Obesity In DSM-5

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Obesity in DSM-5Marsha D. Marcus, PhD; and Jennifer E. Wildes, PhDThe Eating Disorders Work Groupof the Diagnostic and StatisticalManual of Mental Disorders,Fifth Edition Task Force was given thecharge of considering whether obesityis a mental disorder that should be included.There were several reasons for considering the salience of obesity for thepsychiatric nomenclature. First, phenotypic similarities in the behaviors associated with obesity and both eatingdisorders and substance use disorders,as well as findings documenting different brain responses to food-related cuesin lean and obese individuals,1 have ledto consideration of obesity as a mentaldisorder.Next, there is growing evidence documenting a relation between obesityand numerous psychiatric disorders.2-4Finally, increasing concern about theassociation of psychotropic drugs withweight gain and increases in cardiomet-abolic risk has led to enhanced awareness of obesity in psychiatry.5 Nevertheless, there currently is insufficientevidence to include obesity in DSM-5.In the sections that follow, we outlineresearch findings that informed the decision making of the Eating DisordersWork Group.CHARACTERISTICS OF OBESITYObesity refers to an excess of bodyfat. In the broadest sense, obesity isPSYCHIATRIC ANNALS 42:11 NOVEMBER 2012 ShutterstockMarsha D. Marcus, PhD, is Professor ofPsychiatry and Psychology, Departmentof Psychiatry, University of PittsburghSchool of Medicine. Jennifer E. Wildes,PhD, is Assistant Professor of Psychiatryand Psychology, Department of Psychiatry, University of Pittsburgh School ofMedicine.Address correspondence to: Marsha D.Marcus, PhD, Western Psychiatric Instituteand Clinic, 3811 O’Hara Street, Pittsburgh,PA 1521; fax: 412-246-6370; email: marcusmd@upmc.edu.Disclosure: The authors have no relevant financial relationships to disclose.Copyright 2012, American PsychiatricAssociation. All rights reserved.doi: 10.3928/00485713-20121105-10Healio.com/Psychiatry 431

caused by a long-term imbalance between energy intake and energy expenditure resulting in the storage of nonessential lipids in adipose cells. Thereis no clear demarcation between normaland abnormal levels of body fat, andobesity is most commonly estimated byvarious proxies. Currently, body massindex (BMI), which is a ratio of weightto height that is calculated by weightin kilograms divided by height in meters squared, is used most commonlyto define obesity operationally. BMI isstrongly associated with adiposity andobesity-related morbidity, and categorythresholds have been established (BMI 18.5 – underweight; BMI 18.5-24.9– normal weight; BMI 25-29.9 – overweight; BMI 30 – obese).6Since the middle of the 20th century,rates of obesity in the United Stateshave increased dramatically in menand women, and in all racial/ethnic andsocioeconomic groups. There is someevidence that the striking increases inobesity have leveled off; nevertheless,the prevalence of obesity in the US in2009-2010 was 35.5% in adult men and35.8% among adult women, and thereis no indication that prevalence is decreasing.7Obesity has profound medical consequences8 and is associated with cardiovascular disease, hypertension, type2 diabetes, and certain types of cancer.Obesity also is related to psychosocialimpairments and poorer quality of life.Health care costs associated with obesity were estimated to account for 9.1%of US medical expenses in 1998,9 andif current trends continue, obesity willaccount for 16% of US health care expenditures by 2030.10The substantial personal and societalburden incurred by obesity has led TheObesity Society to declare on utilitariangrounds that obesity is a disease in order to promote research, reduce stigma,and facilitate professional care.11 Indeed, in light of the medical morbidity432 Healio.com/Psychiatryand costs associated with obesity, research focusing on the causes, consequences, and treatment of obesity is apublic health priority.ETIOLOGY OF OBESITYThe causes of obesity are incompletely understood. At a populationlevel, many epidemiologists have concluded that the increased prevalence ofobesity may be due primarily to modestincreases in calorie intake and decreases in physical activity that have led tooverall upward shifts