Complete Nurse's Guide to Diabetes Care, 3rd Edition

Chapter 5:

Issues Associated with Obesity

Alison B. Evert, MS, RD, CDE1

1University of Washington Medical Center, Diabetes Care Center, Seattle, WA.

Overweight and obesity are both labels for ranges of weight that are greater than what generally is considered healthful for a given height. Overweight and obesity have been shown to increase the likelihood of health problems, such as type 2 diabetes (T2D), coronary vascular disease (CVD), certain types of cancer, osteoarthritis, and sleep apnea. The prevalence of obesity has increased and is a source of concern because the negative consequences start as early as childhood. Because of obesity’s association with many illnesses, it is now one of the leading preventable causes of death worldwide. Once established, obesity, like other chronic illnesses, requires long-term treatment.


Using data based on measured values of weight and height from the 2011–2012 National Health and Nutrition Examination Survey (NHANES), the age-adjusted estimates indicate that more than two-thirds of adults were either overweight or obese, of whom 34.9% were obese, and 6.4% were extremely obese.1 The prevalence of obesity in youth in the U.S. was 16.9% for the same time period.1 Unfortunately the increase in prevalence of T2D has closely followed the rise in obesity. According to the Centers for Disease Control and Prevention, diabetes now affects more than 29 million Americans—or 9% of the U.S. population. More than 9 million of those people do not know they have diabetes.2

Causes of Obesity

Despite the recognized trends in increasing body weight, experts hold varying explanations for its causes. One of the most commonly held views is that changes in diet, including increased fast food and sugar-sweetened beverage consumption, have resulted in calories in excess of what is needed to maintain weight. Others argue that substantially reduced levels of physical activity during work and leisure time have contributed to weight gain. Many feel it is a combination of unhealthy food choices, physical inactivity, and other socioecological determinants, such as poverty, poor access to healthful foods, and an environment not conducive to promoting health. Other causes may include genetic3 or epigenetic factors,4 medications, or lifestyle factors (e.g., stress, insufficient sleep). It is likely that all or a combination of these factors contribute to the increase in obesity.

Energy Balance

Energy balance is an important concept to understand when examining treatment and management strategies for obesity. Simply stated, energy balance is defined as the state achieved when energy intake is equal to energy expenditure. When individuals are in a state of energy balance over time, body weight (i.e., energy stores) is maintained. This concept has led to the theory that weight change is due to an energy gap or a gap in energy balance.5 Higher intakes (increased calories) result in weight gain and relatively higher expenditure (increased levels of physical activity) results in weight loss.6 Research conducted in this field reveals that energy balance is influenced by a fairly complex set of interactions and adjustments by the body in response to calories consumed, physical activity, individual biology, and the environment.7

Maintaining Weight Loss Is Difficult

Achieving weight loss is often feasible over the short term. It has been well established that participants in intensive weight-loss interventions (lifestyle or medication) can achieve an average loss of 5% to 10% of starting weight at 6 months.8 It is also known that some individuals will lose more and some will lose less than others. Plateaus and regain of weight loss typically occurs after 6 months, as compensatory mechanisms protect the body against weight loss. If treatment is discontinued, weight gain occurs, but with support, modest weight loss can be maintained.9 In particular, behavioral methods such as self-monitoring, goal setting, stimulus control, reinforcement, and cognitive change are key components of long-term weight loss.10 Social support from family, friends, or significant others also has been shown to be helpful.11 A systematic review of weight-loss trials lasting a minimum of 1 year found study participants benefited from continued professional support through either face-to-face encounters, phone calls, or Internet-based interactions.9 Furthermore, research suggests it is more difficult for people with diabetes to lose weight than it is for those without diabetes.12

Unfortunately, maintaining weight loss long term is difficult because body weight is tightly regulated by neural, hormonal, and metabolic factors. For example, hormonal adaptations (decreased leptin, peptide YY, cholecystokinin, insulin, and increased ghrelin, gastric inhibitory polypeptide, pancreatic polypeptide) may occur after weight loss that encourage weight gain after diet-induced weight loss.13 These findings suggest that relapse among obese people who have lost weight may not be due to the resumption of old eating habits, but rather may be a result of physiologic changes in hormones that regulate weight. Research reveals that weight loss also results in adaptive thermogenesis (i.e., a decrease in resting metabolic rate), and therefore, the body requires fewer calories for basal energy needs.13,14 These findings indicate that in obese people who have lost weight, multiple compensatory mechanisms encouraging weight gain that persist for at least 1 year, must be overcome to maintain weight loss.

Finally, long-term maintenance of weight loss is a daunting task because most people live in what has been termed an obesogenic environment, that is, settings that positively encourage weight gain.15 Many 21st-century chronic health problems can be attributed to poor nutrition knowledge and lack of financial resources to purchase healthful foods. A growing body of evidence confirms that well-designed behavior-focused nutrition education improves eating plans and behaviors among families with limited resources.16

Defining Weight Status

For adults, the most commonly used anthropometric tool to assess relative weight and classify obesity is the body mass index (BMI). The BMI is expressed as the ratio of total body weight over height squared (kg/m2). BMI defines people as overweight (preobese) when their BMI is between 25 kg/m2 and 30 kg/m2 (23–27.4 kg/m2 in Asian Americans) and defines them as obese when it is >30 kg/m2 (≥27.5 kg/m2 in Asian Americans). After BMI exceeds that point, obesity is graded into three categories: grade 1 (30–34.9 kg/m2), grade 2 (35–39.9 kg/m2), and grade 3 (≥40 kg/m2). In Asians the cutpoint for the definition of overweight is > 23 kg/m2 and is a criteria for testing for diabetes or prediabetes in this population.17 A position statement addressing the research surrounding at-risk Asian Americans found that this population has a higher risk for type 2 diabetes at a lower BMI. The ADA does not change the definitions and has not redefined overweight or obesity for Asian Americans, only the BMI cut point for screening for type 2 diabetes.18 The American Heart Association (AHA) has proposed additional obesity subgroups taking into consideration the increasing prevalence of massive obesity, grade 4 (≥50 kg/m2) and grade 5 (≥60 kg/m2; see Table 5.1).19 The definition of obesity in children involves BMIs greater than the 85th (commonly used to define overweight) or the 95th (commonly used to define obesity) percentiles, respectively, for age-matched and sex-matched control subjects.

Table 5.1—BMI Classification

BMI (kg/m2)





normal weight




class 1


class 2


class 3 (severe, extreme, or morbid obesity)


class 4


class 5

Source: Reprinted with permission from American Heart Association, Circulation. 2013;129:S102–S138.

