Journal of the American Association of Nurse Practitioners
Purpose: To highlight the prevalence and impact of obesity in the United States and provide nurse practitioners (NPs) with an overview of pharmacotherapy options for treatment of overweight and obese individuals.
Data source: A comprehensive review of the literature was conducted using multiple databases, including PubMed, MEDLINE, and Ovid. Keywords used to obtain relevant articles included obesity and drug, or orlistat, topiramate/phentermine, lorcaserin, bupropion/naltrexone, and liraglutide.
Conclusions: Obesity is a prevalent disease with more than two thirds of Americans being considered overweight and one third being obese. Obesity places patients at an increased risk for many comorbidities that impact patient health as well as public health. There are currently five approved medications for the chronic management of obesity, two of which were approved in 2014. These pharmacological therapies are options to aid weight loss in patients that are obese or those who are overweight with additional risk factors.
Implications for practice: NPs can assist patients struggling with their weight. With new pharmacotherapy options, there is an opportunity to add to diet and exercise in order to achieve increased weight loss. A decrease in obesity would potentially alleviate the burden on the healthcare system, both socially and economically, and improve patient quality of life.
More than one third of adults in the United States are obese (body mass index [BMI] > 30 kg/m2) and two thirds are overweight (BMI 25–29.9 kg/m2; Ogden, Carroll, Kit, & Flegal, 2012). The obesity rate in the United States has not changed significantly since 2004, but the prevalence of morbid obesity (BMI > 40 kg/m2) has increased 70%, from 3.9% to 6.6% from 2000 to 2010 (Sturm & Hattori, 2013; Ogden, Carroll, Kit, & Flegal, 2012). Obesity is recognized as a chronic disease requiring evaluation and treatment by most organizations, including the National Institutes of Health (NIH), American Medical Association (AMA), the U.S. Center for Medicare and Medicaid Services (CMS), and the World Health Organization (WHO) (AMA, 2013; U.S. Department of Health and Human Services, CMS, 2011; James, 2008; U.S. Department of Health and Human Services, National Institutes of Medicine National Heart, Lung, and Blood Institute [NIH NHLBI], 2000).
Obesity is closely associated with type 2 diabetes (T2DM), hypertension (HTN), coronary heart disease, stroke, dyslipidemia, obstructive sleep apnea (OSA), gallstones, infertility, depression, as well as many types of cancers (NIH NHLBI, 1998). Estimates suggest that obesityrelated treatment costs are nearly 10% of annual U.S. medical spending (Finkelstein, Trogdon, Cohen, & Dietz, 2009). On average, obese people spend 42% more on health care, with the majority of the spending on treating obesity-related diseases.
The American Heart Association (AHA), American College of Cardiology (ACC), and The Obesity Society (TOS) released guidelines for the management of overweight and obese patients by providing specific recommendations regarding assessment, lifestyle interventions, and bariatric surgery; however, provided little insight on pharmacotherapy (Jensen et al., 2014). At the time the guidelines were written, only one agent, orlistat, was Food and Drug Administration (FDA) approved. Since 2012, four new agents, lorcaserin (Belviq), topiramate/phentermine (Qsymia), bupropion/naltrexone (Contrave), and liraglutide (Saxenda), have gained FDA approval (Eisai, 2012; Novo Nordisk, 2015; Takeda, 2014; Vivus, 2014). The Endocrine Society released clinical practice guidelines for the pharmacological management of obesity encouraging the use of FDA-approved pharmacotherapy in patients unable to achieve permanent weight loss with lifestyle interventions (Apovian et al., 2015). They also encourage practitioners to select medications that have a favorable weight profile when treating comorbid conditions in obese/overweight patients.
Pharmacotherapy is approved for use as an adjunct to diet and exercise in adults with an initial BMI of 30 kg/m2 or 27 kg/m2 in the presence of at least one weight-related comorbid condition including HTN, dyslipidemia, T2DM, OSA, and cardiovascular disease (NIH NHLBI, 1998). Selection of pharmacotherapy should be individualized based on the patient’s medical history, concomitant medications, and preference. No one medication will work for every patient; therefore, prescribers should be aware of the mechanism of actions, potential adverse effects, and likely benefits to advise patient and to reach a shared decision regarding drug selection. This article reviews the FDA-approved medications for chronic, 12 weeks, treatment of obesity.
