Ovid: Primary Care Medicine

Chapter 10

Evaluation of Overweight and Obesity

Overweight and obesity have become major health concerns in modern postindustrial societies, affecting an estimated 55% of Americans older than the age of 20 years. The personal and social costs are enormous, approaching $100 billion annually when medical complications, lost wages, and expenditures for weight reduction efforts are taken into account, not to mention the accompanying emotional pain, social stigmatization, and discrimination that may ensue. Excessive weight, through its promotion of the metabolic syndrome, is a major risk factor for cardiovascular disease, type 2 diabetes mellitus, dyslipidemia, and hypertension, and it is also associated with increased risks of stroke, heart failure, and cancer. In addition, obese patients manifest heightened risks of impaired pulmonary function (including sleep apnea), osteoarthritis, gallbladder disease, and surgical complications.

The tasks for the primary physician in the evaluation of patients with excess weight include not only an attempt to identify etiologic factors, but also a careful assessment of weight status and fat distribution as risk factors for major disease. This chapter focuses on the diagnostic evaluation; see Chapter 233 for the approach to treatment.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1,2,3,4,5,6,7,8,9,10,11,12,13,14,15)

Definitions

The preferred definitions of overweight and obesity are based on body mass index (BMI) determinations, which approximate total body fat content and correlate with disease risk (Table 10.1). Overweight is defined as a BMI of 25 to 29.9 kg/m². Obesity is defined as a BMI greater than 30 kg/m², and morbid obesity by a BMI greater than 40 kg/m² (Table 10.1).

Table 10.1. Definition and Classification of Excess Weight

CLASS	BMI (KG/M²)	WAIST CIRCUMFERENCE^a	RELATIVE RISK^b
Normal	18.5–24.9	Normal	Normal
		Increased	Increased
Overweight	25.0–29.9	Normal	Increased
		Increased	High
Obese	30.0–34.9	Normal	High
		Increased	Very High
	35.0–39.9	Normal	Very high
		Increased	Very high
Obese, morbid	40.0+	All are increased	Extremely high
BMI, body mass index.
^a Increased, >102 cm (40 in.) in men, >88 cm (35 in. in women).
^b For diabetes type 2, hypertension, coronary artery disease.
Adapted from Expert Panel on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998;158:1855, with permission.

Physiology

Caloric intake and energy expenditure are linked through hypothalamic regulation of appetite and metabolism. The hypothalamus integrates a complex and redundant set of afferent signals, including leptin, released from adipose tissue; norepinephrine, from the autonomic nervous system; epinephrine, insulin, androgens, glucocorticoids, progesterone, and estrogens, from endocrine glands; peptide YY, glucagon, cholecystakinin, bombesin peptides, neurotensin, growth hormone–releasing hormone, somatostatin, and glucose, from the gastrointestinal tract; and dopamine, gamma-amino butyric acid, ghlanin, opioids, growth hormone–releasing factor, somatostatin, and serotonin, from the central nervous system. The efferent output from the hypothalamus controls energy expenditure and appetite by the release of alpha-melanocyte-stimulating hormone (alpha-MSH), norepinephrine, serotonin, neuropeptide Y, glucagon-like peptide I, thyrotropic hormone, and corticotropin-releasing hormone, which act on the autonomic nervous system and the thyroid gland. Increasingly appreciated as a factor in appetite control is the role of alpha-MSH on the melanocortin 4 receptor (MC4R), which, when stimulated, suppresses appetite.

Pathophysiology

Obesity is often the consequence of physical inactivity, especially in persons with an underlying disturbance in metabolism, appetite control, or dietary composition. In most instances, the etiology is multifactorial, although one factor may predominate. Susceptibility is influenced by genetic determinants that were once advantageous in regard to evolution, such as those that reduce energy expenditure or encourage the intake of energy-rich foods. However, such inherited traits can be counterproductive to good health in postindustrial societies, in which physical demands are greatly reduced and high-calorie food is plentiful and inexpensive.

