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American Heart Association task force on practice guidelines. Circulation. 2014;129(25 Suppl 2):S1–45.
11. Eckel RH, etal. AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association task force on prac­tice guidelines. J Am Coll Cardiol. 2014;63(25 Pt B):2960–84.
12. Fowkes FG, et al. Development and validation of an ankle brachial index risk model for the prediction of cardiovascular events. Eur J Prev Cardiol. 2014;21(3):310–20.
13. Polonsky TS, et al. Coronary artery calcium score and risk classification for coronary heart disease prediction. JAMA. 2010;303(16):1610–6.
14. Ranthe MF, etal. A detailed family history of myocardial infarc­tion and risk of myocardial infarction—a nationwide cohort study. PLoS One. 2015;10(5):e0125896.
15. Ridker PM, et al. C-reactive protein and parental history improve global cardiovascular risk prediction: the Reynolds Risk Score for men. Circulation. 2008;118(22):2243–51. 4p fol­lowing 2251
16. Bilheimer DW, etal. Mevinolin and colestipol stimulate receptor­mediated clearance of low density lipoprotein from plasma in familial hypercholesterolemia heterozygotes. Proc Natl Acad Sci U S A. 1983;80(13):4124–8.
1 7. Bruckert E, et al. Mild to moderate muscular symptoms with
high-dosage statin therapy in hyperlipidemic patients—the PRIMO study. Cardiovasc Drugs Ther. 2005;19(6):403–14.
18. Finegold JA, etal. What proportion of symptomatic side effects in patients taking statins are genuinely caused by the drug? Systematic review of randomized placebo-controlled trials to aid individual patient choice. Eur J Prev Cardiol. 2014;21(4):464–74.
19. Thompson PD, et al. Statin-associated side effects. J Am Coll Cardiol. 2016;67(20):2395–410.
20. Cohen DE, etal. An assessment of statin safety by hepatologists. Am J Cardiol. 2006;97(8A):77C–81C.
21. Swerdlow DI, etal. HMG-coenzyme A reductase inhibition, type 2 diabetes, and bodyweight: evidence from genetic analysis and randomized trials. Lancet. 2015;385(9965):351–61.
22. Elam MB, et al. Association of fenofibrate therapy with long­term cardiovascular risk in statin-treated patients with type 2 diabetes. JAMA Cardiol. 2017;2(4):370–80.
23. Keech A, et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mel-
Chapter 9. Lipids
litus (the FIELD study): randomized controlled trial. Lancet. 2005;366(9500):1849–61.
24. Blais JE, et al. Comparative efficacy and safety of statin and fibrate monotherapy: a systematic review and meta- analysis of head-to-head randomized controlled trials. PLoS One. 2021;16(2):e0246480.
25. Bhatt DL, et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia (REDUCE-IT). N Engl J Med. 2019;380:11–22.
26. Cannon CP, et al. Ezetimibe added to statin therapy after acute coronary syndromes (IMPROVE-IT). N Engl J Med. 2015;372(25):2387–97.
2 7. Writing C, et al. ACC expert consensus decision pathway on
the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk: a report of the American College of Cardiology task force on clinical expert consensus documents. J Am Coll Cardiol. 2016;68(1):92–125.
28. Robinson JG, et al. Efficacy and safety of alirocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015;372(16):1489–99.
29. Sabatine MS, et al. Efficacy and safety of evolocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015;372(16):1500–9.
30. Ray KK, etal. Two phase 3 trials of inclisiran in patients with elevated LDL cholesterol. N Engl J Med. 2020;382:1507–19.
31. Goldberg AC, etal. Effect of bempedoic acid vs placebo added to maximally tolerated statins on low-density lipoprotein choles­terol in patients at high risk for cardiovascular disease: CLEAR wisdom randomized clinical trial. JAMA. 2019;322(18):1780–8.