in populationweights.12 At an individual level, however, there is agreement that causes areheterogeneous and involve an intricateinterplay among genetic, individual,environmental, and societal factors.13Research in obesity has increased exponentially with work across multiplelevels of analysis from the molecular tothe macroeconomic.Findings suggest that obesity resultsfrom varying alterations of complex internal and environmental milieus thatinteract to result in a diversity of phenotypes. In light of the multiple pathwaysto obesity, the DSM-5 Eating DisordersWork Group concluded that there is little evidence to support the conclusionthat obesity per se is a mental disorder.14 Nevertheless, it certainly is possible that particular obesity phenotypesare the consequence of mental disorder.BEHAVIORAL PHENOTYPESOF OBESITYObesity and Binge EatingIn a paper examining the potentialrole for obesity-related diagnoses in theDSM-5, Devlin15 proposed eating disorders (EDs), in particular binge eatingdisorder (BED), or substance use disorders (SUDs) as two models for including obese phenotypes characterizedby “non-normative obesity-promotingovereating.” BED, which has been recommended for inclusion in the DSM-5as an ED, is characterized by persistentand frequent ingestion of large amountsof food coupled with a loss of controlover the aberrant eating, which are associated with clinically significant distress and dysfunction.Available evidence has indicatedthat recurrent binge eating is associatedwith weight gain.16 Moreover, there is astrong relationship between BED andobesity in clinical and community samples, as well as an association betweenseverity of binge eating and degree ofoverweight.17 Thus, there already is a diagnosis in the DSM for an obesity phenotype characterized by aberrant eating.Nevertheless, it is important to recognizethat not all individuals with BED areobese, and conversely, the vast majorityof obese individuals do not have BED.Thus, inclusion of BED in the DSM-5will not address the question of obesityas a psychiatric disorder completely.Obesity as an SUDAnalternateconceptualizationwould be to classify obesity as an SUDbased on phenotypic similarities between drug-seeking in individuals whoare addicted to drugs and food-seekingin obese individuals, who ostensibly areaddicted to food. In an addiction modelof obesity, certain foods, in particularthose that are highly palatable, are theorized to co-opt central reward neurocircuitry in a manner analogous to thatseen in other SUDs.18Observers have noted evidence ofcompulsive food-seeking and the development of tolerance, withdrawal, andloss of control over eating in obese individuals, with persistence of overeatingdespite adverse consequences for theindividual.19However, considering obesity as anSUD is problematic for several reasons, including that food, unlike drugsof abuse, is necessary for survival, andthere is no compelling evidence of human withdrawal symptoms from foods.In addition, not all obese individualsPSYCHIATRIC ANNALS 42:11 NOVEMBER 2012

report patterns of behavior consistentwith food addiction or substance abuse.A more nuanced stance might be toconsider whether the concept of foodaddiction is most salient for individualswith clearly aberrant eating, ie, thosewith BED. Nevertheless, not all individuals with BED are phenotypicallysimilar to those with SUD,20 and thereare compelling arguments that modelsutilizing clinical phenomenology ofEDs or SUDs to conceptualize psychiatric phenotypes of obesity are too imprecise to evaluate critically.21Advances in understanding arelikely to emerge from work examiningthe neurobiology of obese phenotypesacross these psychiatric disorders. Forexample, there has been an explosion ofwork in neuroscience, particularly fromstudies utilizing functional neuroimaging, which has focused on the potentialdysfunction of central pathways thatmay be involved in obesity-related eating behavior.The notion that obesity may be understood in the context of the neurobiological framework of addiction, if notas a SUD per se, has gained increasingattention. In particular, Volkow and colleagues,18 informed by work in animaland human models of addiction, haveposited that in vulnerable people (byvirtue of genetic liability or other individual factors), reinforcers