BMI commonly is used as a screening tool to identify possible weight problems for adults (Tables 5.2 and 5.3). For most people, BMI correlates to their body fat (BF). BMI, however, cannot be used to make the distinction between an elevated body weight resulting from high levels of lean body mass versus fat body mass as evident in some athletes of skeletal frame size. Excess body fat more frequently is associated with metabolic abnormalities, such as cardiovascular disease (CVD) and T2D than a high level of lean body mass.20

Table 5.2—Body Mass Index

Table 5.2—Body Mass Index

To use the table, find the appropriate height in the left-hand column labeled Height. Move across to a given weight (in pounds). The number at the top of the column is the BMI at that height and weight. Pounds have been rounded off.

Source: Reprinted with permission from National Heart, Lung, and Blood Institute. Aim for a healthy weight. Available from Accessed 9 August 2014.

Table 5.3—Body Mass Index Greater Than 35 kg/m2

Table 5.3—Body Mass Index Greater Than 35 kg/m2

To use the table, find the appropriate height in the left-hand column labeled Height. Move across to a given weight (in pounds). The number at the top of the column is the BMI at that height and weight. Pounds have been rounded off.

Source: Reprinted with permission from National Heart, Lung, and Blood Institute. Aim for a healthy weight. Available from Accessed 9 August 2014.

Despite the fact that obesity is recognized as a major risk factor in the development of CVD and diabetes, a higher BMI may be associated with a lower mortality and a better outcome in several chronic diseases and health circumstances compared with nonobese patients.21 This inverse relationship fuels a controversy in the literature, named the “obesity paradox.”22 Overweight and obese individuals may show dramatically different CVD risk factor profiles on the basis of their body fat distribution, which may be one explanation for this paradox.15

Waist circumference is a measurement of abdominal obesity and provides risk information that is not accounted for by BMI. People with abdominal obesity (also called central adiposity, visceral, android, or male-type obesity) are at greater risk of metabolic and cardiovascular disorders, including insulin resistance, T2D, hypertension, and CVD. A man whose waist circumference is >40 inches (>102 cm) or a nonpregnant woman whose waist circumference is >35 inches (>88 cm) is considered elevated and indicative of increased cardiometabolic risk.23 To measure waist circumference, locate the upper hip bone and the top of the right iliac crest. Place a measuring tape in a horizontal plane around the abdomen at the level of the iliac crest. Before reading the tape measure, ensure that the tape is snug but does not compress the skin and is parallel to the floor. The measurement is made at the end of a normal expiration.24

The waist circumference measurement is particularly useful in people who are categorized as normal or overweight in terms of BMI. Experts recommend using both BMI and waist circumference up to a BMI of 30.19 For individuals with a BMI ≥35 kg/m2, waist circumference adds little to the predictive power of the disease risk classification of BMI. In some populations (e.g., Asian Americans or people of Asian descent who may have smaller frame size), waist circumference may be a better indicator of relative disease risk than BMI. BMI is not a flawed screening tool, but it may be just one piece of the puzzle when defining weight status.

Twin Epidemics Diabetes and Obesity

Obesity is strongly linked to T2D. In a nationally representative sample of 21,205 U.S. adults, 2,894 had diabetes (13.6%).25 The prevalence of diabetes was found to increase with increasing weight classes. Among adults with diabetes, 80.3% were considered overweight and 49.1% were considered obese. The survey revealed that nearly one-fourth of adults with diabetes in this sample had poor glycemic control (defined as A1C >8.0%). These findings of the high prevalence of obesity in adults with diabetes suggest that more effort should be taken to combat obesity because it is a modifiable risk factor for the development of diabetes.


The mechanism by which obesity induces insulin resistance is poorly understood and is an area of significant research. Obesity causes peripheral resistance to insulin-mediated glucose uptake (insulin resistance) and also may decrease the sensitivity of the β-cells to glucose.26 Being obese with diabetes increases insulin resistance and deteriorates glucose tolerance, thereby making glycemic targets much more difficult to achieve with lifestyle intervention as well as pharmacologically.

Numerous research studies also have focused on the role of inflammation as a common mediator linking obesity to both the pathogenesis of diabetes and atherosclerosis.26 Adipose tissue is an endocrine organ, and central adiposity in particular has been associated with elevated levels of circulating proinflammatory cytokines.27 The cytokine, interleukin-6 (IL-6; produced by the adipocytes) stimulates platelet activity and secretion of C-reactive protein.22 The incidence of T2D also is correlated with increased levels of markers of inflammation, including C-reactive protein, IL-6, plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor–α (TNF-α), and white cell count.28-30


Weight control encompasses a variety of techniques and strategies, including lifestyle intervention strategies such as nutrition therapy, physical activity, and behavioral therapy; pharmacotherapy; or metabolic surgery. The treatment strategies should be tailored to the individual to promote long-term weight control and prevention of weight gain. Reducing body weight as little as 5% in overweight and obese people not only helps reduce the risk of comorbidities such as diabetes and CVD from developing but also helps in ongoing management.31 This amount of weight loss is often much less than the individual (as well as their health-care provider) expects to lose. Everyone on the treatment team needs to help set realistic expectations for weight loss.

Lifestyle Intervention

In 2014 the AHA, American College of Cardiology (ACC) and The Obesity Society (TOS) published a guideline report based on a systematic evidence review that summarized the current literature for the risks of obesity and the benefits of weight loss.8 The publication includes a treatment algorithm for the management of this chronic disease for primary care of overweight and obese individuals (Figure 5.1). The guidelines recommend that health-care providers develop individual weight loss plans that include three components: a moderately reduced-calorie eating plan, a program of regular physical activity, and use of behavioral strategies to help achieve and maintain a healthful body weight. The AHA/ACC/TOS report also presented evidence showing that the greater the BMI, the greater the risk of CVD, stroke, T2D, and all-cause mortality. The American Diabetes Associaiton Standards of Medical Care in Diabetes—2017 include specific recommendations for obesity management for treatment of type 2 diabetes.32

• At each patient encounter, BMI should be calculated and documented.

• Diet, physical activity, and behavioral therapy designed to achieve >5% weight loss should be prescribed for overweight and obese patients with type 2 diabetes ready to achieve weight loss.

• Such interventions should be high-intensity (≥16 sessions in 6 months) and focus on diet, physical activity, and behavioral strategies to achieve a 500–750 kcal/day energy deficit.

• Diets should be individualized, as those that provide the same caloric restriction but differ in protein, carbohydrate, and fat content are equally effective in achieving weight loss.