A comprehensive search, using PubMed, MEDLINE, and Ovid databases, was conducted from inception to April 1, 2015, to find long-term, >12 weeks, studies investigating drugs used alone or in combination for an obesity or weight-relating treatment. Keywords included obesity and drug, or orlistat, topiramate/phentermine, lorcaserin, bupropion/naltrexone, and liraglutide. Only clinical trials in English including more than 100 human subjects were included. The bibliographies of articles were reviewed for other relevant articles not included in the original search. All references included were published between 1998 and 2015. Studies were excluded if attempts for an obesity indication have ceased (i.e., fluoxetine) or if the drug has been withdrawn from the market (i.e., sibutramine). Five drugs were included in this review (Table 1).
Orlistat is the oldest chronic obesity pharmacotherapy agent in the market having been approved in 1999. It is a reversible inhibitor of lipase enzymes in the gastrointestinal (GI) tract, which leads to reduced absorption of fat (Roche, 2012). Orlistat is approved as a prescription-only product, Xenical 120 mg capsules, and as an over-thecounter product (OTC), Alli 60 mg capsules (U.S. Department of Health and Human Services, FDA, 2007). Both the prescription and OTC versions are taken orally three times daily just prior to meals. Orlistat has been studied in 17 randomized, placebo-controlled, clinical trials (RCTs) and the mean reduction in weight of participants in the orlistat 120 mg orally three times daily groups at 1 year ranged from 3.9% to 10.2% (Derosa, Cicero, D’Angel, Fogari, & Maffioli, 2012; Kelley et al., 2002—see Table S2). Significant reductions in weight were also seen at 2 and 4 years (Torgerson, Hauptman, Boldrin, & Sjostrom, 2004).
Additionally, orlistat is associated with significant improvements in cardiovascular risk factors including reductions in systolic and diastolic blood pressures (BPs), total and low-density lipoprotein (LDL) cholesterol, and fasting glucose after 1 year of treatment (Zhou et al., 2012). Lastly, orlistat can slow the progression to diabetes in patients with at least one risk factor (Torgerson et al., 2004).
Because of orlistat’s mechanism of action, increased excretion of undigested fats causes significant GI adverse events including fecal urgency, oily spotting, abdominal discomfort, and flatus with discharge (Table 1; Roche, 2012). These adverse events decrease with chronic use and reduction of fat intake to <30% of daily dietary calories; however, long-term adherence to orlistat is low because of the GI adverse effect profile. Patients taking orlistat are at risk for fat-soluble vitamin deficiencies, so the manufacturer recommends all patients take an OTC multivitamin once daily at least 2 h before or after orlistat.
Lorcaserin, a selective serotonin 2C receptor (5-HT2C) agonist, binds to the 5-HT2C receptors on the anorexigenic pro-opiomelanocortin neurons located in the hypothalamus to decrease food consumption and promote satiety (Eisai, 2012). Lorcaserin is available as a 10 mg tablet taken orally twice a day (BID). Lorcaserin therapy should be reevaluated after 12 weeks of therapy and if weight loss is <5% from baseline, then lorcaserin should be discontinued as the patient will not likely see clinically significant weight loss.
Lorcaserin has been studied in three phase III RCTs: BLOSSOM, BLOOM-DM, and BLOOM (Fidler et al., 2011; O’Neil et al., 2012; Smith et al., 2010). The BLOSSOM trial included patients aged 18–65, BMI of 30–45 kg/m2 or BMI of 27–29.9 kg/m2 with comorbid conditions of HTN, dyslipidemia, cardiovascular disease, impaired glucose tolerance, or OSA on lorcaserin 10 mg once or twice daily or placebo for 1 year (Fidler et al., 2011). A significantly higher proportion of patients on lorcaserin achieved a decrease of 5% and 10% bodyweight as compared to placebo (p < .001 for both). The BLOOMDM trial included patients with treated T2DM, aged 18– 65, with BMI 27–45 kg/m2, and HbA1c between 7.0% and 10.0% (O’Neil et al., 2012). Patients were given lorcaserin 10 mg once or twice daily or placebo for 1 year.
