Currently Viewing:
Supplements Impact of Obesity Interventions on Managed Care
Currently Reading
Obesity: Definition, Comorbidities, Causes, and Burden
Caroline M. Apovian, MD, FACP, FACN
The Role of Managed Care Organizations in Obesity Management
Kenneth L. Schaecher, MD, FACP, CPC
Impact of Obesity Interventions on Managed Care
Impact of Obesity Interventions on Managed Care

Obesity: Definition, Comorbidities, Causes, and Burden

Caroline M. Apovian, MD, FACP, FACN
Obesity has been shown to increase the risk of chronic conditions such as rheumatoid arthritis (RA). A meta-analysis of 13 studies, involving 400,609 participants, found that the relative risk (RR) of RA was 1.21 (95% CI, 1.02-1.44) for patients who were obese and 1.05 (95% CI, 0.97-1.13) for patients who were overweight. A 13% increase in the risk of RA was seen for every 5 kg/m2 increase in BMI.58

Nonallergic Rhinitis

Adults and children who are overweight or obese are at an increased risk of nonallergic rhinitis, with adjusted OR of 1.43 (95% CI, 1.06-1.93) for adults and 0.88 (95% CI, 0.63-1.22) for children.59 However, being overweight or obese does not appear to increase the risk of allergic rhinitis.

Major Depressive Disorder

Obesity is also a risk factor for major depressive disorder (MDD). For women with a baseline BMI of 30 or higher, the odds of MDD rose significantly (OR, 5.25; 95% CI, 1.41-19.58) independent of other risk factors such as age, education, prior depressive symptoms, marital status, chronic disease, low social support, and financial strain.60 Persons with a higher BMI showed a slightly increased risk of developing depression (over a 6-year study period).61 However, no relationship has been found between BMI and the persistence of depres-sion. A temporal connection was also reported between obesity and general anxiety disorder (GAD). Women with a BMI of 30 or higher had a greater chance of devel-oping GAD (OR, 6.27; 95% CI, 1.39-28.16); this was not found for women with a baseline BMI of 25 or higher (OR, 2.15; 95% CI, 0.78-5.93).60 Similarly, a meta-analysis showed that baseline excess weight was associated with depression in people 20 years or older, but not younger.62 People who were obese had a 55% increased risk of depression, and people who were depressed had a 58% increased risk of becoming obese.


Additionally, patients who are obese have an increased risk of cancer. Prospectively collected data from the UK Clinical Practice Research Datalink were evaluated, including BMI values and the prevalence of 22 different cancers for 5.2 million people. The mean BMI of the pop-ulation was 25.5 kg/m2; 3.8% developed any cancer, and 3.2% developed 1 of the 22 cancers recorded in the study. Thirteen of the 22 cancers were associated with being overweight or obese; 41% of cases of uterine cancer and more than 10% of gallbladder, kidney, liver, and colon cancers were attributable to being overweight or obese. Higher BMI was positively correlated with an increased risk of uterine, gallbladder, kidney, cervical, and thyroid cancers, along with leukemia, and positive associations were seen with liver, colon, ovarian, and postmenopausal breast cancers.63 A similar relationship between obesity and cancer was observed in cancer-related deaths in the United States. Death from cancer was attributed to being overweight, and obesity ranged from 4.2% to 14.2% for men and 14.3% to 19.8% for women. If people could potentially maintain a BMI under 25 kg/m2, an estimated 90,000 deaths per year from cancer could be avoided.64

Pharmacotherapy for Other Conditions and Associated Weight Gain

Several medication classes have been associated with weight gain, including antidepressants, atypical antipsychotics, antiepileptic drugs, and beta-blockers.


Common treatments of MDD may increase the risk of obesity. Grundy and colleagues reported that women who took antidepressants were more likely to be obese (OR, 1.71; 95% CI, 1.16-2.52).65 Weight gain appears to occur in a large proportion of patients taking antidepres-sants. One study of 362 patients (mostly women) showed that antidepressant use promoted weight gain in 55.2% of patients, with a mean gain of 4.97 ± 6.16 kg, usually occurring in the first 3 months of treatment. Treatment with escitalopram, sertraline, or duloxetine is associated with significant weight gain; patients gain 7% or more from their baseline weight in the first 3 months of use. Mirtazapine, citalopram, venlafaxine, or paroxetine is associated with a 20% or higher weight gain.66