• For patients who achieve short-term weight-loss goals, long-term (≥1-year) comprehensive weight maintenance programs should be prescribed. Such programs should provide at least monthly contact and encourage ongoing monitoring of body weight (weekly or more frequently), continued consumption of a reduced-calorie diet, and participation in high levels of physical activity (200–300 min/week).

• To achieve weight loss of >5%, short-term (3-month) interventions that use very low-calorie diets (≤800 kcal/day) and total meal replacements may be prescribed for carefully selected patients by trained practitioners in medical care settings with close medical monitoring. To maintain weight loss, such programs must incorporate long-term comprehensive weight maintenance counseling.

Figure 5.1—Treament algorithm

Figure 5.1—Treatment algorithm. Chronic disease management model for primary care of patients with overweight and obesity. BMI, body mass index; CVD, cardiovascular disease; FDA, U.S. Food and Drug Administration.

*BMI cut point determined by the FDA and listed on the package inserts of FDA-approved obesity medications.

Source: Reprinted with permission from Circulation 2013;129:5102–5138.8

In a recent position statement for the management of hyperglycemia in T2D the American Diabetes Association (the Association) and European Association for the Study of Diabetes endorsed a patient-centered approach that utilizes diabetes self-management education, including lifestyle intervention.33 Current recommendations for management of type 2 diabetes indicates that metformin monotherapy should be started at diagnosis unless there are contraindications.34 This along with lifestyle changes is believed to increase the chances of success in managing blood glucose levels, and does not promote weight gain.

The 2012 U.S. Preventive Services Task Force (USPSTF) also has recommended that physicians offer or refer their patients with a BMI of >30 kg/m2 for high-intensity multicomponent behavioral interventions.35 The USPSTF found adequate evidence that these types of interventions can lead to an average weight loss of 4–7 kg (8.8–15.4 lb). They noted that these interventions also improve glucose tolerance and other physiologic risk factors for CVD. The USPSTF report that the most effective interventions were comprehensive and of high intensity (12–26 sessions per year). The behavioral interventions included multiple behavioral management activities, such as meeting in individual and group sessions, setting weight-loss goals, improving nutrition or eating plan, participating in physical activity sessions, actively using self-monitoring, addressing barriers to change, and strategizing how to maintain lifestyle changes. It was noted that weight-loss outcomes improved when interventions involved more sessions (12–26 sessions in the first year). In an effort to recognize the chronic nature of obesity and the chronic health effects, in 2013 the American Medical Association classified obesity as a disease in an effort to increase screening, treatment, and reimbursement for obesity care.

Landmark diabetes research trials, such as the Diabetes Prevention Program (DPP) and the Look AHEAD (Action for Health in Diabetes) trials, have included intensive lifestyle intervention treatment arms.36 Research reveals that lifestyle intervention seems to be particularly beneficial early in the natural history of T2D, before loss of β-cell function and mass is so extensive that multidrug pharmacotherapy is required to achieve optimal glycemic control.37,38 It also has been reported that diabetes prevention trials that have included intensive lifestyle interventions have been shown to decrease markers of inflammation.39

Lifestyle Intervention Research: Look AHEAD Trial

Because of the size and length of the Look AHEAD trial, it is important to review this study in more detail. Look AHEAD is the longest randomized controlled evaluation to date of intensive lifestyle interventions for weight management. The Look AHEAD was a 14-year multicenter randomized control trial. It is the first trial in subjects with T2D to assess whether weight reduction combined with physical activity could reduce CVD morbidity and mortality.36 Half of the 5,145 people enrolled in the study were randomly assigned to receive an intensive lifestyle intervention (ILI), and the other half were assigned to a control group that received a general program of diabetes support and education (DSE). Both groups received routine medical care from their own health-care providers. The ILI was modeled after the landmark DPP research trial. Look AHEAD, however, set a more ambitious individual goal of losing ≥7% of initial weight loss at year 1 (versus 7% in the DPP) and >175 min moderate-intensity physical activity per week (versus >150 min/week in the DPP). Table 5.4 gives the intervention strategies used in the Look AHEAD trial. At year 1, ILI participants lost a mean of 8.5% initial weight, compared with 0.6% DSE (P < 0.001). At 4 years, participants in the ILI group averaged a weight loss of 4.7 kg compared with 1.1 kg in the control group.40Look AHEAD’s long-term weight-loss maintenance intervention included monthly or twice-monthly individual contacts combined with periodic group meetings (i.e., refresher groups and national campaigns).

Table 5.4—Lifestyle Intervention Strategies Used in the Look AHEAD Trial

• Nutrition

—Energy goals to achieve a weight-loss goal of ≥7% of initial weight

* 1,200–1,500 kcal/day (40–50 g fat) for individuals whose initial weight was <250 lb

* 1,500–1,800 kcal/day (50–60 g fat) for individuals whose initial weight was >250 lb

—Self-monitoring of food intake, such as counting calories or fat grams

—Use of meal replacements (mainly beverages and bars provided at no charge)

—Weekly self-weighing

—Regular consumption of breakfast

—Reduced intake of fast foods

—Reduced size of portions

• Physical Activity

—Goal of >175 min moderate-intensity physical activity per week, such as the following:

* Aerobic exercise in the form of brisk walking on level ground, cycling, or recumbent cycling for those with joint pain with walking are preferred activities for overweight or obese elderly patients with diabetes.63

* Resistance exercise performed two or three times per week provides additional benefits that complement those of aerobic training (e.g., increased lean mass and strength, reduced body fat, increased resting metabolic rate).61

• Behavioral Support

—Regular and ongoing use of behavior modification, such as motivational interviewing, self-monitoring, and individualized goal setting, are also key elements of lifestyle intervention to support long-term results.40

Sources: Modified from: Delahanty LM, Nathan DM. Implications of Diabetes Prevention Program and Look AHEAD Clinical Trials. JAMA 2008;108(Suppl. 1):S66–S72

The National Institutes of Health stopped the trial early, acting on the recommendation of the study’s data and safety monitoring board. The independent advisory board found that the ILI did no harm but was not on a course that would result in greater decreases in cardiovascular events compared with the control group. All participants had the opportunity to complete 8 years of intervention when Look AHEAD was halted in September 2012. At study end, the mean weight loss from baseline was 6% in the intervention group and 3.5% in the control group.41 Overall, Look AHEAD advances the management of obesity by showing that a comprehensive, long-term lifestyle intervention produced 5% weight loss at 8 years in 50% of participants.42 It is doubtful, however, whether the intensity of the Look AHEAD interventions could be implemented in regular clinical practices outside of a research setting.