Significantly more patients taking lorcaserin achieved 5% reduction in bodyweight, 37.5% in the lorcaserin twice daily group, 44.7% in lorcaserin once daily group compared to 16.1% in placebo group (p < .001 for both doses), while 16.3%, 18.1%, and 4.4% achieved 10% reduction in bodyweight (p < .001 for both doses). The mean reduction in bodyweight at 1 year in the lorcaserin 10 mg BID group ranged from 4.7% to 5.8% in the BLOSSOM and BLOOM-DM trials (Fidler et al., 2011; O’Neil et al., 2012). The BLOOM trial included patients similar to the BLOSSOM trial with three treatment groups: lorcaserin 10 mg orally BID for 2 years, lorcaserin 10 mg orally BID daily for 1 year then a crossover to placebo for 1 year, and placebo BID for 2 years (Smith et al., 2010). Similar to the BLOSSOM trial, 47.5% of patients taking lorcaserin and 20.3% taking placebo achieved 5% reduction in bodyweight (p < .001). This trend was also seen for patients that achieved 10% reduction in bodyweight (22.6% vs. 7.7%, p < .001). At 52 weeks, mean reduction in bodyweight was 2.2% in the placebo group and 5.8% in the lorcaserin group (p < .001). The 2-year lorcaserin group had significantly more patients maintaining a 5% decrease in bodyweight compared to patients who were reassigned to receive placebo for the second year (67.9% vs. 50.3%, p < .001). In fact, patients in the crossover group had similar weight loss as the placebo group at year 2.
Various secondary end points were measured in all three trials and lorcaserin showed improvements compared to placebo for many secondary outcomes in the individual trials; however, only glycemic parameters (fasting glucose and HbA1c) were significantly reduced in all three trials. Specifically in patients with diabetes, lorcaserin 10 mg BID lead to significant reductions in HbA1c when compared with placebo (−1.0% vs. −0.4%; p < .001; O’Neil et al., 2012).
Lorcaserin has a favorable tolerability profile (Table 1). Completion rates in the above studies ranged from 55.4% to 69.5% with discontinuation because of an adverse event related to lorcaserin occurring in 7.1%–8.6% of patients compared to 4.3%–6.7% of patients treated with placebo. Because of valvulopathy with prior 5-HT2B agonists for weight loss (i.e., fenfluramine), Weissman et al. (2013) evaluated the risk of new valvulopathy in patients treated with lorcaserin and found that valvulopathy occurred in 2.37% of lorcaserin patients and 2.04% of placebo patients (RR 1.16; 95% CI, −0.46 to −1.13). Patients with diabetes taking lorcaserin should monitor for hypoglycemia as the risk of hypoglycemia can occur in up to 29% of patients (Eisai, 2012). Because of lorcaserin’s activity on serotonin receptors, it should be used with caution in patients taking other serotonergic agents because of risk of serotonin syndrome.
Phentermine, a sympathomimetic amine anorectic, and topiramate extended release (ER), an antiepileptic drug, was approved in 2012 (Vivus, 2014). Phentermine/topiramate is available in multiple fixed doses and must be titrated upon initiation and at discontinuation, to reduce the risk of seizures with abrupt discontinuation (Table 1).
Phentermine/topiramate has been studied in four large RCTs: EQUIP, CONQUER, SEQUEL, and OB-202/DM-230 (Allison et al., 2011; Gadde et al., 2011; Garvey et al., 2012, 2014). The EQUIP trial included patients aged 18– 70, BMI of >35 kg/m2 with triglycerides 102 cm for men; >88 cm for women); however, no lower BMI limit was set for patients diagnosed with diabetes (Gadde et al., 2011). After 4 weeks of dose titration patients took high-dose phentermine/topiramate orally once daily, moderate-dose phentermine/topiramate ER (7.5/46 mg) orally once daily, or placebo once daily for 1 year. Both phentermine/topiramate ER treatment groups had a statistically significant proportion of patients achieving 5% decrease in bodyweight compared to placebo (62% moderate dose; 70% high dose; 21% placebo). The mean reduction in bodyweight at 1 year with high-dose phentermine/topiramate in the EQUIP and CONQUER trials ranged from 7.8% to 10.9% (Allison et al., 2011; Gadde et al., 2011). The SEQUEL trial was a 1 year extension of the CONQUER trial completed by Garvey et al. (2012). Patients continued in the same treatment arm as they did in the CONQUER trial. At 108 weeks, mean reduction in bodyweight was 10.5% in the highdose phentermine/topiramate group (p < .0001) and 9.3% in the moderate-dose group (p < .0001) as compared to 1.8% in the placebo group. Both phentermine/topiramate treatment groups had a statistically significant proportion of patients achieving 5% decrease in bodyweight compared to placebo (75.2% moderate dose; 79.3% high dose; 30% placebo).