Physical Inactivity

Physical inactivity emerges as a leading cause of obesity in modern society, underscored by the increasing prevalence of obesity despite a decline in average daily caloric intake. When daily life makes few physical demands, caloric needs drop precipitously, which leads to an epidemic of excess weight, even among those without major genetic susceptibility to weight gain. Some genetic variability in the propensity for exercise has been described, which may contribute to inactivity in some.

Metabolic Factors

Metabolic factors are important, genetically determined contributors to excessive weight and include resting energy expenditure, thermic effect of food, and exercise-induced energy expenditure. Among these, a reduction in energy utilization with exercise correlates the most strongly with risk for weight gain. Ninefold to 30-fold variations have been observed. Because exercise-induced energy expenditure accounts for about 30% of total energy demand, any genetic propensity for reduced energy expenditure with exertion could substantially increase the risk for obesity.

Dietary Composition

Dietary composition actually plays a much smaller role than might be expected. In most persons, changing the percentages of dietary fat, protein, and carbohydrate without changing the number of calories consumed has little or no influence on the development of obesity. Diets high in fat contribute to obesity mostly because they are rich in calories, not because they are rich in fat. Despite claims to the contrary by those promoting weight-loss diets, there is no evidence that dietary composition alone is a major determinant of obesity for the vast majority of persons. Almost all weight loss diets work by restricting total calories (see Chapter 233). The timing of food intake may contribute modestly to obesity; eating once daily, particularly before going to bed, predisposes to the accumulation of adipose tissue in some persons.

Appetite Disturbances

Appetite disturbances have long been suspected as a cause of obesity. Many obese individuals

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appear to eat without satiety. This has led to intensive study of appetite regulation and its disruption. In some, there appears to be resistance to normal appetite controls, such as the appetite suppressant leptin, serum levels of which actually increase in obese subjects. In some obese persons, the postprandial production of appetite suppressing gut hormone fragment polypeptide YY (PYY) is reduced compared with normal controls. In others, there is genetic alteration of the MC4R (see later discussion). In some animals, the effects of appetite suppressants can be overcome by providing easy access to palatable, energy-rich foods.

Genetic Factors

Genetic factors, as noted earlier, play a substantial role by influencing energy utilization, appetite, food preferences, and even propensity for physical activity. The importance of genetic factors is underscored by findings from studies of twins, families, and adoptees, which reveal a strong relation between weight class of adoptees and their biologic parents, but none between adoptees and their adopted parents. Parental obesity doubles the risk for adult obesity in obese and nonobese children younger than the age of 10 years. Obese children younger than the age of 3 years who have an obese parent have a very high risk for adult obesity, but they experience no increase in risk if neither parent is obese. The alpha-MSH/MC4R axis appears important in some cases of morbid obesity. Patients with a mutation in the MC4R gene manifest hyperphagia, binge eating, and morbid obesity. Genetic factors are estimated to account for nearly 50% of the risk of becoming overweight, and even more for becoming obese.

Developmental and Environmental Factors

Developmental and environmental factors, manifested by parental influences and childhood environment, contribute to the development of adult obesity. As the age of the child increases, the influence of environment increases. At ages greater than 10 years, heredity becomes a less-dominant determinant of adult obesity, and environment increases in importance. Persons growing up in the current era of plentiful, inexpensive high-calorie fast food are at greater risk of obesity than are cohorts from earlier eras. Teenagers, especially, consume large amounts of such food, with potentially serious long-term consequences. Natural history studies find a strong relation between increased weight during the teenage and young adult years, and risk of becoming frankly obese later in life. Those who become obese tend to remain obese their entire lives.