Other Intervention Studies

The Association’s 2013 nutrition therapy recommendations for the management of adults with diabetes reported interventional studies lasting ≥12 months and targeting individuals with T2D to reduce excess body weight resulted in only modest weight loss ranging from 1.9 to 8.4 kg.43 Studies achieving the greatest weight losses at 1 year, 6.2 kg and 8.4 kg, respectively, included the Mediterranean-style eating pattern and the intensive lifestyle interventions followed by the Look AHEAD participants. In addition, the Mediterranean-style eating pattern reported the largest improvement of A1C at 1 year (21.2%),37 and the Look AHEAD study intensive lifestyle intervention participants reported the next largest improvement (20.64%).36 From a lifestyle perspective, a reduced energy intake with an emphasis on nutrient-dense (Table 5.5), fiber-rich foods along with regular physical activity continue to be priorities for all individuals living with longer-duration T2D. The Association’s 2013 nutrition therapy recommendations are listed in Table 5.6.

Table 5.5—Nutrient-Dense Foods

Nutrient density is a measure of the amount of nutrients a food contains in comparison to the number of calories. A food is more nutrient dense when the level of nutrients is high in relationship to the number of calories the food contains.

Following are nutrient-dense food choices:

• Grains, especially whole grains

• Fruits and vegetables—fresh, frozen, or canned with light sodium

• Fat-free or low-fat milk or dairy-like products

• Leaner protein sources or meat alternatives, such as beans, lentils, and unsalted nuts

• Substitute unsaturated (liquid fats such as olive, canola, corn, safflower oil) for foods higher in saturated (solid fats) or trans fats as much as possible.

Table 5.6—The 2013 American Diabetes Association Nutrition Therapy Recommendations for Energy Balance, Overweight, and Obesity

• For overweight or obese adults with type 2 diabetes or at risk for diabetes, reducing energy intake while maintaining a healthful eating pattern is recommended to promote weight loss.

• Modest weight loss may provide clinical benefits (improved glycemia, blood pressure, and/or lipids) in some individuals with diabetes, especially those early in the disease process. To achieve modest weight loss, intensive lifestyle interventions (counseling about nutrition therapy, physical activity, and behavior change) with ongoing support are recommended.

Source: From Evert et al.43


Many obese individuals take multiple medications, some of which are associated with significant weight gain. It is helpful to evaluate medication regimens for drugs that may be contributing to weight gain. Medications can be added or subtracted with weight-neutral or weight-loss potential when medically appropriate.44 As the obese individual with hypertension or diabetes loses weight, medication adjustment is also necessary to reduce risk of hypoglycemia or hypotension.

As of 2011, approximately 2.7 million people were estimated to use obesity drugs in the U.S., a small number relative to the prevalence of obesity.45 Barriers to sustained use or initiation of obesity medications include safety concerns, costs, perception of limited efficacy, and reluctance to view obesity as a disease requiring medical treatment.45 Regardless of initial weight-loss success with high-intensity multicomponent behavioral interventions, long-term weight maintenance, as stated, is difficult. Therefore, adjunctive therapies, such as pharmacotherapy, are needed to assist people who are not able to lose or sustain sufficient weight loss to improve health in addition to lifestyle changes. The goal of obesity medication use is to improve the individual’s health and quality of life.44

Medicine for Glycemic Control

As T2D progresses in the patient over the years with the continued loss of β-cell function and enduring insulin resistance, medications frequently are added to the treatment plan to achieve optimal glycemic control. Unfortunately, people with diabetes, as well as their health-care providers, often are reluctant to initiate the use of medication for fear of weight gain. Diabetes medications that have been shown to result in weight gain include insulin, insulin secretagogues, and thiazolidinediones. The weight gain attributed to these diabetes medications in part actually might be a consequence of the improvement in glucosuria and retention of calories previously lost in the urine. Diabetes medications that are weight neutral or weight reducing include metformin, the glucagon like peptide-1 analogs (GLP-1 analogs) and amylin, and sodium glucose co-transporter 2 (SGLT-2) inhibitors (see Table 5.7).

Table 5.7—A1C Reduction and Weight Change of Diabetes Medications

Table 5.7—A1C Reduction and Weight Change of Diabetes

ACE, Acarbose Cardiovascular Evaluation11; ACTID, Early Activity in Type 2 Diabetes4; DAFNE, Dose Adjusted for Normal Eating1; DCCT, Diabetes Complications and Control Trial7; DIGAMI, Diabetes Mellitus, Insulin Glucose Infusion in Acute Myocardial Infarction6; LOADD, Lifestyle Over and Above Drugs in Diabetes5; NAVIGATOR, Nateglinide and Valsartan in Impaired Glucose Tolerance Outcomes Research10; NPG, Nutrition Practice Guidelines2; PROACTIVE, Prospective Pioglitazone Clinical Trial in Macrovascular Events8; RECORD; Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycaemia in Diabetes9; TECOS, Trial to Evaluate Cardiovascular Outcomes12; UKPDS, United Kingdom Prospective Diabetes Study3.

Source: Adapted from Inzucchi et al.30 The effect of oral antidiabetic agents on A1C levels: a systematic review and meta-analysis. Diabetes Care 2010;33:1859–1864.33

The Association’s 2013 nutrition therapy recommendations for the management of adults with diabetes reported that the unwanted side effect of treatment intensification often can be mitigated by referral to a registered dietitian or intensive diabetes self-management education program that includes lifestyle counseling.43,46–50 Therefore, regardless of duration of diabetes in years, nutrition therapy and physical activity remain key treatment strategies.

Medicine for Weight Loss

The U.S. Food and Drug Administration (FDA) has approved several medications for long-term use for the treatment of obesity, including orlistat, lorcaserin, phentermine/topiramate, bupropion-naltrexone, and liraglutide. Orlistat inhibits gastrointestinal lipases, reducing fat absorption. Lorcaserin and phentermine/topiramate-extended release (ER) are appetite suppressants, and bupropion-naltrexone reduce hunger and cravings. Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that works like a hormone produced by the body to regulate appetite.

Studies of these drugs have demonstrated improvements, compared with placebo, in progression to diabetes and in many CVD risk factors.44 No obesity medication has been shown to reduce cardiovascular mortality or morbidity. However, the Liraglutide Effect and Action in Diabetes (LEADER) trial of the glucose-lowering drug liraglutide recently concluded that this medication when used for the treatment of type 2 diabetes significantly reduced the rates of major adverse cardiovascular events in type 2 diabetes patients at elevated cardiovascular risk.51

A recent systematic review reported that obesity medications approved for long-term use, when prescribed with lifestyle interventions, produce additional weight loss relative to placebo ranging from ~3% of initial weight loss for orlistat and lorcaserin to 9% for top dose of phentermine/topiramate-ER at 1 year.44 Orlistat is available over the counter.

