs) are established, they are not easily overcome. Thesetypes of behaviors appear to be rooted in the omnivore strategy that hasserved us well over evolutionary history. Together, shunning toxic foodsand eating very palatable ones guarantee avoiding proven toxins and selec-ting energy dense foods. This is understandable from a pre-agricultural his-tory that was somewhat capricious in providing food. When a tasty mealpresented itself, especially in a safe place, short term satiety signals could beignored and more eaten, thereby protecting against short-term food scar-city. The pattern reaches its extreme when hibernators “fatten up” inadvance of the long winter and lower their metabolism. Although this stra-tegy has worked well along the calendar of evolution, technological agricul-tural and transportation advances have upset this balance by providing see-mingly unlimited CDFs to a feeding system that had been crafted to exploitsuch previously rare meals.

Add to this that behavioral reinforcement systems are functional atbirth (Blass et. al., 1984) and may contribute to the development of foodpreferences, which are not fully specified in the first years of life. As will bediscussed below, the ingestion of fats and sweets has neurobiological rein-forcing properties. Since today’s human cultures are offering diets increa-singly rich in fats and sweets, the addictive properties of these highly pala-table foods provide a robust point of entry in early childhood (andpotentially even prenatally) for lifelong obesity.

Like any syndrome, addiction demarcates a constellation of events andconsequences that surround a common theme, including common physiolo-gical and behavioral manifestations. Addicts, by definition, need that towhich they are addicted. Urges to consume addictive substances or toengage in addictive behaviors, like gambling or sex, reflect psychologicalneeds. Unlike natural urges such as thirst, CDF needs do not rise out ofphysiological deficit. Rather, addictive qualities are acquired; originally asubstance was wanted, as in recreational drugs. Over time and withrepeated use, wanting becomes transformed into needing. Identifying theorigins as behavioral/cognitive and acquired does not at all diminish painof withdrawal, or urgency. It does, however, provide a point of impact.

The neurology of addiction underlies all motivation; i.e., the neuro-logies of urge and affect. They follow the rules of reinforcement and habitformation, most notably, the larger the reward, the greater the urge toobtain them again, and the more likely the success in doing so. Effects arecumulative so that obtaining the third “hit” is more likely than the secondand so on. At some point in the individual’s history, the relationshipbetween user and object shifts from wanting the commodity to needing it,the hallmark of addiction. Need is especially triggered by stimuli or events

DEVELOPMENTAL CONTRIBUTIONS... 291

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that have predicted or been regularly associated with previous “hits”. Com-monalities shared by overeating and other addictions include difficulty inquitting, dieting ineffectiveness and vulnerability to stress, which rekindlesthe habits. Categories of structure, neural function, and behavior presentedin Table provide a matrix of recognized addictions against which ingestingsweet and fatty foods match up. The concordance between establishedaddictions and overeating is remarkable: some of the major factors requirefurther comment.

Commonalities between overeating/obesity and all recognized addictions

Characteristic Overeating/obesity Addiction

Neurology Medial forebrain bundle Medial forebrain bundleNeurochemistry Dopamine,

Opioid/CannabinoidDopamine,Opioid/Cannabinoid

Addicting substances Manufactured ManufacturedCravings Profound ProfoundCompliance Poor PoorReinstatement Conditioned Stimuli Yes YesReinstatement: drug/taste Yes YesStress Yes YesPsychological dependence Yes YesPhysiological dependence ? YesWithdrawal Delayed Immediate

EPIDEMIOLOGICAL EVIDENCE

FOR OVEREATING AS AN ADDICTION

Inverse relationships between obesity and addictive disorders are therule. Obese adults have a 25% lower lifetime prevalence of substance abuse,despite a higher incidence of affective disorders (Simon et al., 2006). Thisalso holds for alcohol consumption in obese women (Kleiner et al., 2004).In addition, adolescents in substance abuse treatment programs who suc-cessfully abstain from drug-use exhibit weight gain (Hodgkins et al., 2004).In short, drug/alcohol use and energy-dense food consumption were inver-sely correlated in studies of very different populations. “Self-medicating”through sweets and fats may have made obese individuals less likely to turnto drugs or alcohol.