Polypharmacy, either adding a second antidepressant or an atypical antipsychotic, may become necessary for the management of MDD. Examining antidepressant plus anti-depressant co-treatment (AD + AD) versus antidepressant monotherapy (AD) showed that AD + AD therapy is asso-ciated with an increased risk of weight gain (RR, 3.15; 95% CI, 1.34-7.41; P = .009). Specific classes of antidepressants are associated with greater weight gain than others. For example, the addition of noradrenergic and specific sero-tonergic antidepressants (NaSSAs) to selective serotonin reuptake inhibitors (SSRIs) is associated with a greater incidence of weight gain than SSRI therapy alone. The RR of 7% or higher weight gain was 3.81 (95% CI, 1.37-10.55).67


Antipsychotics used as adjunctive treatment in MDD are associated with weight gain, diabetes, and lipid disorders. A randomized study examining the effectiveness of atypical antipsychotics reported a weight gain of more than 7% from baseline in 30% of patients taking olanzap-ine, 16% of patients taking quetiapine, 14% of patients taking risperidone, 12% of patients taking perphenazine, and 7% of patients taking ziprasidone.68 Long-term treatment, even at low doses, can lead to increases in blood lipids, triglycerides, and glucose, eventually leading to weight gain.69 It is recommended that potential weight gain be considered when selecting an antipsychotic and that patients be informed of the estimated weight gain for the medications.15 Once an antipsychotic is prescribed, clinical guidelines recommend that clinicians monitor a patient’s height, weight, BMI, and waist circumference throughout treatment with antipsychotics; if the patient gains 5% or more of his/her baseline weight, the clinician should consider a different antipsychotic.70

Sulfonylureas, Thiazolidinediones, and Insulin

Many treatments for T2D are associated with weight gain, with the potential of patients gaining up to 10 kg within 6 months after the start of treatment.15 Weight gain of 3.0 kg has been reported for thiazolidinediones; sulfonylureas, 1.12 kg; and insulin, 1.7 to 2.5 kg.15,71 Other classes of medications, such as sodium-glucose cotrans-porter 2 (SGLT-2) inhibitors, GLP-1 receptor agonists, and dipeptidyl peptidase 4 (DDP4) inhibitors, have been shown to be weight-reducing or weight-neutral therapies. Metformin is also associated with weight loss. Patients who are obese and require treatment for T2D should be prescribed weight-loss or weight-neutral medications as first- or second-line treatment. It is recommended that patients with obesity and T2D who require insulin also be prescribed metformin, pramlintide, or GLP-1 agonists to offset insulin-associated weight gain.15

Antiepileptic Drugs

Valproic acid, carbamazepine, and gabapentin are antiepileptic medications that are associated with weight gain. The most significant weight gain has been reported with valproic acid, in the range of 5 to 49 kg.72


Steroid therapy is essential to the treatment of inflam-matory disorders; however, steroids are associated with weight gain. Glucocorticosteroid therapy is associated with a 4.4% increase in weight after a year of treatment, and that weight gain is often maintained even after gluco-corticosteroid therapy is stopped.73 Treatment guidelines recommend against chronic steroid treatment to avoid weight gain in individuals who are overweight or obese.15


Beta-blockers, which are used for migraine and myocardial infarction prophylaxis and for the management of hypertension and heart failure, have also been associated with a mean weight gain of 1.2 kg.72 A study examined the effects of beta-blockers on weight loss and reduction of waist circumference in 3582 patients (173 were taking beta-blockers) involved in an intensive calorie-restriction program of 900 kcal/day. Participants taking beta-blockers lost a mean 0.67 kg less than par-ticipants in the control group and had a smaller decrease in waist circumference (–24.2 vs –25.2 cm, respectively).74 The authors recommend that alternate hypertensive treatment should be considered for patients with obesity. Treatment guidelines recommend a selective or nonse- lective beta-blocker (eg, carvedilol or nebivolol) because these agents have less potential of weight gain.15


The paradigm shift from thinking of obesity as a character flaw to an understanding that it is a disease is monumental. Hopefully, this will motivate healthcare professionals to be proactive and intervene sooner when individuals are identified at risk or meet the definition of obesity. Prescribers and pharmacists should be aware of the pathophysiology of obesity to understand the rationale for medication therapy. Awareness of the risk factors of obesity, especially those that are preventable, is important so that clinicians can counsel patients on how to avoid or minimize them. Obesity is a serious public health concern, and the associated financial and health consequences to Americans can be addressed by prescribers and pharmacists.