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Chapter 10
Obesity
JacinthS.Ruddock andGayotriGoswami

Introduction

Obesity is a chronic, relapsing, multifactorial, neurobehav­ioral disease, where an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass resulting in adverse metabolic, biomechanical, and psychosocial health conse­quences [1]. Obesity is defined as having a body mass index (BMI) of ≥30kg/m2. It is estimated that about 42.5% of the US population are obese, and almost 10% of the country are severely obese with a BMI >40% [2].
By 2030 it is estimated that 51% of the US population will be obese [3]. Obesity is associated with an increased risk for developing many common chronic medical conditions. This significant and increasing prevalence of obesity poses public
J. S. Ruddock (*) Department of Internal Medicine, Albert Einstein College of Medicine, New York City Health and Hospitals/Jacobi + North Central Bronx, Bronx, NY, USA e-mail: Jacinth.Ruddock@nychhc.org
G. Goswami Division of Endocrinology, Department of Medicine, Westchester Medical Center, Valhalla, NY, USA e-mail: Gayotri.Goswami@wmchealth.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_10
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health as well as economic concerns. According to data from the 2012 National Ambulatory Medical Survey, there were 11 million visits by adults age >20 years old to a physician’s office where obesity was listed as a primary diagnosis; this number was up to 12.7 million by 2014, and additional chronic medical condition was associated with 73% of these visits [4, 5].
However there has not been an equivalent increase in the proportion of health care visits by adults with obesity that include counseling on weight loss, nutrition, or physical activity or prescription of weight loss drugs [5]. Primary care physicians are faced with the challenge of screening for and treating obesity and its related complications. The USPSTF recommends screening all adults for obesity and treating those with a BMI of >30kg/m2 [6]. The primary care provider remains integral in getting patients engaged in the conversa­tion about weight loss. Primary care providers cite limited time, inadequate knowledge of obesity treatment, and lack of reimbursement as reasons obesity is not addressed [7]. New evidence suggests that under medicalization of this dis­ease may also be a contributing barrier to appropriate obe­sity care [5].
This text hopes to aid in bridging the knowledge deficit and to add to the expanding body of knowledge on obesity as a medical condition in an effort to enhance patient access to meaningful and successful treatment options for obesity. We provide a review of current and updated best practices for medical evaluation and management of patients with obesity. Approaches to the conversation about weight management and algorithms for treatment will be highlighted.
Key History andPhysical Exam
History
Starting the conversation about weight loss is important. Patients considered even a brief conversation with their pri-
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213
mary care provider about how weight loss may improve their health to be motivating, helpful, and appropriate [8]. As with most health issues, the conversation should be broached sen­sitively. It is recommended that the physician asks the patients’ permission to engage in a conversation about their weight and share their concerns regarding the impact on the patient’s health [9]. If patients are agreeable, utilize a strategy that focuses on information sharing rather than blaming patients for their weight. Recognize obesity as a medical con­dition by using language that is agreeable, inoffensive, and clear [10]. The terms fat, obese, and morbidly obese are most associated with stigmatization and blaming, while the terms excess weight, high body mass index, or unhealthy weight are more acceptable and motivating [11]. In addition to further medicalize the condition, it’s been recommended that physi­cians use phrases such as “patients with obesity” rather than “obese patients” [9].
Taking an obesity-focused history includes assessment of historical events surrounding weight gain or loss, paying close attention to the patient’s own perception of weight. Major life events that may contribute to weight gain include changes in marital status or employment status, quitting tobacco, preg­nancy, and menopause. These events can be plotted on a weight graph to aid in presenting a visual depiction of the trends [10]. The review of medical history should be thorough and include any history of childhood or adolescent obesity.
Assess for any symptoms or signs suggestive of secondary causes of weight gain. For example, a body habitus suggestive of a specific hormone imbalance or genetic anomaly might prompt further testing. A careful review of all medications including all over-the-counter medications should be com­pleted in order to identify and modify any drugs or substances known to promote weight gain. Common weight-inducing prescription medications include beta- blockers, oral cortico­steroids, anti-epileptics, sulfonylureas, insulin, atypical anti­psychotics, some SSRIs, and hormonal treatments such as progesterone.