in the formof food or drugs become overvaluedrelative to other reinforcers as a resultof conditioned learning.Then, an elevated expected or anticipated reward from food or drugs overactivates memory and reward circuitsand inhibits cognitive control circuitry,which in turn, leads to an inability toself-manage the drive to consume drugsor foods.Support for various componentsof the model come from burgeoningevidence documenting differences between obese and lean individuals inneural responding in pathways that in-PSYCHIATRIC ANNALS 42:11 NOVEMBER 2012volve reward sensitivity, conditionedlearning and cognitive control, as wellas data that elucidate how hypothalamic neuropeptides that regulate energybalance affect the activity of dopaminecells in reward pathways.22Nevertheless, numerous questionsremain. There is little evidence that differences in neural activation in responseto food-related or non–food-related re-The exact causes for thecomorbidity of obesity andnon-eating or substancerelated mental disordersremain unknown.ward are directly associated with theonset or maintenance of obesity or invivo eating behavior.14 Moreover, findings from functional neuroimagingstudies have not been consistent, whichmay be due to the highly heterogeneousnature of obesity, or the need for moreprecise tools to measure potential differences in responding and more sophisticated characterizations of potentially aberrant human eating behavior.21COMORBID PSYCHIATRICDISORDERS AND OBESITYThe relation between obesity andpsychiatric disorder is not limited toEDs and SUDs. A growing body ofevidence from epidemiologic and community samples has documented a relationship between obesity and other psychiatric disorders, including mood andanxiety disorders,23 as well as personality disorder.24 Moreover, developingevidence has suggested a relationshipbetween obesity and attention-deficit/hyperactivity disorder (ADHD)2 andposttraumatic stress disorder.3The exact causes for the comorbidity of obesity and non-eating or sub-stance-related mental disorders remainunknown. However, there are severalpossible explanations. For example,obesity shares a number of symptomatic features in common with mooddisorders, including increased appetite, decreased activity levels, and sleepdisturbance. Indeed, changes in weightstatus or eating behavior are included inthe current DSM criteria for major depressive episodes, dysthymia, and borderline personality disorder.25Obesity also shares a number ofcorrelates in common with mental disorders in addition to those noted withregard to EDs and SUDs, includinghypothalamic-pituitary-adrenal (HPA)axis dysregulation and environmentalprecipitants such as childhood trauma.Thus, it is possible that increased adiposity in psychiatric patients may signalthe presence of clinically relevant thirdvariables that might have relevance forcourse or outcome.The ubiquity of the relationshipsbetween obesity and numerous psychiatric disorders highlights both theheterogeneity of obesity and the limitations inherent in descriptive diagnosticcategories.The current understanding of mentaldisorder encompasses multiple levelsof analysis, including genetics, braincircuitry, and behavioral factors, anddoes not always correspond clearly tothe current symptom-based psychiatricnosology. This has led to increased interest in efforts to examine conceptually relevant dimensions associated withpsychiatric disorder that will guideinvestigations designed to identifymeaningful distinctions and similaritiesacross the range of psychiatric diagnoses. This approach is exemplified bythe National Institute of Mental Health(NIMH) Research Domain Criteria(RDoC) project.26Thus, a more complete understanding of the relationships among eatingpathology, obesity and the range ofHealio.com/Psychiatry 433