The majority of prescriptions that are written are for noradrengenic medications: phentermine, diethylpropion, benzphetamine, and diethylpropion. The FDA has approved these four medications for short-term use (usually considered ≤12 weeks). These drugs reduce appetite by increasing activation of adrenergic and dopaminergic receptors. Data about long-term safety and efficacy are limited (but see Tables 5.8 and 5.9 for FDA-approved weight-loss drugs for short- and long-term use).

Table 5.8—Short-Term Management Weight-Loss Drugs

Table 5.8—Short-Term Management Weight-Loss Drugs

Table 5.9—Long-term Management Weight-Loss Drugs

Table 5.9—Long-term Management Weight-Loss Drugs

Table 5.9—Long-term Management Weight-Loss Drugs, continued

*Prescribing information for Contrave, Orexigen Therapeutics, Takeda Pharmaceuticals America, September 2016

Source: Adapted from Yanovski et al.44

Weight-loss medications should only be used as an adjunct to therapy to lifestyle intervention. If a weight-loss medication is prescribed, a decrease in dosages of insulin or sulfonylureas may be needed to reduce risk of hypoglycemia. Further research is needed to determine the efficacy of these weight-loss medications among people with type 2 or type 1 diabetes on insulin therapy.

Metabolic Surgery

Most people who present for metabolic surgery already have failed multiple attempts to achieve a sustained weight loss by using nonsurgical treatment options.52 Metabolic surgery has been found to attenuate not only obesity but also major risk factors for T2D.53 There is now a large amount of reseach that has demonstrated that metabolic surgery achieves superior glycemic control and a reduction of cardiovascular risk factors in obese people with type 2 diabetes compared with various lifestyle and medical interventions. In 2016, an international panel of experts issued a consensus statement and new guidelines for metabolic surgery for people with type 2 diabetes.54The 2017 American Diabetes Association Standards of Care recommend metabolic surgery in people with BMI ≥40 kg/m2 or BMI ≥37.5 kg/m2 in Asian Americans, regardless of glycemic control or complexity of glucose-lowering regimens, and in adults with BMI 35–39.9 kg/m2 (32.5–37.4 kg/m2 in Asian Americans) when hyperglycemia is inadequately controlled despite lifestyle and optimal medical thereapy. Metabolic surgery should be considered for adults with type 2 diabetes and BMI 30.0–34.9 kg/m2 (27.5–32.4 kg/m2 in Asian Americans) if hyperglycemia is inadequately controlled despite optimal medical control by either oral or injectable medications (including insulin). ADA also states that metabolic surgery should be performed in high-volume centers with multidisciplinary teams that understand and are experienced in the management of diabetes and gastrointestinal surgery. Long-term lifestyle support and routine monitoring of micronutrient and nutritional status must be provided to patients after surgery, according to guidelines for postoperative management of metabolic surgery by national and international professional societies.55

The two major classes of metabolic surgery are gastric bypass and adjustable gastric banding procedures. Gastric bypass procedures restructure the digestive system; they include Roux-en-Y gastric bypass, vertical sleeve gastrectomy, biliopancreatic diversion, and biliopancreatic diversion with duodenal switch. Laparoscopic adjustable gastric banding procedures are less invasive but result in less weight loss. The biliopancreatic diversion procedures result in higher rates of micronutrient deficiencies and malnutrition than the gastric bypass and sleeve procedures. See Table 5.10 for a description of commonly available metabolic procedures.

Table 5.10—Types of Surgical Bariatric Procedures

Roux-en-Y Gastric Bypass (RYGBP)

The RYGBP technique was developed by Mason and Ito in 1967 using a surgical stapler to create a gastric pouch holding only ~30 cc.a The upper pouch is entirely divided from the gastric remnant and anastomosed to the jejunum via a narrow gastrojejunal anastomosis. An entero-entero anastomosis between the excluded biliopancreatic limb and the alimentary limb is made, typically performed 100–150 cm distal to the gastrojejunostomy.b

Laparoscopic Adjustable Banding (LAGB)

The LAGB is a purely restrictive procedure involving implanting a silicon band-like tubing along the upper portion of the stomach to encircle it, forming a pouch-like area of stomach above the band and the larger part of the stomach below it. Laparoscopic adjustable banding (LAGB) constricts the cardia of the stomach and is secured in place to help decrease the risk of retrograde slippage of the stomach through the band. Adjustments can be made to the band by injecting or withdrawing saline solution from the hollow core of the band via a subcutaneous port that is connected to the tubing and subsequent ring that encircles the top part of the stomach.b

Vertical Sleeve Gastrectomy (VSG)

VSG, commonly referred to as a “sleeve,” creates a 100–150 mL stomach via the creation of a partial gastrectomy of the greater curvature side of the stomach, whereas the last 6–8 cm of antrum stays intact. Therefore, with the sleeve, the pylorus is kept intact, which aids in preventing gastric emptying issues.b A two-staged approach in high-risk individuals seeking laparoscopic biliopancreatic diversion with duodenal switch (BPD-DS) is a high-risk malabsorptive surgery that will be discussed in the next section.c The VSG is performed first and the BPD-DS several months later as a second procedure among high-risk individuals or individuals with very high BMIs (e.g., >60 kg/m2). This procedure was found to lower the surgical morbidity and mortality versus the one-stage approach. A contraindication of this procedure is reflux or GERD. Surprisingly, individuals often exhibit significant weight loss after the VSG first stage, and the VSG is now gaining ground as an independent bariatric procedure, with some insurance carriers reimbursing for it as a stand-alone procedure.