Psychological and Behavioral Factors

Psychological and behavioral factors have long been thought to be important; however, there is no known psychological explanation for why reactive hyperphagia develops in some persons as a response to emotional stress, whereas anorexia is the reaction of others. Considerable research has been unable to determine any particular personality organization or cluster of psychological defense mechanisms clearly linked to obesity. Nonetheless, psychological problems frequently contribute to the onset and perpetuation of obesity-inducing behavioral changes. For example, some individuals characteristically overeat in response to stress, loss, or frustration. Those with the night-eating syndrome, characterized by insomnia, massive late-evening “refrigerator raids,” and morning anorexia, also experience particular emotional distress when they try to reform their eating behaviors. Usually, coinciding social stresses are present as well. The appetite disturbance associated with major depression may lead to either an increase or a decrease in weight.

Social Factors

Social factors are key determinants of the frequency and nature of feasts, timing of meals, role and meaning of food, types of foods consumed, and norms of appearance. In U.S. society, excess weight occurs far more frequently among minorities and the socioeconomically disadvantaged than among others. Young African American and Hispanic women are 2.1 and 1.5 times, respectively, more likely to become obese than are young white women. Whether this difference represents dietary preference, socially motivated behavior, or interactional factors is unclear. In certain occupations, such as wrestling, obesity is a help, not a hindrance. In former times, corpulence was a sign of prosperity and was cultivated by bankers and businessmen.

Clinical Presentation

Most cases of overweight and obesity occur independent of an underlying medical condition, although they may exacerbate or lead to illness. Onset of exogenous obesity is often evident by early adulthood and tends to persist. Those who are overweight by their early 20s are at considerable risk of developing frank

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obesity by their late 30s. Persons with an underlying hereditary etiology usually manifest obesity before age 10 years.

In 5% to 10% of adult cases, an underlying medical condition or medication that affects energy expenditure, fuel utilization, appetite, or physical activity may be responsible. Often, the mechanism is an effect on one of the substances involved in regulating energy intake or expenditure (see earlier discussion).

Pharmacologic Agents

Pharmacologic agents prescribed for clinical conditions other than obesity may cause weight gain. Beta-blockers and central sympatholytics (e.g., clonidine) can decrease metabolic rate and energy expenditure. Glucocorticosteroids cause hypertrophic obesity in a characteristic truncal pattern. Antidepressants, such as the tricyclics and selective serotonin reuptake inhibitors, and some antihistamines (e.g., cyproheptadine) act as appetite stimulants. Weight gain is also common with oral contraceptive use.

Endocrine Disturbances

Endocrine disturbances are more often the result, rather than the cause, of excess weight. However, hypothyroidism (see Chapter 104) has been found to account for up to 5% of cases in some series. Cushing's syndrome is a rare cause and is usually accompanied by characteristic features of truncal obesity and peripheral muscle wasting. Stein–Leventhal syndrome—polycystic ovaries, absent menses, moderate hirsutism, and hyperinsulinism (see Chapter 112)—often goes unrecognized as an endocrinologic form of obesity; the precise mechanism of the obesity is unknown. Eunuchism may also be associated with obesity. Of great concern is the marked increase in frequency of insulin resistance and its attendant metabolic syndrome, characterized by hyperinsulinism, elevated triglycerides, and low high-density-lipoprotein (HDL) cholesterol, all important risk factors for diabetes, hypertension, and cardiovascular disease. Serum insulin and triglyceride levels are elevated, and HDL cholesterol is reduced.

Neurologic Causes

Neurologic causes of obesity are usually not cryptic; they mostly result from hypothalamic injury, as occurs with craniopharyngiomas, encephalitis, or trauma. Visual field defects or headaches are usually present. Two rare types of neurologic disease without obvious central nervous system symptoms have been described. Kleine–Levin syndrome consists of periodic hyperphagia and hypersomnia. A second syndrome is characterized by preoccupation with food and accompanying electroencephalographic abnormalities that respond to phenytoin.

Mental Illness

Mental illness may be heralded by weight gain. The appetite disturbance of major depression is one of the cardinal manifestations of the condition and may be a presenting complaint (see Chapter 227).

