1 INTRODUCTION

Evaluation and management of obesity is an essential step in the treatment of patients with obstructive sleep apnea (OSA) and snoring based on three important facts. First, 66% of US adults are currently categorized as overweight or obese,¹ placing obesity as one of the most common conditions seen among primary care providers and medical and surgical specialists. Second, obesity is a contributor to poor quality of life and increased morbidity and mortality that involves nine organ systems. Obesity, particularly upper body obesity, is a well-documented risk factor for OSA and is reported to be present in 60% to 90% of OSA patients evaluated in sleep clinics.² Additionally, the severity of OSA is directly related to increasing body weight. Population-based studies have consistently shown an increased incidence of sleep disordered breathing with weight gain and obesity.^3–5 Third, weight reduction by dietary and surgical treatment has been shown to improve co-morbid conditions including sleep disordered breathing and sleep quality.⁶ For these reasons, a thorough evaluation and treatment plan for OSA should specifically address weight loss for patients who are overweight or obese. This chapter will review current evaluation and treatment guidelines for overweight and obesity with a special focus for the otolaryngologist. For a more comprehensive review, readers are referred to the American Medical Association’s Assessment and Management of Adult Obesity: A Primer for Physicians.⁷

2 EVALUATION OF THE OVERWEIGHT AND OBESE PATIENT

Screening for overweight and obesity should not rely on subjective visual inspection alone. Rather, screening is carried out by performing three simple anthropometric measurements: weight, height and waist circumference. These measurements can be easily obtained by ancillary office personnel. The Body Mass Index (BMI), calculated as weight (kg)/height (m)², or as weight (pounds)/height (inches)²×703, is used to define classification of weight status and risk of disease (Table 8.1). A BMI table is more conveniently employed for simple reference (Table 8.2). BMI is used since it provides an estimate of body fat and is related to risk of disease.

Excess abdominal fat, assessed by measurement of waist circumference or waist-to-hip ratio, is independently associated with higher risk for metabolic abnormalities, diabetes mellitus, cardiovascular disease and OSA.⁸ Although protocols and guidelines differ among investigators, measurement of waist is most commonly performed in the horizontal plane above the iliac crest or at the narrowest point between the costal margin and iliac crest. Cut points that define higher risk are a waist circumference >102 cm (>40 inches) in men and >88 cm (>35 inches) in women when measured superior to the iliac crest.⁹ Overweight persons with waist circumferences exceeding these limits should be urged more strongly to pursue weight reduction since it categorically increases disease risk for each BMI class. Measurement of waist circumference should be obtained in those individuals with a BMI ≤35 kg/m².

Although not specified in the clinical guidelines, it may be useful to measure neck circumference in obese patients presenting with signs and symptoms of OSA. Large neck girth in both men and women who snore is highly predictive of sleep apnea.¹⁰ Some studies suggest that neck circumference is a more useful predictor of sleep apnea than BMI¹¹ or waist circumference.¹² In general, a neck circumference of 17 inches in men or 16 inches in women indicates a higher risk for sleep apnea.

3 TAKING AN OBESITY-FOCUSED HISTORY

Once the overweight or obese patient is identified, inclusion of obesity-focused questions in an expanded history will allow the physician to provide tailored treatment recommendations that are more consistent with the needs and goals of the individual patient. Information from the history should address factors that have contributed to the patient’s weight gain, how obesity affects the patient’s perceived health, the patient’s understanding of the relationship between weight and OSA, what the patient’s goals and expectations are regarding obesity treatment, whether the patient is ready and motivated to begin a weight management program, and what kind of help the patient needs for treatment.

Although the vast majority of overweight and obesity can be attributed to behavioral changes in diet and physical activity patterns, the patient’s history may suggest several less common secondary causes that may warrant further evaluation, such as polycystic ovarian syndrome (PCOS), hypothyroidism, Cushing’s syndrome, and hypothalamic tumors or damage to this part of the brain as a consequence of irradiation, infection or trauma. Drug-induced weight gain as well as medications interfering with weight loss also needs to be considered. Common causes include anti-diabetes agents (insulin, sulfonylureas, thiazolidine-diones), steroid hormones, psychotropic agents, mood stabilizers (lithium), antidepressants (tricylics, MAOIs, paraxetine, mirtazapine), and antiepileptic drugs (valproate, gabapentin, carbamazapine).

A history of the patient’s current diet and physical activity patterns along with existing or potential barriers to change is used to both understand the contributing factors toward the development of obesity as well as target behaviors for treatment. A dietary and physical activity history can be assessed as part of the patient interview.

3.1 ASSESSING RISK

The medical history, physical examination and laboratory evaluation should be focused on assessing obesity co-morbid diseases. There is no single laboratory test or diagnostic evaluation that is indicated for all patients with obesity. The specific evaluation performed should be based on presentation of symptoms, risk factors and index of suspicion. However, based on several other screening guideline recommendations, all patients should have a fasting lipid panel (total, LDL and HDL cholesterol and triglyceride levels) and blood glucose measured at presentation along with blood pressure determination. Symptoms and diseases that are directly or indirectly related to obesity are listed in Table 8.3. Although individuals will vary, the number and severity of organ specific co-morbid conditions usually rise with increasing levels of obesity.

Table 8.3 Obesity-related organ systems review

Cardiovascular	Respiratory
Hypertension Congestive heart failure Cor pulmonale Varicose veins Pulmonary embolism Coronary artery disease	Dyspnea Obstructive sleep apnea Hypoventilation syndrome Pickwickian syndrome Asthma
Endocrine	Gastrointestinal
Metabolic syndrome Type 2 diabetes Dyslipidemia Polycystic ovarian syndrome (PCOS)/angrogenicity Amenorrhea/infertility/menstrual disorders	Gastroesophageal reflux disease (GERD) Non-alcoholic fatty liver disease (NAFLD) Cholelithiasis Hernias Colon cancer
Musculoskeletal	Genitourinary
Hyperuricemia and gout Immobility Osteoarthritis (knees and hips) Low back pain Carpal tunnel syndrome	Urinary stress incontinence Obesity-related glomerulopathy End-stage renal disease Hypogonadism (male) Breast and uterine cancer Pregnancy complications
Psychological	Neurologic
Depression/low self-esteem Body image disturbance Social stigmatization	Stroke Idiopathic intracranial hypertension Meralgia paresthetica Dementia
Integument
Striae distensae (stretch marks) Stasis pigmentation of legs Lymphedema Cellulitis Intertrigo, carbuncles Acanthosis nigricans Acrochordon (skin tags) Hidradenitis suppurativa

An increased waist circumference has been found to be predictive of a constellation of metabolic risk factors termed the metabolic syndrome that includes elevated blood pressure, impaired fasting glucose or glucose intolerance, hypertriglyceridemia, and low HDL cholesterol.⁶ Although the components and cutoff values selected to define the metabolic syndrome are useful for clinical practice, the constellation of abnormalities associated with insulin resistance is much broader. These ‘non-traditional risk factors’ include increased biomarkers of chronic inflammation (C-reactive protein, tumor necrosis factor-a, interleukin-6), a prothrombotic state (increased plasma plasminogen activator inhibitor (PAI)-1 and fibrinogen), endothelial dysfunction (decreased endothelium-dependent vasodilatation), hemodynamic changes (increased sympathetic nervous activity and renal sodium retention), hyper-uricemia, and non-alcoholic fatty liver disease (NAFLD). OSA often co-exists with these traditional and non-traditional cardiovascular risk factors, leading one author to coin the term ‘Syndrome Z’.¹³

Measurement of waist circumference is a surrogate marker for visceral adipose tissue (VAT) which refers to adipose tissue located within the abdominal cavity, below abdominal muscles, and comprising omental and mesenteric adipose tissue, as well as adipose tissue of the retroperitoneal and perinephric regions (Fig. 8.1). Visceral fat accumulation has also been shown to have a significant negative impact on glycemic control in patients with type 2 diabetes. Recent studies have linked the metabolic and inflammatory abnormalities seen in abdominal obesity to the secretion of adipocyte and adipose connective tissue products called adipokines. Secreted factors include leptin, IL-6, TNF-α, angiotensinogen, PAI-1, transforming growth factor (TGF)-β, and adiponectin among many others.¹⁴ Secretion of these products results in altered endocrine, paracrine and autocrine functions. The metabolic dysregulation and systemic inflammation seen in OSA is likely related, in part, to VAT- derived secretory products.^15–17

Fig. 8.1 Waist circumference is an independent prediction of metabolic risk and is a surrogate marker for intra-abdominal or visceral adipose tissue (VAT). VAT is considered an active endocrine organ that is associated with metabolic and inflammatory abnormalities and secretion of adipocyte and adipose connective tissue adipokines. To measure waist, place a measuring tape in a horizontal plane around the abdomen at the level of the iliac crest.

4 TREATMENT OF THE OVERWEIGHT AND OBESE PATIENT

Guidance for weight loss should be part of the non-surgical treatment for all obese patients with OSA.¹⁸ The evidence that treatment of obesity improves OSA is reasonably well established. Both medical and surgical approaches to weight loss have been associated with a consistent but variable reduction in number of respiratory events, as well as improvement in oxygenation.¹⁰ A critical review of the literature by Strobel and Rosen⁶