psychiatric disorders is likely to involve examination of these phenomenaacross psychiatric classes to identifyneurobiological factors that underliephenotypic similarities (eg, binge eating in mood disorder, BED, and borderline personality disorder) and distinguish lean from obese individuals. Asthere is complexity and redundancy ofcentral and peripheral mechanisms involved in the regulation of energy, thiswill require additional studies focusingon the neurobiology of reward, but alsobroadening the investigative focus toexamine patterns of responding in otherdisorders where obesity and aberranteating are common.Such studies will need to include other relevant domains of neural responding such as those involved in threat orarousal systems that govern sleep. Inaddition, these data will need to be integrated with findings that explicate thehomeostatic systems involved with energy regulation (ie, hunger and satiety)and their interaction with central systems implicated in psychiatric disorder.Overall, the research designed to elucidate the role and function of centralmechanisms associated with psychiatric and obese phenotypes shows greatpromise for promoting understandingof the relationship between obesity andpsychiatric dysfunction. However, thecomplex and heterogeneous nature ofthis relationship highlights the problems of including obesity as a distinctdisorder in DSM-5.PSYCHOTROPIC DRUGSAND OBESITYAn additional factor that has prompted interest in the salience of obesity topsychiatry is the effect of psychotropicdrugs on body weight. Many psychiatric medications available currentlyare associated with weight gain,5 butthere has been a particular focus onthe potential iatrogenic effects of second-generation antipsychotic agents,434 Healio.com/Psychiatryespecially clozapine and olanzapine.27Medication-induced weight gain hasbeen linked to noncompliance withtreatment and the development of obesity and its related comorbidities.28However, because psychiatric medications affect multiple and diverse aspects of central functioning, there is noObesity is a heterogeneouscondition with a complex andincompletely understood etiology,and thus cannot be considered amental disorder.single cause of psychotropic-associated weight gain.29 There also is markedvariation in medication-induced weightgain across patients.Future research may help to identifypatients at highest risk for significantweight gain and metabolic risk. For example, a recent study documented thata locus near the melanocortin 4 receptor gene was associated with extremeweight gain from second-generationantipsychotic medications.30In light of the potential effects ofpsychiatric medications on the development of obesity and associated medicalcomorbidities, it is critical that clinicians select medications carefully andmonitor side effects closely. Moreover,it is advisable to include BMI as an index of adiposity in the assessment andmanagement of all psychiatric illnesses.Referral for additional medical assessment is recommended for individualswith marked increases in weight duringtreatment.CONCLUSIONIn summary, the Eating DisordersWork Group concluded that obesityshould not be included in DSM-5. Obesity is a heterogeneous condition with acomplex and incompletely understoodetiology, and thus cannot be considereda mental disorder per se. There may beobesity phenotypes that are caused bymental disorder, but research focusingon the role of neural mechanisms in theonset and maintenance of obesity andobesity-related behaviors (eg, overeating) is in its infancy.Future work focusing on conceptually relevant biological dimensions thatmay underlie both obesity and psychiatric disorders could shed light onthe role of mental dysfunction in theexpression of psychiatrically relevantobesity subtypes. Nevertheless, obesityis associated with numerous psychiatric disorders, and several classes ofpsychotropic medications are associated with weight gain, metabolic riskfactors, and obesity. Consequently, clinicians are advised to monitor weightand BMI closely and to consider the salience of overeating and weight-relatedissues in patients with psychiatric disorders.REFERENCES1. Stice E, Spoor S, Ng J, Zald DH. Relationof obesity to consummatory and anticipatoryfood reward. Physiol Behav. 2009;97(5):551560.2. Pagoto SL, Curtin C, Lemon SC, et al. Association between adult attention deficit/hyperactivity disorder and obesity in theUS Population. Obesity (Silver Spring).2009;17(3):539-544.3. Pagoto SL, Schneider KL, Bodenlos JS,et al. Association of post-traumatic stressdisorder and obesity in a nationally representative sample. Obesity (Silver Spring).2012;20(1):200-205.4. Allison DB, Newcomer JW, Dunn AL, et al.Obesity among those with mental disorders:a National Institute of Mental Health meeting report. Am J Prev Med. 2009;36(4):341350.5. Schwartz TL, Nihalani N, Virk S, Jindal S,Chilton M. Psychiatric medication-inducedobesity: treatment options. Obes Rev.2004;5(4):233-238.6. National Institutes of Health. Clinical Guidelines on the Identification, Evaluation, andTreatment of Overweight and Obesity inAdults–The Evidence Report. National Institutes of Health. Obes Res. 1998;6(Suppl2):51S-209S.PSYCHIATRIC ANNALS 42:11 NOVEMBER 2012