DIFFERENTIAL DIAGNOSIS (16)

The causes of obesity can be primary or secondary, with the latter being medical conditions that result in obesity. Some forms of secondary weight gain are a consequence of salt retention and fluid overload rather than an increase in fat cell mass. Among the important causes of sodium retention are congestive heart failure, severe hepatocellular disease, and renal failure (see Chapters 32, 71, and 142). Primary forms of obesity can be classified by their underlying pathophysiology. The vast majority of cases are primary in nature. An etiologic/pathophysiologic diagnosis is essential to the design of an effective management program (Table 10.2).

Table 10.2. Important Causes of Obesity

Primary

Psychological factors
   Depression
   Anxiety
   Frustration

Biologic factors
   Reduced thermogenesis
   Increased fat cell mass
   Autonomic dysfunction
   Altered hypothalamic set point
   Single large daily meal taken before bedtime
   Decreased energy expenditure
   Drugs (e.g., tricyclic antidepressants, oral contraceptives, corticosteroids, phenothiazines)

Genetic influences
Familial obesity

Social and occupational factors
Lower socioeconomic class
Social/occupational situation

Secondary

Endocrine disease
   Hypothyroidism
   Stein-Leventhal syndrome
   Cushing's syndrome

Neurologic disease
Hypothalamic injury (e.g., trauma, encephalitis, craniopharyngioma)

WORKUP (16,17,18,19)

Particular attention should be paid to detection and early intervention in persons at greatest risk for becoming obese, namely overweight teenagers and young adults, especially women from minority groups.

A principal objective of the overweight/obesity evaluation is to determine how much risk the weight problem confers. The risk assessment begins with an estimate of the amount and distribution of fat, followed by a consideration of other risk factors and underlying conditions that add to morbidity and mortality risks; it concludes with estimates of relative and absolute risk. Additional components of the workup pertinent to management include elucidation of the underlying mechanism(s) responsible for the patient's weight problem, detection of any underlying illnesses presenting as weight excess, and assessment of the patient's motivation to lose weight.

Weight Assessment

To establish whether an individual has a weight problem that poses a health risk, an estimation of the amount and distribution of fat is required. Both are independent determinants of disease risk. Fat distribution is particularly important, even among persons who are not obese.

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Measurement of Body Fat

This is best accomplished by calculating the BMI. The BMI determination assumes that weight is measured with shoes and heavy clothing removed. If weight is obtained with shoes and all clothing on, then 5 lb should be subtracted for men and 3 lb for women. The BMI is calculated by taking the weight in kilograms and dividing it by the square of the height in meters (or by multiplying by 703 the weight in pounds divided by the square of the height in inches). This ratio of weight to height actually calculates total body mass rather than fat mass, but it correlates highly with the amount of body fat and its associated health risks except in very muscular individuals, who might be falsely labeled as overweight with use of the BMI. The BMI range of 20 to 24.9 is classified as “normal” because no actuarial increase in disease mortality is noted within it. Mortality begins to increase as the BMI exceeds 25, and it is here that health professionals should be concerned. Most expert consensus panels recommend that health professionals adopt the BMI as the preferred measure for evaluating weight status because it provides the best estimate of disease risk (Fig. 10-1 and Table 10.1).

Figure 10-1. Nomogram for body mass index (kg/m²). Weights and heights are without clothing. With clothes, add 5 lb (2.3 kg) for men and 3 lb (1.4 kg) for women. Add 1 in. (2.5 cm) in height for shoes. (From New weight standards for men and women. J Am Diet Assoc 1985;85:1119, with permission. Based on data from Stat Bull Metropolitan Life Insurance Company 1959;40:1.)