30% placebo). Lastly, Garvey et al. (2014) further evaluated the CONQUER trial in combination with the OB-202/DM-230 trial, which included patients 18–70 years old with treated T2DM, BMI of 27–45 kg/m2, and HbA1c of 7.0%–12.0%. Treatment groups were phentermine/topiramate (high dose only in OB-202/DM-230; high or moderate dose in CONQUER) or placebo for 1 year. At 56 weeks, OB202/DM-230 subset patients taking placebo achieved an average reduction in their HbA1c of 1.2% as compared to 1.6% in the high-dose group (p = .038). This trend was also seen in the CONQUER subset, with an average reduction of HbA1c of 0.1% in the placebo group and 0.4% in both phentermine/topiramate groups (moderate dose p = .03, high dose p = .004). Various secondary end points were measured in the trials and phentermine/topiramate showed dose-related improvements compared to placebo for WC, multiple lipid parameters, and HTN (Vivus, 2014).
An increase in heart rate was seen in trials with phentermine/topiramate, especially at higher doses (56.1%) as compared to placebo (42.1%; Gadde et al., 2011). Consequently, patient’s heart rate should be monitored. Topiramate carries the potential for oral clefts in offspring of women who become pregnant while on therapy. The FDA created a Risk Evaluation and Mitigation Strategy (REMS) for phentermine/topiramate to decrease the likelihood of pregnancy. This REMS includes clinician training, which must be completed prior to prescribing, dispensing only through certified retail and mail-order pharmacies, supplying patients with educational materials regarding the risks and need for using effective contraception plus baseline and monthly pregnancy tests in women of child-bearing potential (Vivus, 2014). Adverse effects (Table 1), especially the cognitive and psychiatric adverse events, occurred early in treatment, were dose dependent, and usually resolved with discontinuation. Discontinuation rates because of adverse events reported in the clinical trials where 4.5%–16.7% for phentermine/topiramate and 3.1%–8.9% for placebo.
Naltrexone SR/bupropion SR
The combination of naltrexone, a pure opioid antagonist, and bupropion, an antidepressant agent that inhibits dopamine and norepinephrine reuptake, was approved as a fixed-dose combination agent for the treatment of obesity in September 2014. Each tablet contains 8 mg naltrexone and 90 mg bupropion. Doses must be titrated by one tablet each week until a total daily dose of 32 mg naltrexone and 360 mg bupropion is achieved, given in divided doses (Table 1; Takeda, 2014).
Naltrexone SR/bupropion SR was studied in various Contrave Obesity Research (COR) RCTs: COR-I, COR-II, COR-behavior modification (BMOD), and COR-Diabetes. Patients included in the COR-I, COR-II, and COR-BMOD were aged 18–65, BMI of 30–45 kg/m2 or 27–45 kg/m2 with codiagnosis of controlled dyslipidemia and/or HTN and were given naltrexone/bupropion or placebo for 28–56 weeks (Apovian et al., 2013; Greenway et al., 2010; Wadden et al., 2011). Patients included in CORDiabetes were diagnosed with T2DM, aged 18–70, BMI 27–45 kg/m2, HbA1c between 7.0% and 10.0%, fasting blood glucose <270 mg/dL, and taking stable doses of oral antidiabetes medications (Hollander et al., 2013). The mean decrease in bodyweight for the naltrexone 32 mg/bupropion 360 mg treatment groups in COR-I, COR-II, and COR-Diabetes ranged from 5.0% to 6.4% at week 56 (Apovian et al., 2013; Greenway et al., 2010; Hollander et al., 2013). Patients in the COR-BMOD trial received intensive group behavior modification, which consisted of weekly group sessions, extensive education and follow-up concerning food intake, physical activity, and meal planning, in addition to pharmacotherapy. At week 56, the mean decrease in bodyweight was higher than in the other COR studies, 5.1% with placebo and 9.3% in the naltrexone/bupropion group (p < .001). It appears that the intensive lifestyle modification boosted results seen with weight loss. In all four trials, a significant proportion of patients in the naltrexone/bupropion groups achieved 5% weight loss at the end of the trial when compared to placebo (Apovian et al., 2013; Greenway et al., 2010; Hollander et al., 2013; Wadden et al., 2011).