7. Flegal KM, Carroll MD, Kit BK, Ogden CL.Prevalence of obesity and trends in the distribution of body mass index among US adults,1999-2010. JAMA. 2012;307(5):491-497.8. Bray GA. Medical consequences of obesity.J Clin Endocrinol Metab. 2004;89(6):25832589.9. Finkelstein EA, Fiebelkorn IC, Wang G. National medical spending attributable to overweight and obesity: how much, and who’spaying? Health Aff (Millwood). 2003;SupplWeb Exclusives:W3-219-226.10. Wang Y, Beydoun MA, Liang L, Caballero B,Kumanyika SK. Will all Americans becomeoverweight or obese? estimating the progression and cost of the US obesity epidemic.Obesity (Silver Spring). 2008;16(10):23232330.11. Allison DB, Downey M, Atkinson RL, et al.Obesity as a disease: a white paper on evidence and arguments commissioned by theCouncil of the Obesity Society. Obesity (Silver Spring). 2008;16(6):1161-1177.12. Sturm R. Increases in morbid obesityin the USA: 2000-2005. Public Health.2007;121(7):492-496.13. Bray GA, Champagne CM. Beyond energybalance: there is more to obesity than kilocalories. J Am Diet Assoc. 2005;105(5 Suppl1):S17-23.14. Marcus MD, Wildes JE. Obesity: is ita mental disorder? Int J Eat Disord.2009;42(8):739-753.15. Devlin MJ. Is there a place for obesity in DSMV? Int J Eat Disord. 2007;40(Suppl):S83-88.16. Wonderlich SA, Gordon KH, Mitchell JE,Crosby RD, Engel SG. The validity and clinical utility of binge eating disorder. Int J EatDisord. 2009;42(8):687-705.17. Hudson JI, Hiripi E, Pope HG, Jr., KesslerRC. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry.2007;61(3):348-358.18. Volkow ND, Wang GJ, Fowler JS, Telang F.Overlapping neuronal circuits in addictionand obesity: evidence of systems pathology. Philos Trans R Soc Lond B Biol Sci.2008;363(1507):3191-3200.19. Gearhardt AN, Corbin WR, Brownell KD.Food addiction: an examination of the diagnostic criteria for dependence. J Addict Med.2009;3(1):1-7.20. Gearhardt AN, White MA, Masheb RM,Morgan PT, Crosby RD, Grilo CM. An examination of the food addiction construct inobese patients with binge eating disorder. IntJ Eat Disord. 2012;45(5):657-663.21. Ziauddeen H, Farooqi IS, Fletcher PC.Obesity and the brain: how convincing isthe addiction model? Nat Rev Neurosci.2012;13(4):279-286.22. Grosshans M, Vollmert C, Vollstadt-Klein S,et al. Association of leptin with food cue-induced activation in human reward pathways.PSYCHIATRIC ANNALS 42:11 NOVEMBER 2012Arch Gen Psychiatry. 2012;69(5):529-537.23. Simon GE, Von Korff M, Saunders K, et al.Association between obesity and psychiatricdisorders in the US adult population. ArchGen Psychiatry. 2006;63(7):824-830.24. Petry NM, Barry D, Pietrzak RH, WagnerJA. Overweight and obesity are associatedwith psychiatric disorders: results from theNational Epidemiologic Survey on Alcoholand Related Conditions. Psychosom Med.2008;70(3):288-297.25. American Psychiatric Association. Diagnostic and Statistical Manual of MentalDisorders. Fourth, Text Revision ed. Arlington, VA: American Psychiatric Association;2000.26. Insel T, Cuthbert B, Garvey M, et al. Research domain criteria (RDoC): toward anew classification framework for researchon mental disorders. Am J Psychiatry.2010;167(7):748-751.27. Henderson DC. Weight gain with atypicalantipsychotics: evidence and insights. J ClinPsychiatry. 2007;68(Suppl)12:18-26.28. Zimmermann U, Kraus T, Himmerich H,Schuld A, Pollmacher T. Epidemiology, implications and mechanisms underlying druginduced weight gain in psychiatric patients. JPsychiatr Res. 2003;37(3):193-220.29. Virk S, Schwartz TL, Jindal S, Nihalani N,Jones N. Psychiatric medication inducedobesity: an aetiologic review. Obes Rev.2004;5(3):167-170.30. Malhotra AK, Correll CU, Chowdhury NI,et al. Association between common variantsnear the melanocortin 4 receptor gene andsevere antipsychotic drug-induced weightgain. Arch Gen Psychiatry. 2012;69(9):904912.AD INDEXSLACK INCORPORATED6900 Grove Rd., Thorofare, NJ 08086Healio.com/Psychiatry. 397SUNOVION PHARMACEUTICALS INC.84 Waterford Dr.Marlborough, MA 01752Latuda.436-440, C3, C4While every precaution is taken to ensure accuracy, wecannot guarantee against occasional changes or omissions in the preparation of this index.Healio.com/Psychiatry 435