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Assessment of psychological health including a thorough psychiatric history is essential. Assess for mood or anxiety disorders, eating disorders, post-traumatic stress disorder, psychotic disorders, and substance abuse disorders. Any posi­tive findings should trigger a mental health referral for fur­ther assessment prior to initiating any weight management treatment [10].
Assessment of readiness to engage in a weight manage­ment regimen should be evaluated. Readiness is primarily determined by the patients’ level of motivation and the feasi­bility of implementing and adhering to a weight-loss plan. Identifying and addressing patient-specific barriers are criti­cal in order for patients to achieve their weight-loss goals. Clarify the patient’s expectations and goals and reconcile them with the physician’s medical recommendations. It is pos­sible that it may not be the optimal time for the patient to undertake a weight-loss plan. The patient may still be in the pre-contemplative or contemplative stages of behavior change, and physician counseling may serve to catapult them to a stage of readiness to engage in weight-loss activities. Physicians’ use of the 5A approach (Assess, Advise, Agree, Assist, Arrange) has been found to lead to improved weight­loss outcomes [12].
Physical Examination andDiagnostics
It has been deemed necessary in more recently developed guidelines to improve upon the diagnosis of obesity by requiring not only BMI calculations but also a system of indi­cating the degree to which excess adiposity negative affects a patient’s health [13]. The focus should be on further assess­ment for objective findings to quantify and qualify obesity, to determine if any comorbid conditions or secondary contribu­tors to obesity exist, and to direct specific screening or diag­nostic testing for obesity related health conditions.
Patients who are obese may experience a great amount of trepidation when seeking medical care as many offices do not
Chapter 10. Obesity
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have the appropriate instruments readily available for an accurate and comfortable examination [14]. Always use suit­able instruments for a patient’s body habitus especially when measuring weight and blood pressure. Often examination gowns/drapes and tables may be too small. These factors may limit the comfort of the patient and also the usefulness and even safety of proceeding with the exam.
Calculate BMI based on an accurate height and weight. Measurement of waist circumference provides additional information regarding predisposition to metabolic disease among individuals with BMI <35kg/m2 [10, 13]. Percentage of body fat may be more useful in patients at the extremes in muscle mass and may be a more accurate measure of body composition. Assess blood pressure using an appropriately sized cuff. Examine the skin for signs suggestive of glucose intolerance such as acanthosis nigricans. Conduct a thorough cardiorespiratory, abdominal, and musculoskeletal exam and observe for signs of obesity-related complications (Table10.1).
The measurement of neck circumference may be useful as part of calculating the STOP-BANG score as a screening tool for sleep apnea [15]. Please see Chap. 15 for more information.
Diagnostic and screening laboratory values such as lipid panel, hemoglobin A1c, thyroid-stimulating hormone level, liver function tests, and an EKG should be completed in addition to any other appropriate evaluations for associated conditions (listed below) based on history and exam findings [10, 13].
T . Weight classications based on BMI
Body mass index
Weight
Normal 18.5–24.9
Overweight 25.0–29.9
Class 1 obesity 30.0–34.9
Class 2 obesity 35.0–39.9
Class 3 obesity ≥40
(BMI) (kg/m2)
216
BMI – Body mass index in kg/m
J. S. Ruddock and G. Goswami
*prediabetes *metabolic syndrome *type 2 diabetes *dyslipid-
emia *hypertension *cardiovascular disease *nonalcoholic fatty
liver disease *polycystic ovarian syndrome *female infertility
*depression *male hypogonadism *obstructive sleep apnea
*asthma *osteoarthritis *urinary stress incontinence *gastro-
esophageal reflux disease
Who Should Lose Weight?
Results of diagnostic and laboratory testing can be one of the key factors in determining which patients need to lose weight. Weight loss is recommended for individuals with a BMI ≥30kg/m2 or BMI 25–29.5kg/m2 with adiposity-related com- plications (see Fig.10.1). The Edmonton obesity staging sys­tem may offer clinical guidance in assessing obesity-related risk and prioritizing treatment (see Table10.2) [16, 17].