Various secondary end points were also measured in the four mentioned trials. Naltrexone/bupropion showed significant improvements compared to placebo for WC, triglycerides, high-density lipoprotein (HDL) cholesterol, and various quality of life questionnaires. The CORDiabetes trial showed that the naltrexone/bupropion also resulted in a greater reduction in HbA1c when compared to placebo (−0.6% vs. −0.1%, p < .001) and a greater percent of patients achieving HbA1c < 7.0% when compared to placebo (44.1% vs. 26.3%, p < .001; Hollander et al., 2013).
Naltrexone/bupropion was well tolerated with study discontinuation rates ranging from 41% to 54% (Takeda, 2014). More patients in the naltrexone/bupropion groups dropped out of the studies because of adverse effects while patients in the placebo groups potentially discontinued because of insufficient weight loss. Nausea was the most common adverse event seen in naltrexone/bupropion groups (Table 1). Transient increases in systolic BP (SBP) and pulse for the naltrexone/bupropion were also seen. There is currently a boxed warning for increased risk of suicidal thoughts. It is important to titrate the dose upon initiation and avoid the use of this medication in patients with a history of seizures, eating disorders, or those with chronic opioid use.
Liraglutide is a glucagon-like peptide analog, which increases glucose-dependent insulin secretion, decreases inappropriate glucagon secretions, slows gastric emptying, and increases satiety. Liraglutide was originally approved for the treatment of T2DM in doses up to 1.8 mg subcutaneous daily (Novo Nordisk, 2013) and in December 2014 was approved for the treatment of obesity at a dose of 3.0 mg subcutaneous daily (Novo Nordisk, 2015).
Liraglutide has been studied in various RCTs, as part of the Satiety and Clinical Adiposity—Liraglutide Evidence (SCALE) studies. These four studies include SCALE Maintenance, SCALE Diabetes, SCALE Obesity and Prediabetes, and SCALE Sleep Apnea (U.S. FDA, 2014; Wadden et al., 2013). The SCALE Sleep Apnea trial had nonobesity related primary outcomes and will not be discussed in this article. The SCALE Diabetes trial included patients with T2DM, a BMI of 27 kg/m2 and HbA1c 7.0%–10.0%. Treatment groups included placebo, liraglutide 1.8 mg, and liraglutide 3 mg subcutaneously once daily. The 3 mg liraglutide group had a mean change of −5.93% in bodyweight compared to a mean change of −1.98% in the placebo group (p < .0001; U.S. FDA, 2014). The SCALE Obesity and Prediabetes trial included patients with a BMI of 30 kg/m2 or 27 kg/m2 with a diagnosis of HTN and/or dyslipidemia. Eligible patients were randomized to liraglutide 3 mg subcutaneously once daily or placebo. At week 56, the liraglutide group had a mean change of −7.99% in bodyweight compared to a mean change of −2.60% in the placebo group (p < .0001). In the SCALE Diabetes and SCALE Obesity and Prediabetes trials a statistically significant proportion of patients in the liraglutide group achieved 5% weight loss compared to placebo and had >10% weight loss from baseline (p < .0001; U.S. FDA, 2014). In the SCALE Maintenance trial patients needed to lose 5% of baseline bodyweight during a 3-month lowcalorie diet run-in period (Wadden et al., 2013). If patients achieved the required weight loss, they were randomized to either placebo or 3 mg liraglutide subcutaneous daily injection. At week 56, a significantly higher proportion of patients in the liraglutide group maintained the 5% weight loss achieved during the run-in period compared to placebo (81.4% vs. 48.9%, p < .0001). The liraglutide group had a mean change of −6.3% of bodyweight and the placebo group had a change of −0.2% (p < .0001). Various secondary outcomes were assessed during the SCALE trials. Liraglutide showed statistically significant improvement compared to placebo for WC, HbA1c, fasting plasma glucose, and SBP. In the SCALE Diabetes trial, the liraglutide group had a statistically significant mean HbA1c reduction of 1.32% versus 0.38% in the placebo group. Higher proportions of patients in the liraglutide group achieved HbA1c < 7.0% and 6.5%. The risk of hypoglycemia was low in patients without T2DM (U.S. FDA, 2014). The extension of the SCALE Obesity and Prediabetes study is ongoing to investigate the long-term potential of liraglutide to delay the onset of T2DM.