Obesity is a complex interaction between multiple genetic, socioeconomic, and cultural factors that also are associated with existing or resulting comorbidities and their treatments. The prevalence of obesity continues to be high, as are associated comorbidities and healthcare costs. Early intervention and effective treatment of obesity are needed to reduce costs and improve outcomes for these patients. 

Author affiliation: Boston Medical Center and Boston University School of Medicine, Boston, MA.

Funding source: This activity is supported by educational grants from Novo Nordisk and Takeda Pharmaceuticals U.S.A., Inc.

Author disclosure: Dr Apovian has disclosed being a consultant for Amylin, Arena, EnteroMedics, Gelesis, Johnson and Johnson, Merck, Novo Nordisk, Nutrisystem, Orexigen, Sanofi-Aventis, Scientific Intake, Takeda, and Zafgen; she also reports research funding from Amylin, Aspire Bariatrics, the Dr. Robert C. and Veronica Atkins Foundation, GI Dynamics, Lilly, MetaProteomics, MYOS Corporation, Orexigen, Pfizer, and Sanofi-Aventis, as well as owning stock in Science Smart LLC.

Authorship information: Concept and design, drafting of the manuscript, critical revision of the manuscript for important intellectual content, and supervision.

Address correspondence to:
1. Jensen MD, Ryan DH, Apovian CM, et al; American College of
Cardiology/American Heart Association Task Force on Practice Guidelines; Obesity Society. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. J Am Coll Cardiol. 2014;63(25 Pt B):2985-3023. doi: 10.1016/j. jacc.2013.11.004.
2. Fitch A, Fox C, Bauerly K, et al; Institute for Clinical Systems Improvement. Prevention and management of obesity for chil-dren and adolescents. ICSI website.
S184 n n MAY 2016 Report ObesityChildhood.pdf. Published July 2013. Accessed March 28, 2016.
3. Whitlock G, Lewington S, Sherliker P, et al; Prospective Studies Collaboration. Body-mass index and cause-specific mortal-ity in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet. 2009:373(9669);1083-1096. doi: 10.1016/S0140-6736(09)60318-4.
4. Yusuf S, Hawken S, Ounpuu S, et al. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet. 2005;366(9497):1640-16499.
5. Padwal RS, Pajewski NM, Allison DB, Sharma AM. Using the Edmonton obesity staging system to predict mortality in a popu-lation-representative cohort of people with overweight and obe-sity. CMAJ. 2011;183(14):E1059-E1066. doi: 10.1503/cmaj.110387.
6. Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384(9945):766-781. doi: 10.1016/S0140-6736(14)60460-8.
7. Sturm R. The effects of obesity, smoking, and drinking on medical problems and costs. Health Aff (Millwood). 2002;21(2):245-253.
8. Finkelstein EA, Trogdon JG, Cohen JW, Dietz W. Annual medi-cal spending attributable to obesity: payer- and service-specific estimates. Health Aff (Millwood). 2009;28(5):w822-w831. doi:
9. Geier AB, Foster GD, Womble LG, et al. The relationship between relative weight and school attendance among elemen-tary schoolchildren. Obesity (Silver Spring). 2007;15(8):2157-2161.
10. Han E, Norton EC, Powell LM. Direct and indirect effects of body weight on adult wages. Econ Hum Biol. 2011;9(4):381-392. doi: 10.1016/j.ehb.2011.07.002.
11. Janssen I, Craig WM, Boyce WF, Pickett W. Associations between overweight and obesity with bullying behaviors in school-aged children. Pediatrics. 2004;113(5):1187-1194.
12. Wang LY, Denniston M, Lee S, Galuska D, Lowry R. Long-term health and economic impact of preventing and reduc-ing overweight and obesity in adolescence. J Adolesc Health. 2010;46(5):467-473. doi: 10.1016/j.jadohealth.2009.11.204.
13. Skelton JA, Irby MB, Grzywacz JG, Miller G. Etiologies of obesity in children: nature and nurture. Pediatr Clin North Am. 2011;58(6):1333-1354, ix. doi: 10.1016/j.pcl.2011.09.006.