Biliopancreatic Diversion (BPD)

The BPD procedure consists of a distal, horizontal gastrectomy that allows for a functional upper stomach of 200–500 mL (variable with individual’s needs) and leaving the fundus intact.d The gastric remnant is then anastomosed to the distal 250 cm of small intestine (the alimentary limb). The small bowel that is excluded, including the duodenum, jejunum, and a section of the proximal ileum, carries bile and pancreatic secretions (bilipancreatic limb) and is connected to the alimentary channel 50 cm proximal to the ileocecal valve. Therefore, the only section of the small bowel where digestive secretions and nutrients mix is the 50 cm common limb. The alimentary limb (~200–250 cm in length) allows absorption of some protein and simple carbohydrates, whereas fat and starches are absorbed in the short common limb.b

Biliopancreatic Diversion with Duodenal Switch (BPD-DS)

The BPD-DS involves the sleeve cited previously, leaving a 150–200 mL gastric reservoir. The duodenum is closed 2 cm distal to the pylorus, and a duodeno-ileal anastomosis is created (DS).e,f The gastric fundus is virtually completely removed, whereas the antrum, pylorus, and a small segment of duodenum are left intact, along with the vagus nerve. With the BPD-DS procedure, the entero-entero anastomosis is created more proximally on the alimentary limb, allowing for a longer common channel of 100 cm versus the original BPD procedure.b

Source: Adapted from Furtado M, Evert AB. Nutrition therapy for bariatric surgery and diabetes. In American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Franz MJ, Evert AB, Eds. Alexandria, VA, American Diabetes Association, 2012, p. 371–390.

aFrom Mason EE, Ito C. Gastric bypass in obesity. Obes Res 1967;4:316–319

bFrom Keidar A. Bariatric surgery for type 2 diabetes reversal: the risks. Diabetes Care 2011;34:(Suppl. 2):S362–S366

cFrom Gagner M, Inabnet WB, Pomp A. Laparoscopic gastrectomy with second stage biliopancreatic diversion and duodenal switch in the super-obese. In Laparoscopic Bariatric Surgery. Inabnet WB, DeMaria EJ, Ikramuddin S, Eds. Philadelphia, Lippincott Williams & Wilkins, 2005, p. 143–149

dFrom Scopinaro 2005

eFrom Hess DS, Hess DW, Oakley RS. The biliopancreatic diversion with duodenal switch: results beyond 10 years. Obes Surg 2005;15:408–416

fFrom Marceau P, Hould FS, Simard, S, Lebel S, Bourque RA, Potvin M, Biron S. Biliopancreatic

diversion with duodenal switch. World J Surg 1998;22:947–954

Approximately 40–95% of people with T2D, depending on the study and type of procedure, can achieve near or complete normalization of glucose levels after a bariatric procedure.55–58 A meta-analysis of metabolic surgery studies that included more than 3,000 participants with diabetes reported 78% remission rates from diabetes with enduring rates of remission >2 years in studies that reported follow-up >2 years.59 The surgically restrictive procedures, such as Roux-en Y gastric bypass, vertical sleeve gastrectomy, biliopancreatic diversion, and biliopancreatic diversion with duodenal switch, offer superior weight loss and diabetes remission rates. Remission rates tend to be lower for procedures that constrict only the stomach, such as the less invasive, adjustable lap-band surgery procedure.

Evidence appears to suggest that metabolic surgery may produce anti-diabetes effects beyond that seen with weight loss alone. Studies have shown that a return to normal blood glucose and insulin levels can occur within days following gastric bypass procedures, well before any weight loss starts to happen. People who have higher A1Cs, use insulin, and have had diabetes for a longer duration may have a reduced likelihood of remission. Many people who do not experience remission of diabetes following metabolic surgery still may be able to reduce blood glucose medications.

Ongoing medical care, support, and vitamin/mineral supplementation are important following bariatric procedures to reduce the risk of weight regain and complications such as vitamin and mineral deficiencies, osteoporosis, and rare but often severe hypoglycemia.

Physical Activity

Because of the importance of physical activity in enhancing weight loss, improving insulin resistance, and supporting weight maintenance, and the increasingly strong evidence that increased physical activity and fitness level can affect health regardless of BMI,61 it is important to have interventions available that can lead to sustained changes in physical activity. Physical activity is a critical factor in the energy balance equation, and interventions that attempt only to lower calories are likely to fail.61 Unfortunately, physical activity alone as a treatment strategy for treatment of obesity does not seem to be effective.

The ADA’s Physical Activity/Exercise and Diabetes position statement recommends that most adults with diabetes should engage in 150 min or more of moderate-to-vigorous intensity activity weekly, spread over at least 3 days/week, with no more than 2 consecutive days without activity, as long as this is tolerated.62 Aerobic exercise in the form of brisk walking on level ground, cycling, or recumbent cycling for those with joint pain when walking are preferred activities for overweight or obese elderly people with diabetes. Shorter durations (minimum 75 min/week) of vigorous-intensity or interval training may be sufficient for younger and more physically fit individuals for type 2 diabetes and for type 1 diabetes. Children and adolescents with type 1 or type 2 diabetes should engage in 60 min/day or more of moderate- or vigorous-intensity aerobic activity, with vigorous, muscle-strengthening, and bone-strengthening activities included at least 3 days/week. Adults with diabetes should engage in 2–3 sessions/week of resistance exercise on nonconsecutive days and flexibility and balance training are recommended 2–3 times/week for older adults with diabetes. In addition people with diabetes or prediabetes are encouraged to increase their total daily incidental (nonexercise) physical activity to gain additional health benefits.63

Permanent weight-loss maintenance also may require a very high level of physical activity. The challenge for obesity treatment is not losing weight but keeping it off. According to the 2009 American College of Sports Medicine position stand for strategies for weight maintenance after weight loss, some evidence suggests that >250 min/week of moderate-intensity physical activity will prevent weight regain.64

Low-Calorie Sweeteners: Are They Safe? Do They Cause Weight Gain?

The use of nonnutritive sweeteners (NNS), also commonly referred to as artificial sweeteners, continues to be an area of much debate and misinformation. The U.S. Food and Drug Administration has reviewed several types of low-calorie sweeteners (LCSs; e.g., aspartame, sucralose, saccharin, and sugar alcohols) for safety and approved them for consumption by the general public, including people with diabetes.a Research supports that NNS do not produce a glycemic effect; however, foods containing NNSs may affect glycemia based on other ingredients in the product.b In a recently published meta-analysis that included 15 randomized controlled trials, the authors found the use of NNSs and other LCSs, such as sugar alcohols, were associated with lower body weight, BMI, and waist circumference when substituted for calorically dense alternatives. The meta-analysis also included nine cohort studies that reported the use of NNSs and LCCs were associated with less weight gain but a slightly greater BMI.c The following table provides safe levels of NNS.