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NEUROPHYSIOLOGY OF OVEREATING AS AN ADDICTION

Sweets and fats engage the central reward systems formerly used byaddicting drugs, or successfully compete for and make these systems lessavailable through pre-established obesity. Others have suggested thatsweets and fats enhance dopamine (DA) synthesis and utilization throughopioid release, setting the stage for intense reward, and through standardreinforcement mechanisms, addiction (Hodgkins et al., 2004). In fact,animal research has shown that all addictions share a common path thattraverses the medial forebrain bundle/ventral tegmental area (Wise, 2008).

Imaging studies in humans support this view (Aharon et al., 2001).Reductions in striatal dopamine D2 receptors within central reward circuitsamong drug-addicted subjects and in the morbidly obese have beenobserved using positron emission tomography (Wang et al., 2004). The cli-nical correlates are striking: medications that block dopamine D2 receptorsinduce weight gain, while medications such as methylphenidate (Ritalin)that increase brain DA concentrations, markedly decrease appetite. In short,DA agonists reduce appetite, while DA antagonists increase appetite. Amongthe obese, reduced D2 receptor availability suggests a down-regulation thatmay be compensated for through more intense food stimulation.

Two pathways shared by all addictions, regardless of origin, are themedial forebrain bundle (MFB) and the ventral tegmental area (VTA). DA isthe primary neurotransmitter in each pathway and pockets of opioid andcannabinoid receptors are interspersed throughout. Laboratory rats andprimates work for hours for electrical or chemical (DA, opioid, cannabi-noid) stimulation of these areas (Wise, 2008). Such stimulation evokeseating, especially of sweet foods. Humans who have received electricalMFB/VTA stimulation prior to surgery report generally unspecified pleasure(Wise, 2008). Blocking DA transmission either through lesions or neuroche-mical depletion provokes a syndrome of sensory neglect, motor impair-ment, and anhedonia that is fatal (Marshall & Teitelbaum, 1974). Recoveryensues in animals maintained by tube feeding, and they appear to benormal, albeit rather fragile, as the syndrome can be reinstituted throughstress (Marshall & Teitelbaum, 1974).

We manufacture our own opioids, the endorphins, which are distributedthroughout the brain, spinal cord, stomach and gastrointestinal (GI) tract.The hallmark of the system is its involvement in energy conservation. Thus,energy dense foods cause endorphin and DA release, which, in turn, act in a“feed-forward” manner to secure additional foods and ensure increasedintake. Appetizers are in this manner appetite stimulants and are routinelyprovided to whet our appetites.

Opioids contribute significantly to energy conservation throughout theneuroaxis and in digestion. Gastric and GI opioids facilitate digestion. Cen-


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tral, including spinal opioids, help mitigate pain. Pain-killers such as mor-phine are fabricated for accommodation by endogenous receptors, whichlike all aspects of the nervous system, recognize structure in triggering aresponse. Response magnitude, however, reflects concentration, size andother quantitative aspects of the triggering stimulus. This is especially truein the domains of intake and especially in infants. A series of studies byBlass and colleagues has demonstrated, that sweets and fats, the two majorconstituents in mothers’ milk, calm newborn rats (Blass, Fitzgerald,& Kehoe, 1987) and humans (Smith, Fillion, & Blass, 1990) and alleviatepain (Blass & Hoffmeyer, 1991; Blass & Watt, 1999). Opioid systems arefunctional even during the prenatal period (Smith & Blass, 1996). Sugarsand fats reduce heart rate, as well as crying (Blass & Watt, 1999). Thejustly famous reports by Jacob Steiner (1974) on sweet taste eliciting smilesin newborns testifies to affective change. Naloxone, the opioid antagonist,blocks both the calming and analgesia in rats. Likewise in human newbornswhose mothers had received methadone during pregnancy. Such infants areborn with depleted endogenous opioids, which take a few days to attainnormal levels. Absent endogenous opioids, they are very distressed duringthis early period and cannot be calmed by sucrose taste. But pacifier suc-king and holding, mediated by non-opioid pathways, are effective, as onewould predict (Blass & Ciaramitaro, 1994).