14. McAllister EJ1, Dhurandhar NV, Keith SW, et al. Ten puta-tive contributors to the obesity epidemic. Crit Rev Food Sci Nutr. 2009;49(10):868-913. doi: 10.1080/10408390903372599.
15. Apovian CM, Aronne LJ, Bessesen DH, et al; Endocrine
Society. Pharmacological management of obesity: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2015;100(2):342-362. doi: 10.1210/jc.2014-3415.
16. Skelton JA, DeMattia L, Miller L, Olivier M. Obesity and its therapy: from genes to community action. Pediatr Clin North Am. 2006;53(4):777-794.
17. Crino M, Sacks G, Vandevijvere S, Swinburn B, Neal B. The influence on population weight gain and obesity of the macronu-trient composition and energy density of the food supply. Curr Obes Rep. 2015;4(1):1-10. doi: 10.1007/s13679-014-0134-7.
18. Park S, Blanck HM, Sherry B, Brener N, O’Toole T. Factors associated with sugar-sweetened beverage intake among United States high school students. J Nutr. 2012;142(2):306-312. doi:
19. Ludwig DS, Peterson KE, Gortmaker SL. Relation between con-sumption of sugar-sweetened drinks and childhood obesity: a pro-spective, observational analysis. Lancet. 2001;357(9255):505-508.
20. Du H, van der A DL, Ginder V, et al. Dietary energy density in relation to subsequent changes of weight and waist circumfer-ence in European men and women. PLoS ONE. 2009;4(4):e5339. doi:10.1371/journal.pone.0005339.
21. Savage JS, Marini M, Birch LL. Dietary energy density predicts women’s weight change over 6 y. Am J Clin Nutr.
22. Kershaw KN, Albrecht SS, Carnethon MR. Racial and ethnic residential segregation, the neighborhood socioeconomic envi-ronment, and obesity among Blacks and Mexican Americans. Am J Epidemiol. 2013;177(4):299-309. doi: 10.1093/aje/kws372.
23. Benjamin RM. The Surgeon General’s vision for a healthy and fit nation. Public Health Rep. 2010;125(4):514-515.
24. Glickman D, Parker L, Sim LJ, Del Valle Cook H, Miller EA, eds. Accelerating Progress in Obesity Prevention: Solving the Weight of the Nation. Washington, DC: Institute of Medicine of the National Academies. The National Academies Press; 2012.
25. Gordon-Larsen P, Nelson MC, Page P, Popkin BM. Inequality in the built environment underlies key health disparities in physi-cal activity and obesity. Pediatrics. 2006;177(2):417-424.
26. Li S, Zhao JH, Luan J, et al. Cumulative effects and predic-tive value of common obesity-susceptibility variants identified by genome-wide association studies. Am J Clin Nutr. 2010;91(1):184-190. doi: 10.3945/ajcn.2009.28403.
27. Stunkard AJ, Harris JR, Pedersen NL, McClearn GE. The body-mass index of twins who have been reared apart. N Engl J Med. 1990;322(21):1483-1487.
28. Price RA, Gottesman II. Body fat in identical twins reared apart: roles for genes and environment. Behavior Genetics. 1991;21(1):1-7.
29. Schousboe K, Visscher PM, Erbas B, et al. Twin study of genetic and environmental influences on adult body size, shape, and composition. Int J Obes Relat Metab Disord. 2004;28(1):39-48.
30. Schreiner AB, Kao JY, Young VB. The gut microbiome in health and in disease. Curr Opin Gastroenterol. 2015;31(1):69-75. doi: 10.1097/MOG.0000000000000139.
31. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006;444(7122):1027-1031.
32. Garaulet M, Madrid JA. Chronobiology, genetics and meta-bolic syndrome. Curr Opin Lipidol. 2009;20(2):127-134. doi:
33. Garaulet M, Ordovás JM, Madrid JA. The chronobiology, etiology and pathophysiology of obesity. Int J Obes (Lond). 2010;34(12):1667-1683. doi: 10.1038/ijo.2010.118.
34. Simpson K, Parker J, Plumer J, Bloom S. CCK, PYY and PP: the control of energy balance. Handb Exp Pharmacol. 2012;(209):209-230. doi: 10.1007/978-3-642-24716-3_9.
35. Bataille D, Dalle S. The forgotten members of the glucagon family. Diabetes Res Clin Pract. 2014;106(1):1-10. doi: 10.1016/j. diabres.2014.06.010.