Using pooled information from the four SCALE trials, the proportion of patients withdrawing from the trials because of adverse events was higher with liraglutide 3 mg (9.8%) than with placebo (4.3%; U.S. FDA, 2014). Nausea was the most common adverse event, occurring in 39.3% of patients, with diarrhea and constipation also occurring frequently (Table 1). There were 12 confirmed cases of pancreatitis in the liraglutide group (0.4%) and one case in the placebo group (<0.1%). Additionally, there is a recommendation to avoid liraglutide in patients with a history or family history of medullary thyroid carcinoma (Novo Nordisk, 2015).
While the indications for pharmacotherapy are clear, the widespread utilization of obesity pharmacotherapy has been limited. These barriers can be attributed to many causes, including efficacy, cost, identifying appropriate pharmacotherapy candidates, and a lackluster performance with previously available pharmacotherapy options. This review discussed the available literature evaluating the efficacy of agents approved for chronic management. It has been shown that even modest weightloss, 5%–10%, can improve HbA1c, BP, LDL, HDL, and triglycerides as well as have other various disease related benefits (Skolnik & Ryan, 2014). Additionally, not all patients can succeed at weight loss through lifestyle modification as demonstrated in the LOOK-AHEAD trial where one of three participants were unable to achieve a 5% reduction in bodyweight with intensive behavioral counseling, meal replacement, and incentives (Wadden et al., 2009). The rationale for these medications is to use biology to reinforce behavior and improve a patient’s success rate.
Insurance coverage for these medications has been poor and the out-of-pocket costs can be significant. All of the medications are brand name and do not have available generic products for substitution, only orlistat is available as an OTC medication. With more organizations recognizing obesity as a chronic disease and legislative changes focusing healthcare resources on preventative care, it is hoped that coverage of obesity pharmacotherapy will improve and be an option for more patients.
Identifying appropriate candidates for obesity treatment and selecting an agent can prove to be another challenge. Recognizing patients’ comorbidities can help determine an appropriate therapy (Table 1). As previously mentioned, many of the medications have shown significant improvements in glycemic and cholesterol measures. Concomitant medications also need to be considered; the use of lorcaserin with serotonergic agents may increase the risk of serotonin syndrome (Eisai, 2012) and the use of naltrexone/bupropion in a patient with chronic opioid use may result in opioid withdrawal (Takeda, 2014). Frequency of dosing varies depending on the specific agents, phentermine/topiramate is dosed once daily whereas orlistat is dosed three times daily, which may significantly increase a patient’s pill burden.
Safety has been a major concern leading to the withdrawal or nonapproval of several obesity medications, including most recently, sibutramine and rimonabant. Long-term safety data are lacking for these new agents; however, three of the four recently approved products have been on the market for other indications for many years. This fact does offer some insight into the potential long-term risks with these agents, but does not eliminate the need for long-term trials evaluating cardiovascular outcomes. With the exception of liraglutide, obesity pharmacotherapy options are contraindicated in pregnancy with phentermine/topiramate treatment requiring monthly pregnancy tests in accordance with the REMS program (Vivus, 2014). Lorcaserin and phentermine/topiramate are schedule IV controlled substances, meaning they are subject to additional stipulations.
All trials for the four newly approved medications were sponsored by the drug manufacturers, as evidence for FDA approval. At this time we do not have studies assessing long-term (>2 years) efficacy or safety of the four new agents. A limitation with the available literature is that we do not have any head-to-head studies comparing the agents or any studies using the medications in combination.
Obesity not only affects those practicing in primary care, the impact of obesity spans to many subspecialties. Managing obesity may correspond with lower rates of HTN, hyperlipidemia, T2DM, and overall healthcare costs. Based on the need for monitoring and potential adjustment of doses, patients treated with obesity pharmacotherapy should been reevaluated at a minimum of every 12 weeks. Obesity is a chronic disease and should be treated as such. Looking at results from the BLOOM trial, chronic treatment with medication is likely indicated as weight regain with discontinuation is a concern (Smith et al., 2010).
Pharmacological therapy options for the management of obesity have grown in the past few years. There are currently five FDA-approved medications for chronic treatment. The literature reviewed in this article shows the efficacy of these agents in eligible patients as well as the potential secondary benefits on glucose, BP, cholesterol, and WC. Obesity is a chronic disease that requires a multiaspect approach. Pharmacotherapy is indicated as an adjunct to a reduced calorie diet and increase in physical activity. Therapy should be selected based on patient preference, comorbidities as well as side effect and efficacy profile.
The authors would like to acknowledge and thank Miranda Dimmerling, MSN, CNM, WHNP-BC, for her assistance during the manuscript revision process.
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