INDICATIONS AND USAGELATUDA is an atypical antipsychotic agent indicated for thetreatment of patients with schizophrenia. Efficacy was established infive 6-week controlled studies of adult patients with schizophrenia. Theeffectiveness of LATUDA for longer-term use, that is, for more than6 weeks, has not been established in controlled studies. Therefore,the physician who elects to use LATUDA for extended periodsshould periodically re-evaluate the long-term usefulnessof the drug for the individual patient.IMPORTANT SAFETY INFORMATION FOR LATUDAWARNING: INCREASED MORTALITY IN ELDERLYPATIENTS WITH DEMENTIA-RELATED PSYCHOSISSee full prescribing information for complete boxed warning.ß &MEFSMZ QBUJFOUT XJUI EFNFOUJB SFMBUFE QTZDIPTJT USFBUFE XJUI BOUJQTZDIPUJD ESVHT BSF BU BO JODSFBTFE SJTL PG EFBUI ß "56%" JT OPU BQQSPWFE GPS UIF USFBUNFOU PG QBUJFOUT XJUI EFNFOUJB SFMBUFE QTZDIPTJT CONTRAINDICATIONSLATUDA is contraindicated in the following:ß A ny patient with a known hypersensitivity to lurasidone HCl orany components in the formulation. Angioedema has beenobserved with lurasidone.ß Concomitant use with strong CYP3A4 inhibitors (e.g., ketoconazole).ß Concomitant use with strong CYP3A4 inducers (e.g., rifampin).WARNINGS AND PRECAUTIONS FSFCSPWBTDVMBS "EWFSTF 3FBDUJPOT *ODMVEJOH 4USPLF LATUDA is notapproved for the treatment of patients with dementia-related psychosis.Dyslipidemia: Undesirable alterations in lipids have been observedin patients treated with atypical antipsychotics.Weight Gain: Weight gain has been observed with atypicalantipsychotic use. Clinical monitoring of weight is recommended.)ZQFSQSPMBDUJOFNJB As with other drugs that antagonize dopamineD2 receptors, LATUDA elevates prolactin levels. Galactorrhea,amenorrhea, gynecomastia, and impotence have been reportedin patients receiving prolactin-elevating compounds.-FVLPQFOJB /FVUSPQFOJB BOE "HSBOVMPDZUPTJT Leukopenia/neutropenia has been reported during treatment with antipsychoticagents. Agranulocytosis (including fatal cases) has been reported withother agents in the class. Patients with a preexisting low white bloodcell count (WBC) or a history of drug induced leukopenia/neutropeniashould have their complete blood count (CBC) monitored frequentlyduring the first few months of therapy, and LATUDA should bediscontinued at the first sign of a decline in WBC in the absenceof other causative factors.0SUIPTUBUJD )ZQPUFOTJPO BOE 4ZODPQF LATUDA may causeorthostatic hypotension. Orthostatic vital signs should be monitoredin patients who are vulnerable to hypotension and in patients withknown cardiovascular disease or cerebrovascular disease.4FJ[VSFT LATUDA should be used cautiously in patients with ahistory of seizures or with conditions that lower seizure threshold(e.g., Alzheimer’s dementia).1PUFOUJBM GPS PHOJUJWF BOE .PUPS *NQBJSNFOU In short-term,placebo-controlled trials, somnolence was reported in 17.0%(256/1508) of patients treated with LATUDA compared to 7.1%(50/708) of placebo patients, respectively. Patients should becautioned about operating hazardous machinery, includingmotor vehicles, until they are reasonably certain that therapywith LATUDA does not affect them adversely./FVSPMFQUJD .BMJHOBOU 4ZOESPNF /.4 NMS, a potentiallyfatal symptom complex, has been reported with administration ofantipsychotic drugs, including LATUDA. NMS can cause hyperpyrexia,muscle rigidity, altered mental status and evidence of autonomicinstability (irregular pulse or blood pressure, tachycardia, diaphoresis,and cardiac dysrhythmia). Additional signs may include elevatedcreatine phosphokinase, myoglobinuria (rhabdomyolysis), and acuterenal failure. The management of NMS should include: 1) immediatediscontinuation of antipsychotic drugs and other drugs not essentialto concurrent therapy; 2) intensive symptomatic treatment andmedical monitoring; and 3) treatment of any concomitant seriousmedical problems for which specific treatments are available.