36. Ryan D, Acosta A. GLP-1 receptor agonists: Nonglycemic clinical effects in weight loss and beyond. Obesity (Silver Spring). 2015;23(6):1119-1129. doi: 10.1002/oby.21107.
37. Morris DL, Rui L. Recent advances in understanding leptin signaling and leptin resistance. Am J Physiol Endocrinol Metab. 2009;297(6):E1247-E1259. doi: 10.1152/ajpendo.00274.2009.
38. Lee JH, Reed DR, Price RA. Leptin resistance is associated with extreme obesity and aggregates in families. Int J Obes Relat Metab Disord. 2001;25(10):1471-1473.
39. Considine RV, Sinha MK, Heiman ML, et al. Serum immu-noreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334(5):292-295.
40. Moehlecke M, Canani LH, Silva LO, Trindade MR, Friedman
R, Leitão CB. Determinants of body weight regulation in humans. Arch Endocrinol Metab. 2016. pii: S2359-39972016005002104.
41. Kumar DS, Banji D, Harani A. Physiological factor in obesity. Am-Euras J Toxicol Sci. 2010;2(3):177-189.
42. Pearce EN. Thyroid hormone and obesity. Curr Opin Endocrinol Diabetes Obes. 2012;19(5):408-413. doi: 10.1097/ MED.0b013e328355cd6c.
43. Longhi S, Radetti G. Thyroid function and obesity. J Clin Res Pediatr Endocrinol. 2013;5(suppl 1):40-44. doi: 10.4274/jcrpe.856.
44. Kitahara CM, Platz EA, Ladenson PW, Mondul AM, Menke
A, Berrington de González A. Body fatness and markers of thyroid function among US men and women. PLoS ONE. 2012;7(4):e34979. doi: 10.1371/journal.pone.0034979.
45. Garber JR, Cobin RH, Gharib H, et al; American Association of Clinical Endocrinologists and American Thyroid Association Taskforce on Hypothyroidism in Adults. Clinical practice guide-lines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22(12):1200-1235.
46. Laurberg P, Knudsen N, Andersen S, Carlé A, Pedersen IB, Karmisholt J. Thyroid function and obesity. Eur Thyroid J. 2012;1(3):159-167. doi: 10.1159/000342994.
47. Jonklaas J, Bianco AC, Bauer AJ, et al; American Thyroid Association Task Force on Thyroid Hormone Replacement. Guidelines for the treatment of hypothyroidism: prepared by the American thyroid association task force on thyroid hormone replacement. Thyroid. 2014;24(12):1670-1751. doi: 10.1089/ thy.2014.0028.
48. Guaraldi F, Salvatori R. Cushing syndrome: maybe not so uncommon of an endocrine disease. J Am Board Fam Med. 2012;25(2):199-208. doi: 10.3122/jabfm.2012.02.110227.
49. Boscaro M, Barzon L, Sonino N. The diagnosis of Cushing’s syndrome: atypical presentations and laboratory shortcomings. Arch Intern Med. 2000;160(20):3045-3053.
50. Kirk LF Jr, Hash RB, Katner HP, Jones T. Cushing’s disease: clinical manifestations and diagnostic evaluation. Am Fam Physician. 2000;62(5):1119-1127, 1133-1134.
51. Tiryakioglu O, Ugurlu S, Yalin S, et al. Screening for Cushing’s syndrome in obese patients. Clinics (Sao Paulo). 2010;65(1):9-13. doi: 10.1590/S1807-59322010000100003.
52. Polycystic ovary syndrome (PCOS). American Congress of
Obstetrics and Gynecology (ACOG) website. Patients/FAQs/Polycystic-Ovary-Syndrome-PCOS. Accessed January 30, 2016.
53. Escobar-Morreale HR, Botella-Carretero JI, Alvarez-Blasco F, Sancho J, San Millán JL. The polycystic ovary syndrome associat-ed with morbid obesity may resolve after weight loss induced by bariatric surgery. J Clin Endocrinol Metab. 2005;90(12):6364-6369.
54. Legro RS, Arslanian SA, Ehrmann DA, et al; Endocrine Society. Diagnosis and treatment of polysystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2013;98(12):4565-4592. doi: 10.1210/jc.2013-2350.
55. Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obe-sity, diabetes, and obesity-related health risk factors, 2001. JAMA. 2003;289(1):76-79.
56. Pausova Z, Gossard F, Gaudet D, et al. Heritability estimates of obesity measures in siblings with and without hypertension. Hypertension. 2001;38(1):41-47.