1. Measure height, weight and BMI
2. Measure waist circumference for patients with BMI 25 to <35 kg/m
3. Thorough history and physical exam
4. Laboratory evaluation
2
PHARMACOTHERAPY
BMI > 30 kg/m2 or BMI > 27 kg/m2 + Obesity related complications
Recommendations for waist circumference cut-offs values may vary based on ethnicity Men > 40 in/102 cm, Women > 35 in/88 cm
F . Evaluation of a patient with increased weight
Stratify BMI Category
25 – 29.9 – overweight 30 – 34.9 – Class I Obesity 35 – 34.9 – Class II Obesity > 40 – Class III Obesity
TREATMENT OPTIONS
COMPREHENSIVE
LIFESTYLE
INTERVENTION
2
BARIATRIC SURGERY
BMI > 40 kg/m BMI > 35 kg/m2 + Obesity related complications
2
or
STAGE
0 1 2 3 4
Chapter 10. Obesity
T . Edmonton staging system [16]
217
Clinical Complications
None Mild Moderate Significant Severe or End-Stage

Treatment

Management ofObesity
Obesity is a complex chronic disease that results from the interaction of genetic, environmental, and behavioral determi­nants. Adipose tissue becomes a dysfunctional endocrine organ leading to systemic metabolic disease [13]. Therefore, the cor­nerstone of management of obesity lies on the importance of weight loss which has shown to reduce morbidity (e.g., reduc­tion in the rate of progression to type 2 diabetes, decrease in blood pressure, and plasma lipid levels) and mortality.
Most guidelines have incorporated a “complications cen­tric approach” for management of obesity rather than a pre­set decline in body weight. The therapeutic endpoint is improvement of obesity-related complications leading to improved patient health and quality of life [18, 19].
Initial treatment includes lifestyle therapy which is the cornerstone of all weight-loss interventions (see Fig.10.1). An evidence-based comprehensive lifestyle therapy for treat­ment of obesity includes three components provided by a trained interventionist (e.g., exercise specialists, registered dieticians, psychologists, health counselors). The evidence supporting the efficacy of lifestyle intervention or behavioral modification is supported by data from two large randomized clinical trials which have shown that even modest weight loss of 5–10% has a significant impact on the metabolic distur­bances associated with obesity [20, 21]. The three main com­ponents are as follows:
• Reduced calorie diet
• Physical activity
• Behavior modification to facilitate adherence to diet and
activity
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Diet
To achieve weight loss, an energy deficit is required; therefore current guidelines recommend reducing total energy (caloric) intake (500–750 kcal daily deficit), and this should be the main component of any weight-loss intervention [13]. The meal plan should be individualized based on personal and cultural prefer­ences. Various types of diets such as Mediterranean, DASH, low­carb, low-fat, volumetric, high- moderate- protein, vegetarian, macronutrient-targeted, and the AHA-style Step 1 diet have been studied. Several randomized clinical trials have shown simi­lar weight loss on diets with different macronutrient composition [22–25]. Diet effectiveness is more related to adherence to the diet than the diet composition. A very-low-calorie diet (≤800kcal) is an option in select patients using meal replacement options and requires medical supervision [13]. There is evidence that individuals who consumed more calories in the morning than in the evening lost more weight [26, 27], while food intake at night is linked to obesity independent of energy intake [28].
Due to the limited weight loss from continuous energy restriction (CER), there have been recent interest in newer weight loss strategies that involve restricting energy intake to certain periods of the day or prolonging the fasting interval between meals. These strategies include intermittent fasting (IMF; >60% energy restriction on 2–3days per week or on alternate days) and time-restricted feeding (TRF; limiting the daily period of food intake to 8–10h or less on most days of the week). Current evidence suggests that these newer strate­gies produce comparable weight loss to CER [29].
With dietary intervention in overweight and obese adults, average weight loss is maximal in 6 months, with smaller losses maintained for up to 2years during tapering of treat­ment and follow-up [30].
Physical Activity
The typical prescription included in a lifestyle intervention is as follows [13]: