The most common measure of obesity is the body mass index (BMI). BMI is calculated by dividing a person’s weight (in kilograms) by the square of the height in meters (Fig. 41-2). Individuals with a BMI less than 18.5 kg/m² are considered underweight, whereas those with a BMI between 18.5 and 24.9 kg/m² reflect a normal body weight. A BMI of 25 to 29.9 kg/m² is classified as being overweight, and those with values at 30 kg/m² or above are considered obese. The term severely (morbidly, extremely) obese is used for those with a BMI greater than 40 kg/m² (eFig. 41-1 on the website shows individuals who are severely obese).

FIG. 41-2 Body mass index (BMI) chart. Healthy weight: BMI 18 to 24.9 kg/m²; overweight: BMI 25 to 29.9 kg/m²; obesity: BMI 30 kg/m². BMI = weight (kg)/height (m²).

eTABLE 41-1

COMPARISON OF FAD DIETS

Diet	Philosophy	Diet Composition
Atkins	• Obesity and other health problems caused by eating too many carbohydrates • Ketosis leads to decreased hunger	• Protein: 27% • Carbohydrates: 5% • Fat: 68% (saturated fat: 26%)
Zone	• Eating the right combination of food makes body’s metabolism perform at its best • Ideally, every meal and snack would have a ratio of 40% carbohydrates, 30% protein, and 30% fat • Once individuals determine the amount of protein they should have (size of palm) at each meal, they determine how many carbohydrates they need (size of fist) and how much fat they need	• Protein: 34% • Carbohydrates: 36% • Fat: 29% (saturated fat: 9%) • Alcohol: 1%
South Beach	• Much of excess weight comes from highly processed carbohydrates • To make up for the overall cut in carbohydrates, diet permits ample fats and animal proteins • Diet is in two phases • Phase one is the strictest part of the diet, lasting for 2 weeks, and allows protein, monounsaturated and polyunsaturated fats, and carbohydrates with the lowest glycemic index (GI)* (e.g., chocolate powder [no added sugar]), hard candy, sugar substitute (all sugar free unless otherwise specified) • Phase two reintroduces the body to carbohydrates with low GI (e.g., apples, berries, grapefruit, high-fiber cereal, whole-grain breads)	Phase one • Protein: 50% • Carbohydrates: 10% • Fat: 40%
Sugar Busters	• Sugar is toxic to the body and causes the body to create more insulin • Increases in insulin promote fat storage	• Protein: 27% • Carbohydrates: 5% • Fat: 68% (saturated fat: 26%)

^*Glycemic index is the term used to describe the rise in blood glucose levels after a person has consumed a carbohydrate-containing food.

eTABLE 41–2

NUTRITIONAL THERAPY
Meal Plans for 1200–Calorie–Restricted Weight-Reduction Diet *

General Principles

1. Eat regularly. Do not skip meals.

2. Measure foods to determine the correct portion size.

3. Avoid concentrated sweets, such as sugar, candy, honey, pies, cakes, cookies, and regular sodas.

4. Reduce fat intake by baking, broiling, or steaming foods.

5. Maintain a regular exercise program for successful weight loss.

Meal	Exchanges	Meal Plan 1	Meal Plan 2	Meal Plan 3
Breakfast	1 meat	1 scrambled egg	1 hard-boiled egg	1 oz ham
	2 bread	1 slice toast cup dry cereal (unsweetened)	1 flour tortilla cup Cream of Wheat	2 griddle cakes with diet syrup
	1 fruit	small banana	cup orange juice	cup pineapple juice
	1 fat	1 tsp margarine	1 slice bacon	1 tsp margarine
	1 dairy	1 cup low-fat milk	1 cup low-fat milk	1 cup low-fat milk
	Beverage	Coffee	Coffee	Coffee
Lunch	2 meat	1 slice bologna 1 slice cheese	Cheese enchiladas (made with 2 oz cheese, 2 corn tortillas, chili sauce)	2 oz baked breaded pork chop
	2 bread	2 slices bread		1 corn muffin
	Vegetable	Lettuce, pickles	Tomato wedges	Spinach
	1 fruit	Fresh grapes (12)	2 canned peach halves (packed in water)	Fresh orange
	Beverage	Diet soda	Artificially sweetened lemonade	Unsweetened iced tea
Dinner	2 meat	1 oz roast beef	Chili con carne (made with cup ground beef, cup pinto beans, and chili powder)	2 oz baked chicken
	1 bread	Baked potato with 1 tsp margarine^†		Corn on the cob with 1 tsp margarine
	Vegetable	Cooked carrots	Tossed salad and 1 Tbsp salad dressing^†	Okra
	1 fruit	cup strawberries	Fresh apple	Fruit cocktail (packed in water)
	1 milk	1 cup low-fat milk	1 cup low-fat milk	1 cup low-fat milk

^*For 1000 calories, omit 1 fruit exchange and change low-fat milk to skim milk. For 1500 calories, add 1 meat, 1 fruit, and 2 fat exchanges; change low-fat milk to whole milk. For 1800 calories, add 2 bread, 3 meat, 3 fat, and 1 fruit exchanges; change low-fat milk to whole milk.

^†One extra fat exchange allowed for each cup of 2% low-fat milk; 2 extra fat exchanges allowed for each cup of skim milk.

Table 41-1 shows the classification of overweight and obesity by BMI. The BMI, which provides an overall assessment of fat mass, must be considered in relation to the patient’s age, gender, and body build. For example, a body builder may have a BMI associated with obesity but because of a high muscle mass, the BMI would not be an accurate assessment. In contrast, in individuals who have lost body mass (e.g., older adults), the BMI would underestimate the degree of obesity. For this reason, other measures must be combined with the BMI for an accurate evaluation of a person’s weight.

TABLE 41-1

CLASSIFICATION OF OVERWEIGHT AND OBESITY

			Disease Risk Based on Waist Circumference*
	BMI (kg/m²)	Obesity Class	Men ≤40 in (102 cm) Women ≤35 in (89 cm)	Men >40 in (102 cm) Women >35 in (89 cm)
Underweight	<18.5	—	—	—
Normal†	18.5-24.9	—	—	—
Overweight	25.0-29.9	—	Increased	High
Obese	30.0-34.9	Class I	High	Very high
Obese	35.0-39.9	Class II	Very high	Very high
Severely obese	≥40.0	Class III	Extremely high	Extremely high

BMI, Body mass index.

^*Disease risk for type 2 diabetes, hypertension, and cardiovascular disease relative to person of normal weight.

^†Increased waist circumference can also be a marker for increased risk in persons of normal weight.

Source: National Heart, Lung, and Blood Institute: Classification of overweight and obesity by BMI, waist circumference, and associated disease risks. Retrieved from www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/bmi_dis.htm.

Waist Circumference.

Waist circumference is another way to assess and classify a person’s weight (see Table 41-1). People who have visceral fat with truncal obesity are at an increased risk for cardiovascular disease and metabolic syndrome (discussed later in this chapter). Health risks increase if the waist circumference is greater than 40 inches in men and greater than 35 inches in women.¹

Waist-to-Hip Ratio.

The waist-to-hip ratio (WHR) is another tool used to assess obesity. This ratio is a method of describing the distribution of both subcutaneous and visceral adipose tissue. The ratio is calculated by using the waist measurement divided by the hip measurement. A WHR less than 0.8 is optimal, and a WHR greater than 0.8 indicates more truncal fat, which puts the individual at a greater risk for health complications.

Body Shape.

Body shape is another method of identifying those who are at a higher risk for health problems (Table 41-2). Individuals with fat located primarily in the abdominal area, an apple-shaped body, have android obesity. Those with fat distribution in the upper legs, a pear-shaped body, have gynoid obesity. Genetics has an important role in determining a person’s body shape. Weight and shape are influenced by genetics.³

TABLE 41-2

RELATIONSHIP BETWEEN BODY SHAPE AND HEALTH RISKS

Body Shape	Characteristics	Health Risks
Gynoid (pear)	• Fat mainly located in the upper legs • Has a better prognosis but difficult to treat	• Osteoporosis • Varicose veins • Cellulite • Subcutaneous fat traps and stores dietary fat • Trapped fatty acids stored as triglycerides
Android (apple)	• Fat primarily located in abdominal area • Fat also distributed over upper body (neck, arms, shoulders) • Greater risk for obesity-related complications	• Heart disease • Diabetes mellitus • Breast cancer • Endometrial cancer • Visceral fat more active, causing • ↓ Insulin sensitivity • ↑ Triglycerides • ↓ HDL cholesterol • ↑ BP • ↑ Free fatty acid release into blood

HDL, High-density lipoprotein.

Epidemiology of Obesity

Currently, more than 35% of adults in the United States are obese. Unless Americans change their ways, 50% of the U.S. population will be obese by 2030.⁴ Women having a slightly higher incidence of obesity than men. When those who are overweight are included, the incidence of the adult population with a BMI greater than 25 kg/m² increases to more than 68%.⁵

The highest prevalence of obesity occurs between ages 40 and 59 for women and after 60 years of age for men.⁵ African Americans have the highest incidence of obesity followed by Hispanics (see Cultural & Ethnic Health Disparities box above).

Cultural & Ethnic Health Disparities

Obesity

• African Americans and Hispanics have a higher prevalence of obesity than whites.

• Among women, African Americans have the highest prevalence of being overweight or obese, and 15% are severely obese.

• Among men, Mexican Americans have the highest prevalence of being overweight or obese.

• African American and Hispanic women with low incomes appear to have the greatest likelihood of being overweight when compared with other socioeconomic groups.

• Native Americans have a higher prevalence of being overweight than the general population.

• Among Native Americans ages 45 to 74, more than 30% of women are overweight and more than 40% are obese.

• Asian Americans have the lowest prevalence of being overweight and obese compared with the general population.

Obesity in adulthood is often a problem that begins in childhood or adolescence. Nearly one third of children and teens are currently obese or overweight. It is estimated that almost half of overweight adults were overweight in childhood, and two thirds of obese children remained obese into adulthood.⁶ Reversing the childhood obesity crisis is key to addressing the overall obesity epidemic.

Etiology and Pathophysiology

Obesity is an increase in body weight beyond the body’s physical requirements. This results in an abnormal increase and accumulation of fat cells. However, the processes leading to and sustaining the obese state are complex and still undergoing investigation.

In obesity, there is an increase in the number of adipocytes (hyperplasia) and an increase in their size (hypertrophy). Adipocyte hypertrophy is a process by which adipocytes can increase their volume several thousand–fold to accommodate large increases in lipid storage. In addition, preadipocytes are triggered to become adipocytes once storage of existing fat cells is exceeded.² This process primarily occurs in the visceral (intraabdominal) and subcutaneous tissues. The process of hyperplasia (increase in numbers) of adipocytes is greatest from infancy through adolescence.

The majority of obese persons have primary obesity, which is excess calorie intake over energy expenditure for the body’s metabolic demands. Others have secondary obesity, which can result from various congenital anomalies, chromosomal anomalies, metabolic problems, or central nervous system lesions and disorders.

The cause of obesity involves significant genetic and biologic factors that are highly influenced by environmental and psychosocial factors. Each of these factors can and should be considered individually, but in reality they are interrelated.

Healthy People

Health Impact of Maintaining a Healthy Weight

• Reduces the risk of developing type 2 diabetes mellitus

• Increases chance of longevity and better quality of life

• Lowers the risk of hypertension and elevated cholesterol

• Reduces the risk of heart disease, stroke, and gallbladder disease

• Reduces the likelihood of breathing problems, including sleep apnea and asthma

• Decreases the risk of developing osteoarthritis, low back pain, and certain types of cancers

Genetic Link

Studies of twins, adoptees, and families all suggest the existence of genetic factors in obesity.7,8 The heritability of obesity estimated from twin studies is high, with only slightly lower values in twins raised apart than in those raised together. Similarly, in adoptees the children’s BMI correlated with that of their biologic parents rather than their adoptive parents.⁹ Estimates of obesity as an inherited problem are more than 50%.⁸

A number of genes have been identified as being linked to obesity. Genes actually may influence how calories are stored and energy released. “Energy-thrifty” genes, once protective against long periods where food was not available, are now maladaptive in societies where food availability is no longer a primary issue.⁷ Genes may be responsible for why two individuals living in the same environment can vary considerably in body size.

A strong link exists between a gene known as FTO (fat mass and obesity-associated gene) and BMI. Variants of this gene may explain why some people become overweight whereas others do not. People with two copies of a certain allele at the FTO gene weigh 7 to 8 lb more and have a greater risk of obesity than those who do not have the risk allele.¹⁰ More research is needed to better understand the role of genes in obesity.

Physiologic Regulatory Mechanisms in Obesity.

Research has focused on the physiologic regulatory processes that control eating behavior, energy metabolism, and body fat metabolism. Knowing how appetite is triggered and energy is expended provides important information for understanding obesity and specific targets for the development of drugs.

The hypothalamus, gut, and adipose tissue synthesize hormones and peptides that inhibit or stimulate the appetite (Fig. 41-3). The hypothalamus is a major site for regulating appetite. Neuropeptide Y, produced in the hypothalamus, is a powerful appetite stimulant. When it is imbalanced, it leads to overeating and obesity. Hormones and peptides produced in the gut and adipocyte cells affect the hypothalamus and have a critical role in appetite and energy balance (Table 41-3).

TABLE 41-3

HORMONES AND PEPTIDES IN OBESITY

Where Produced	Normal Function	Alteration in Obesity
Neuropeptide Y
Hypothalamus	Stimulates appetite	Imbalance causes increased appetite.
Ghrelin
Stomach (primarily)	Stimulates appetite ↑ After food deprivation ↓ In response to food in the stomach	Normal postprandial decline does not occur, which can lead to increased appetite and overeating.
Leptin
Adipocytes	Suppresses appetite and hunger Regulates eating behavior	Obesity is associated with high levels. Leptin resistance develops; thus obese people may lose the effect of appetite suppression.
Insulin
Pancreas	Decreases appetite	Increased insulin secretion which stimulates ↑ liver synthesis of triglycerides and ↓ HDL production.
Peptide YY
Colon	Inhibits appetite by slowing GI motility and gastric emptying	Circulating levels are decreased. ↓ Release after eating.
Cholecystokinin
Duodenum Jejunum	Inhibits gastric emptying and sends satiety signals to hypothalamus	Unknown role

HDL, High-density lipoprotein.

Leptin, secreted from adipocytes when they fill with fat, acts in the hypothalamus to suppress appetite, increase physical activity, and increase fat metabolism. A genetic deficiency of leptin causes extreme obesity. In obesity the level of leptin is actually increased, which has raised the question of whether obese people are insensitive to leptin.² Possible causes include failure to produce enough leptin receptors or production of receptors that are faulty.

Ghrelin, a gut hormone, regulates appetite through inhibition of leptin. In a fasting state, ghrelin is increased. Ghrelin acts in the hypothalamus by working on the reward system that triggers overeating. Ghrelin is thought to play a part in compulsive eating. In gastric bypass surgery, ghrelin is decreased significantly, which helps suppress appetite.

The two major consequences of obesity are due to the sheer increase in fat mass and the production of adipokines produced by fat cells. Adipocytes produce at least 100 different proteins. These proteins, secreted as enzymes, adipokines, growth factors, and hormones, contribute to the development of insulin resistance and atherosclerosis.

An increased release of cytokines from fat cells may disrupt immune factors, thus predisposing the person to certain cancers. Because visceral fat accumulation is associated with more alterations of these adipokines, people with abdominal obesity have more complications of obesity.¹¹

Environmental Factors.

Environmental factors play an important role in obesity. In today’s culture, people have greater access to food, particularly prepackaged and fast foods, and soft drinks, which have poor nutritional quality. Portion size of meals has increased dramatically (Table 41-4). The Centers for Disease Control and Prevention has developed visual programs that demonstrate how portions have increased over time.¹² Underestimating portion sizes and therefore caloric intake is common. In addition, eating outside of the home interferes with the ability to control the quality and quantity of food.

TABLE 41-4

PORTION SIZES: YESTERDAY VS TODAY

	25 Yr Ago	Today
Turkey sandwich	320 cal	820 cal
Bagel	3-in diameter, 140 cal	6-in diameter, 350 cal
Cheeseburger	333 cal	590 cal
Soda	6½ oz, 85 cal	20 oz, 250 cal

Lack of physical exercise is another factor that contributes to weight gain and obesity. With increases in use of technology, labor-saving devices, and cars, Americans are expending less energy in their everyday lives. Elimination of physical education programs in schools, along with increased time spent playing video games and watching TV, has contributed to the increase in sedentary habits.

Socioeconomic status is a known risk factor for obesity in a variety of ways.¹³ People with low incomes may attempt to stretch their food dollars by purchasing less expensive foods that often have poor nutritional quality with a greater caloric content. For example, people with low incomes are more likely to purchase pasta, bread, and canned fruit packed with sugar rather than chicken and fresh fruits and vegetables. Low-income residents may also live in environments that do not accommodate outdoor activities (e.g., safe playgrounds, walking tracks, tennis, swimming pools).

Psychosocial Factors.

People use food for many reasons besides their nutritional value. Associations with food begin in childhood, such as the use of food for comfort or rewards. Furthermore, when overeating develops at an early age and continues into adulthood, one’s ability to sense fullness (satiety) is compromised. Whether triggered by specific foods or by the wide variety of choices, some people consume more food than their bodies need. The lack of hunger that drives eating has been termed “mindless eating” and leads to consumption of unnecessary calories and increase in body weight.13,14

Finally, the social component of eating begins early in life when food is associated with pleasure and fun at such events as birthday parties, Thanksgiving, and religious holidays. All of these factors must be included when considering the etiology and treatment of obesity.

Health Risks Associated with Obesity

Hippocrates wrote that “corpulence is not only a disease itself, but the harbinger of others,” thus recognizing that obesity has major adverse effects on health. Many problems occur in obese people at higher rates than people of normal weight (Fig. 41-4).

The medical cost of adult obesity in the United States is difficult to calculate, but estimates range from $147 billion to nearly $210 billion per year. The bulk of the spending is from treating obesity-related diseases such as diabetes. Obese people spend 42% more on health care costs than healthy-weight people.⁴

Mortality rates rise as obesity increases, especially when obesity is associated with visceral fat. For obese persons, mortality rates from all causes, especially from cardiovascular disease, are increased by 50% to 100% above those of persons with a normal BMI. Being overweight in midlife, once thought to have fewer health consequences than being obese, confers a 20% to 40% increase in mortality rate for both men and women.¹¹ In addition to these problems, obese patients have a reduced quality of life. Fortunately, most of these conditions can improve if an individual loses weight.

Cardiovascular Problems

Obesity is a significant risk factor for cardiovascular disease in both men and women.¹¹ Android obesity is the best predictor of these risks and is linked with increased low-density lipoproteins (LDLs), high triglycerides, and decreased high-density lipoproteins (HDLs). Obesity is also associated with hypertension, which can occur because of increased circulating blood volume, abnormal vasoconstriction, increased inflammation (damaging blood vessels), and increased risk of sleep apnea (raises blood pressure [BP]). Altered lipid metabolism and hypertension can increase the long-term risk of heart disease and stroke. Excess body fat can also lead to chronic inflammation throughout the body, especially in blood vessels, thus increasing the risk of heart disease.

Diabetes Mellitus

More than 80% of people with type 2 diabetes are obese or overweight.⁴ Hyperinsulinemia and insulin resistance, common features of type 2 diabetes, are also found in obesity, especially when visceral fat is increased. Excess weight decreases the effectiveness of insulin. When insulin does not work effectively, too much glucose stays in the bloodstream. Thus more insulin is made to compensate. Pancreatic β cells (cells that make insulin) may get overworked and become worn out. Over time, the pancreas is no longer able to keep blood glucose in normal range. It appears that adiponectin, a peptide that increases insulin sensitivity, is decreased in obese people.

Obesity is a major risk factor for development of type 2 diabetes. Furthermore, obesity complicates the management of type 2 diabetes by increasing insulin resistance and glucose intolerance, which makes drug treatment for diabetes less effective. A weight reduction of 7% can decrease the risk of diabetes by 58%.¹⁵