Safe Levels of Nonnutritive Sweeteners Based on 150 lb Adult

Safe Levels of Nonnutritive Sweeteners Based on 150 lb Adult

*The U.S. Food and Drug Administration sets an acceptable daily intake (ADI) for each sweetener, which is the maximum amount considered safe to consume each day during a person’s lifetime. The ADI is set to be about 100 times less than the smallest amount that might cause health concerns, based on studies done in lab animals. **Product information not available; sodas containing stevia are not widely available.


aU.S. Department of Agriculture. Nutritive and nonnutritive sweetener resources. National Agricultural Library, Food and Nutrition Information Center. 2013. Available from http://fnic and-nonnutritive-sweetener-resources. Accessed 23 May 2014

bGardner C, Wylie-Rosett J, Gidding SS, et al.; American Heart Association Nutrition Committee of the Council on Nutrition, Physical Activity and Metabolism, Council on Arteriosclerosis, Thrombosis and Vascular Biology, Council on Cardiovascular Disease in the Young; American Diabetes Association. Nonnutritive sweeteners: current use and health perspectives: a scientific statement from the American Heart Association and the American Diabetes Association. Diabetes Care 2012;35:1798–1808

cMiller PE, Perez V. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. Am J Clin Nut 2014;100:765–777

Implications for Nurses

• Understand that obesity and diabetes are both chronic disease conditions and that effective treatment needs to shift from the “diet and exercise mentality” toward efforts to prevention of weight gain.

• Help set realistic expectations for weight loss.

• Recognize that moderate weight loss of 5–10% and increased levels of physical activity with ongoing behavioral support can lead to a fall in blood glucose concentrations toward normal in overweight or obese people with newly diagnosed diabetes.

• Support lifestyle intervention as a key component for individuals utilizing pharmacotherapy or metabolic surgery for the treatment of obesity and diabetes.

• Refer patients who are overweight or obese for nutritional counseling.


Around the world, lifestyle choices are leading to the increased prevalence and dual diagnosis of T2D and obesity. Research has shown that moderate weight loss of 5–10% and increased levels of physical activity with ongoing behavioral support can lead to a decrease in blood glucose concentrations toward normal in overweight and obese people with newly diagnosed diabetes. With a longer duration of diabetes, effective treatment of overweight and obesity needs to shift from the diet and exercise mentality toward efforts to prevent excessive weight gain.12 Reducing the increasing rates of overweight and obesity worldwide will require population-wide efforts to effect change in energy balance. Until then, a combination of treatment strategies are needed to manage obesity, including modification of energy intake and energy expenditure, pharmacotherapy, and metabolic surgery.


Special thanks to Jaime J. Waliczek, MS, RD, University of Washington Medical Center, Weight Loss and Management Center, Seattle, WA, for her thoughtful review and contributions.


1. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011–2012. JAMA 2014;311:806–814

2. Centers for Disease Control and Prevention. National diabetes fact sheet, United States, 2014. Available from Accessed 23 May 2014

3. Xia Q, Grant SF. The genetics of human obesity. Ann N Y Acad Sci 2013;128:178–190

4. Van Dijk SI, Molloy PL, Varinli H, et al. Epigenetics and human obesity. Int J Obes 2015;39:85–97

5. Hill JO, Peters JC, Wyatt HR. Using the energy gap to address obesity: a commentary. J Am Diet Assoc 2009;109:1848–1853

6. Hand GA, Blair SN. Energy flux and its role in obesity and metabolic diseases. US Endocrin 2014;10:59–63

7. Hill JO, Wyatt HR, Peters JC. Energy balance and obesity. Circulation 2012;126:126–132

8. American Heart Association (AHA), American College of Cardiology (ACC), The Obesity Society (TOS). AHA/ACC/TOS guideline for the management of overweight and obesity in adults. Circulation 2014;129(25 Suppl. 2):S102–138.

9. Franz MJ, VanWormer JJ, Crain AL, Boucher JL, Histon T, Caplan W, Bowman JD, Pronk NP. Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up. J Am Diet Assoc 2007;107:1755–1767

10. Klein S, Burke LE, Bray GA, et al. Clinical implications of obesity with specific focus on cardiovascular disease. A statement for professionals from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism. Circulation 2004;110:2952–2967

11. Burke V, Mori TA, Giangiulio N, et al. An innovative program for changing health behaviours. Asian Pacific J Clin Nutr 2002;11(Suppl. 3):S586–S597

12. Franz MJ. The obesity paradox and diabetes. Diabetes Spect 2016;26:145–151

13. Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, Proietto J. Long-term persistence of hormonal adaptations to weight loss. N Eng J Med 2011;365:1597–1604

14. Camps S, Verhoef S, Westerterp KR. Weight loss, weight maintenance, and adaptive thermogenesis. Am J Clin Nutr 2013;97:990–994

15. Bastien M, Poirier P, Lemieux I, Després JP. Overview of epidemiology and contribution of obesity to cardiovascular disease. Prog Cardiovasc Dis 2014;56:369–381

16. Burney J, Haughton B. EFNEP: a nutrition education program that demonstrates cost-benefit. J Am Dietet Assoc 2002;102:39–45

17. American Diabetes Association. Standards of medical care in diabetes—2017. Diabetes Care 2017;40(Suppl.1):S11–S24

18. Hsu WC, Araneta MR, Kanaya AM, Chiang JL, Fujimoto W. BMI cut points to identify at-risk Asian Americans for type 2 diabetes screening. Diabetes Care 2015;38:150–158

19. Poirier P, Albert MA, Fleisher LA, Thompson PD, Sugerman HJ, Burke LE Marceau P, Franklin BA. Cardiovascular evaluation and management of severely obese patients undergoing surgery. A science advisory from the American Heart Association. Circulation 2009;120:86–95

20. Wormser D, Kaptoge S, Di AE, et al. Separate and combined associations of body-mass index and abdominal adiposity with cardiovascular disease: collaborative analysis of 58 prospective studies. Lancet2011;377(9771):1085–1095

21. Hainer V, Aldhoon-Hainerová I. Obesity paradox does exist. Diabetes Care 2013;36(Suppl. 2):S276–S281

22. De Schutter A, Lavie CJ, Milani RV. The impact of obesity on risk factors and prevalence and prognosis of coronary heart disease—the obesity paradox. Prog Cardiovasc Dis 2014;56:401–408

23. World Health Organization. Classification of body mass index. Available at Accessed 28 July 2014

24. National Heart, Lung, and Blood Institute. The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart Lung and Blood Institute, Bethesda, MD, October 2000. (Graphic 77584 Version 1.0). Available at Accessed 4 August 2104

25. Nguyen NT, Nguyen XM, Lane J, Wang P. Relationship between obesity and diabetes in a US adult population: findings from the National Health and Nutrition Examination Survey, 1999–2006. Obes Surg 2011;21:351–355