#PEZ 5FNQFSBUVSF 3FHVMBUJPO Disruption of the body’s ability toreduce core body temperature has been attributed to antipsychoticagents. Appropriate care is advised when prescribing LATUDA forpatients who will be experiencing conditions that may contribute toan elevation in core body temperature, e.g., exercising strenuously,exposure to extreme heat, receiving concomitant medication withanticholinergic activity, or being subject to dehydration.5BSEJWF %ZTLJOFTJB 5% The risk of developing TD and the likelihoodthat it will become irreversible are believed to increase as the durationof treatment and the total cumulative dose of antipsychotic drugsadministered to the patient increase. However, the syndrome candevelop, although much less commonly, after relatively brief treatmentperiods at low doses. Given these considerations, LATUDA should beprescribed in a manner that is most likely to minimize the occurrenceof TD. If signs and symptoms appear in a patient on LATUDA, drugdiscontinuation should be considered.%ZTQIBHJB Esophageal dysmotility and aspiration have beenassociated with antipsychotic drug use. Aspiration pneumonia isa common cause of morbidity and mortality in elderly patients, inparticular those with advanced Alzheimer’s dementia. LATUDA andother antipsychotic drugs should be used cautiously in patients atrisk for aspiration pneumonia.FUBCPMJD IBOHFTHyperglycemia and Diabetes Mellitus: Hyperglycemia, in somecases extreme and associated with ketoacidosis or hyperosmolarcoma or death, has been reported in patients treated with atypicalantipsychotics. Patients with risk factors for diabetes mellitus(e.g., obesity, family history of diabetes) who are starting treatmentwith atypical antipsychotics should undergo fasting blood glucosetesting at the beginning of and periodically during treatment. Anypatient treated with atypical antipsychotics should be monitoredfor symptoms of hyperglycemia including polydipsia, polyuria,polyphagia, and weakness. Patients who develop symptoms ofhyperglycemia during treatment with atypical antipsychoticsshould undergo fasting blood glucose testing. In some cases,hyperglycemia has resolved when the atypical antipsychotic wasdiscontinued; however, some patients required continuation ofanti-diabetic treatment despite discontinuation of the suspect drug.4VJDJEF The possibility of suicide attempt is inherent in psychoticillness and close supervision of high-risk patients should accompanydrug therapy. Prescriptions for LATUDA should be written for thesmallest quantity of tablets consistent with good patientmanagement in order to reduce the risk of overdose.ADVERSE REACTIONSCommonly Observed Adverse Reactions: (incidence 5% and atleast twice the rate of placebo) in patients treated with LATUDAwere somnolence, akathisia, nausea and parkinsonism.Please see brief summary of prescribing information on adjacentpages, including #PYFE 8BSOJOH.3FGFSFODF LATUDA prescribing information. Sunovion Pharmaceuticals Inc.May 2012.FOR MORE INFORMATION, PLEASE CALL 1-888-394-7377 OR VISITXXX -BUVEB) 1 DPN.

Brief Summary (for Full Prescribing Information, see package insert)WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITHDEMENTIA-RELATED PSYCHOSISt &MEFSMZ QBUJFOUT XJUI EFNFOUJB SFMBUFE QTZDIPTJT USFBUFE XJUI BOUJQTZDIPUJD ESVHT BSF BU BO JODSFBTFE SJTL PG EFBUI [see Warningsand Precautions (5.1)].t -"56%" JT OPU BQQSPWFE GPS VTF JO QBUJFOUT XJUI EFNFOUJB SFMBUFE QTZDIPTJT [see Warnings and Precautions 5.1)]. */%* "5*0/4 "/% 64"(&LATUDA is indicated for the treatment of patients with schizophrenia.The efficacy of LATUDA in schizophrenia was established in five 6-weekcontrolled studies of adult patients with schizophrenia [Clinical Studies (14.1)].The effectiveness of LATUDA for longer-term use, that is, for more than 6 weeks,has not been established in controlled studies. Therefore, the physician who electsto use LATUDA for extended periods should periodically re-evaluate th

grounds that obesity is a disease in or-der to promote research, reduce stigma, and facilitate professional care.11 In-deed, in light of the medical morbidity and costs associated with obesity, re-search focusing on the causes, conse-quences, and treatment of obesity is a public health priority. ETIOLOGY OF OBESITY

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