57. Kitahara CM, Flint AJ, Berrington de Gonzalez A, et al. Association between class III obesity (BMI of 40-59 kg/m2) and mortality: a pooled analysis of 20 prospective studies. PLoS Med. 2014;11(7):e1001673. doi: 10.1371/journal.pmed.1001673.
58. Feng J, Chen Q, Yu F, et al. Body mass index and risk of rheumatoid arthritis: a meta-analysis of observational stud-ies. Medicine (Baltimore). 2016;95(8):e2859. doi: 10.1097/ MD.0000000000002859.
59. Han YY, Forno E, Gogna M, Celedón JC. Obesity and rhinitis in a nationwide study of children and adults in the United States. J Allergy Clin Immunol. 2016;pii:S0091-6749(16)00084-1. doi:
60. Kasen S, Cohen P, Chen H, Must A. Obesity and psychopathol-ogy in women: a three decade prospective study. Int J Obesity (London). 2008;32(3):558-566.
61. Gibson-Smith D, Bot M, Paans NP, Visser M, Brouwer I, Penninx BW. The role of obesity measures in the development and persistence of major depressive disorder. J Affect Disord. 2016;198:222-229. doi: 10.1016/j.jad.2016.03.032.
62. Luppino FS, de Wit LM, Bouvy PF, et al. Overweight, obesity, and depression: a systematic review and meta-analysis of lon-gitudinal studies. Arch Gen Psychiatry. 2010;67(3):220-229. doi:
63. Bhaskaran K, Douglas I, Forbes H, dos-Santos-Silva I, Leon DA, Smeeth L. Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5.24 million UK adults. Lancet. 2014;384(9945):755-765. doi: 10.1016/S0140-6736(14)60892-8.
64. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of US adults. N Engl J Med. 2003;348(17):1625-1638.
65. Grundy A, Cotterchio M, Kirsh VA, Kreiger N. Associations between anxiety, depression, antidepressant medication, obe-sity, and weight gain among Canadian women. PLoS One. 2014;9(6):e99780. doi: 10.1371/journal.pone.0099780.
66. Uguz F, Sahingoz M, Gungor B, Aksoy F, Askin R. Weight gain and associated factors in patients using newer antidepres-sant drugs. General Hospital Psychiatry. 2015;37(1):46-48. doi:
67. Galling B, Calsina Ferrer A, Abi Zeid Daou M, Sangroula D, Hagi K, Correll CU. Safety and tolerability of antidepressant co-treatment in acute major depressive disorder: results from a sys-tematic review and exploratory meta-analysis. Expert Opin Drug Saf. 2015;14(10):1587-1608. doi: 10.1517/14740338.2015.1085970.
68. Lieberman JA, Stroup TS, McEvoy JP, et al; Clinical
Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators. Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. N Engl J Med. 2005;353(12):1209-1223.
69. Wang P, Si T. Use of antipsychotics in the treatment of depres-sive disorders. Shanghai Arch Psychiatry. 2013;25(3):134-140. doi:
70. American Diabetes Association; American Psychiatric
Association; American Association of Clinical Endocrinologists; North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27(2):596-601.
71. Dailey G, Admane K, Mercier F, Owens D. Relationship of insu-lin dose, A1c lowering, and weight in type 2 diabetes: compar-ing insulin glargine and insulin detemir. Diabetes Technol Ther. 2010;12(12):1019-1027. doi: 10.1089/dia.2010.0063.
72. Ness-Abramof R, Apovian CM. Drug-induced weight gain. Drugs Today (Barc). 2005;41(8):547-555.
73. Wung PK, Anderson T, Fontaine KR, et al; Wegener’s Granulomatosis Etanercept Trial Research Group. Effects of glu-cocorticoids on weight change during the treatment of Wegener’s granulomatosis. Arthritis Rheum. 2008;59(5):746-753. doi: 10.1002/ art.23561.
74. Azar M, Nikpay M, Harper ME, McPherson R, Dent R. Adverse effects of β-blocker therapy on weight loss in response to a controlled dietary regimen. Canadian J Cardiol. 2016;1-6. doi:10.1016/j.cjca.2015.10.10.016.
Copyright AJMC 2006-2020 Clinical Care Targeted Communications Group, LLC. All Rights Reserved.
Welcome the the new and improved, the premier managed market network. Tell us about yourself so that we can serve you better.
Sign Up