26. DeFronzo R. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes Care 2009;58:773–795

27. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004;89:2548–2556

28. Pradhan AD, Manson JE, Rifai N, et al. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001;286:327–334

29. Vozarova B, Weyer C, Lindsay RS, et al. High white blood cell count is associated with a worsening of insulin sensitivity and predicts development of type 2 diabetes. Diabetes 2002;51:455–461

30. De Rekeneire N, Peila R, Ding J, et al. Diabetes, hyperglycemia, and inflammation in older individuals: The health, aging, and body composition study. Diabetes Care 2006;29:1902–1908

31. Diabetes Prevention Program Research Group (DPP). Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2011;346:393–403

32. American Diabetes Association. Obesity management for the treatment of type 2 diabetes. Sec. 7. In Standards of medical care in diabetes—2017. Diabetes Care 2017;40(Suppl. 1):S57–S63

33. Inzucchi SE, Bergenstal RM, Buse JB, et al., American Diabetes Association (ADA), European Association for the Study of Diabetes (EASD)Management of hyperglycemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 2012;35:1364–1379

34. American Diabetes Association. Standards of medical care in diabetes—2017. Diabetes Care 2017;40(Suppl. 1):S64–S74

35. Moyer VA, on behalf of the U.S. Preventive Services Task Force. Screening for and management of obesity in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2012;157:373–378

36. Pi-Sunyer X, Blackburn G, Brancati FL, et al.; Look AHEAD Research Group. Reduction in weight and cardiovascular disease risk factors in individuals with type 2 diabetes: one-year results of the Look AHEAD trial. Diabetes Care 2007;30:1374–1383

37. Esposito K, Maiorino MI, Ciotola M, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomized trial. Ann Intern Med2009;151:306–314

38. Feldstein AC, Nichols GA, Smith DH, et al. Weight change in diabetes and glycemic and blood pressure control. Diabetes Care 2008;31:1960–1965

39. Haffner S, Temprosa M, Crandall J, et al. Intensive lifestyle intervention or metformin on inflammation and coagulation in participants with impaired glucose tolerance. Diabetes 2005;54:1566–1572

40. Look AHEAD Research Group. Long-term effects of a lifestyle intervention on weight and cardiovascular risk factors in individuals with type 2 diabetes mellitus: four year results of the Look AHEAD trial. Arch Intern Med 2010;170:1566–1575

41. Look AHEAD Research Group. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med 2013;369:145–154

42. Look AHEAD Research Group. Impact of intensive lifestyle intervention on depression and health-related quality of life in type 2 diabetes: the Look AHEAD Trial. Diabetes Care 2014;37:1544–1553

43. Evert AB, Boucher JL, Cypress M, Dunbar SA, et al. Nutrition therapy recommendations for the management of adults with diabetes. Diabetes Care 2013;36:3821–3842

44. Yanovski SZ, Yanovski JA. Long-term drug treatment for obesity: a systematic and clinical review. JAMA 2014;311:74–86

45. Hampp C, Kang EM, Borders-Hemphill V. Use of prescription anti-obesity drugs in the United States. Pharmacotherapy 2013;33:1299–1307

46. Andrews RC, Cooper AR, Montgomery AA, et al. Diet or diet plus physical activity versus usual care in patients with newly diagnosed type 2 diabetes: the Early ACTID randomized controlled trial. Lancet 2011;378:129–139

47. Coppell KJ, Kataoka M, Williams SM, Chisholm AW, Vorgers SM, Mann JI. Nutritional intervention in patients with type 2 diabetes who are hyperglycaemic despite optimized drug treatment—Lifestyle Over and Above Drugs in Diabetes (LOADD) study: randomized controlled trial. BMJ 2010;341:c3337

48. Battista MC, Labonté M, Ménard J, et al. Dietitian-coached management in combination with annual endocrinologist follow up improves global metabolic and cardiovascular health in diabetic participants after 24 months. Appl Physiol Nutr Metab 2012;37:610–620

49. Banister NA, Jastrow ST, Hodges V, Loop R, Gillham MB. Diabetes self-management training program in a community clinic improves patient outcomes at modest cost. J Am Diet Assoc 2004;104:807–810

50. Barratt R, Frost G, Millward DJ, Truby H. A randomized controlled trial investigating the effect of an intensive lifestyle intervention v. standard care in adults with type 2 diabetes immediately after initiating insulin therapy. Br J Nutr 2008;99:1025–1031

51. Marso SP, et al. Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med 2016;375:311–322

52. Buchwald H: Health implications of bariatric surgery. J Am Coll Surg 2005;200:593–604

53. Sjöström L, Lindroos AK, Peltonen M, Torgerson J, Bouchard C, Carlsson B, Dahlgren S, Larsson B, Narbro K, Sjöström CD, Sullivan M, Wedel H, for Swedish Obese Subjects Study Scientific Group. Lifestyle, diabetes and car- diovascular risk factors 10 years after bariatric surgery. N Engl J Med 2004:351:2683–2693

54. Rubino F, Nathan DM, Eckel RH, et al. Metabolic surgery in the treatment algorithm for tpe 2 diabetes: A joint statement by international diabetes organizations. Diabetes Care 2016;39:861–877

55. American Diabetes Association. Standards of medical care in diabetes—2017. Diabetes Care 2017;40(Suppl. 1):S59–S61

56. Ikramuddin S, Korner J, Lee WJ, et al. Roux-en-Y gastric bypass vs intensive medical management for the control of type 2 diabetes, hypertension, and hyperlipidemia: the Diabetes Surgery Study randomized clinical trial. JAMA 2013;309:2240–2249

57. Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 2012;366:1567–1576

58. Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med 2012;366:1577–1585

59. Dorman RB, Serrot FJ, Miller CJ, et al. Case-matched outcomes in bariatric surgery for treatment of type 2 diabetes in the morbidly obese patient. Ann Surg 2012;255:287–293

60. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med 2009;122:248–256.e5

61. Lee DC, Sui X, Church TS, Lavie CJ, Jackson AS, Blair SN. Changes in fitness and fatness on the development of cardiovascular disease risk factors hypertension, metabolic syndrome, and hypercholesterolemia. J Am Coll Cardiol 2012;59:665–672

62. Shook RP, Blair SN, Duperly J, Hand GA, Matsudo SM, Slavin J. What is causing the worldwide rise in obesity? US Endocrin 2014;10:44–52

63. Colberg SR, Sigal RJ, Yardley JE, et al. Physical activity/exercise and diabetes: a position statement of the American Diabetes Association. Diabetes Care 2016;39: 2065–2079

64. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK, American College of Sports Medicine. American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009;41:459–471