DEVELOPMENT OF OVEREATING

AS AN ADDICTION DURING CHILDHOOD

Two pitfalls await children younger than 4 years who overeat sweetsand fats to the detriment of natural, nutritious, balanced diets, adequate inminerals and vitamins and low in calories. First, the windows for selectingbroader proven foods of the culture close (Skinner et al., 2002), furtherconstraining choice. Consequently, children eating nutritionally inadequatediets risk deficiency in one or more vital nutrients or minerals. Paradoxi-cally, they will tend to be obese for having selectively eaten energy-rich,nutritionally poor foods and drinks. Food neophobias are very difficult toovercome because the foods that have been eaten and accepted into the dietalready have proven safe and palatable; there is little incentive to expandthe diet to relatively less palatable, unfamiliar and potentially unsafe foods.In other words, the pleasant taste of sweet and fatty foods and sweetliquids only exacerbates neophobia, thereby keeping children from trying“new”, healthy foods.

Multiple pathways can lock children into calorie-dense food addictions,but the feeding environment is in most cases either the primary or a majormoderating factor. Children’s feeding environments are extremely confined,particularly in poorer neighbourhoods in major US cities in which small


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stores stock their limited shelf space with popular high calorie foods thatdo not spoil. Perishable fruits and vegetables are minimized. The availabi-lity of cheap, high-calorie foods, makes common the phenomenon ofEating in the Absence of Hunger (EAH), a behavioral phenotype that is rela-tively stable within individual children (Fisher & Birch, 1999, 2002). Thephenotype has been studied in laboratory settings by allowing children toeat freely until they report satiety. Within a few minutes, palatable snackfoods are offered. Some children will resume eating despite just reportingsatiety. Others either decline the foods or eat minimally. The children whoeat in the absence of hunger are exhibiting the EAH phenotype. The etiologyof the EAH phenotype is as yet unknown, but these children have greateradiposity (Fisher & Birch, 1999, 2002). The role of the reward centers and“addictive” mechanisms in the brain in prompting these children to eatrequires study.

Some children use food to regulate mood, ease agitation, or soothe.Having food tantrums at age 3 years (Agras et al., 2004) and a having adifficult temperament (Carey et al., 1988) have both been connected toincreased risk of obesity in middle childhood, presumably because food isused for its soothing properties. Childhood psychiatric disorders (Mustilloet al., 2003) and behavioral problems (Lumeng et al., 2003) have also beenlinked with an increased risk of obesity. Whether food holds this propertymore for some individuals than others, or whether the soothing propertiesof food are potentiated through experience, remain areas for futureresearch. It also remains unclear whether mental health disorders portendincreased obesity, obesity portends increased mental health disorder, or asingle underlying but as yet unidentified factor increases the risk of both.

CONCLUSIONS

Obesity is a health crisis that is behavioral in origin. The impact of ano-ther crisis also springing from an addictive behavior, smoking, has beenblunted somewhat by the appropriate public health interventions. Vestedinterests made it difficult to impact smoking through legislation, which isremarkable given that smoking is nothing but harmful. The fight againstovereating is comparatively more difficult because eating is mandatory forsurvival and thus, unlike smoking, cannot be simply stopped. Like smo-king, however, we also must overcome barriers originating within industrythat impede the ability to pass health-promoting legislation and developeffective interventions. Some of these interventions are already in place inthe European Union, and are only just beginning on a very small scale inthe US Keep up the good work.


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developmental contributions to the obesity epidemic - cairn

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