Height and Weight Tables

Height and weight tables have the advantage of simplicity. However, there are serious limitations to their use. Standard charts typically list “ideal” or desired weights based on actuarial data, yet it is not weight per se that minimizes morbidity or the incidence of disease. The person having a significant percentage of lean body mass, such as a physical laborer, may well exceed “ideal” body weight, yet not be obese. On the other hand, some individuals may be within the ideal range but have non-insulin-dependent diabetes mellitus, hypertension, or other conditions that would benefit from weight reduction. The Metropolitan Life Insurance Company has published revised reference weights in an attempt to isolate the effect of weight alone on longevity; individuals with major diseases, such as cancer, diabetes, or heart disease, were omitted from the study (Table 10.3). Life tables, based only on mortality, ignore possible nonfatal risks associated with increased weight.

Table 10.3. Optimal Weights,a in Pounds, for Adults Ages 25 Years and Older (Light Clothing)

HEIGHT (IN SHOES)	SMALL FRAME	MEDIUM FRAME	LARGE FRAME
Men
5 ft 2 in.	112–120	118–129	126–141
5 3	115–123	121–133	129–144
5 4	118–126	124–136	132–148
5 5	121–129	127–139	135–152
5 6	124–133	130–143	138–156
5 7	128–137	134–147	142–161
5 8	132–141	138–152	147–166
5 9	136–145	142–156	151–170
5 10	140–150	146–160	155–174
5 11	144–154	150–165	159–179
6 0	148–158	154–170	164–184
6 1	152–162	158–175	168–189
6 2	156–167	162–180	173–194
6 3	160–171	167–185	178–199
6 4	164–175	172–190	182–204
Women
4 10	92–98	96–107	104–119
4 11	94–101	98–110	106–122
5 0	96–104	101–113	109–125
5 1	99–107	104–116	112–128
5 2	102–110	107–119	115–131
5 3	105–113	110–122	118–134
5 4	108–116	113–126	121–138
5 5	111–119	116–130	125–142
5 6	114–123	120–135	129–146
5 7	118–127	124–139	133–150
5 8	122–131	128–143	137–154
5 9	126–135	132–147	141–158
5 10	130–140	136–151	145–163
5 11	134–144	140–155	149–168
6 0	138–148	144–159	153–173
^aWeights associated with the lowest mortality rates (derived from actuarial data, Metropolitan Life Insurance Company).

Height and Weight Formulas

Height and weight formulas are sometimes used to determine ideal body weight and estimate the degree of obesity, but they provide only the crudest of estimates and should not be used to set goals for weight reduction. They are provided here only because they are sometimes referred to. (Appropriate weight goals for patients can be determined only by a thorough analysis of their medical history and physical findings, supplemented by appropriate laboratory evaluation.)

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Female weight: Allow 100 lb for first 5 ft of height plus 5 lb for each additional inch.
Male weight: Allow 106 lb for first 5 ft of height plus 6 lb for each additional inch.

The measurement of skinfold thickness is used by some to quantify adiposity. Calipers are used to measure skinfold thickness in the triceps and subscapular regions. However, reliability can be a problem when skinfold measurements are used because body fat increases with age, grossly obese patients are difficult to measure, and results vary among providers using the calipers.

Bioelectric Impedance Analysis

Bioelectric impedance analysis is sometimes used to measure body fat. Electrodes are applied to one arm and leg, and the impedance is measured. Impedance is proportional to the aqueous composition of the body. Formulas are used to estimate the percentage of fat in the body. Although accurate, this method is expensive and not readily available.

The old-fashioned eyeball test remains a mainstay of assessment: If a person looks fat, he or she is likely to be fat. However, quantification and correlation with risk are crude with this commonsense method.

Measurement of Fat Distribution

The other independent determinant of health risk associated with excess weight is fat distribution, which can be quantified by measuring waist circumference. The circumference of the waist is obtained at the narrowest area above the umbilicus. Measurements in excess of gender-specific cutoffs (>102 cm, or 40 in., in men and >88 cm, or 35 in., in women) confer an increased relative risk of disease morbidity and mortality (see Table 10.3). The effect of fat distribution on risk is so strong that waist circumference is important even in persons who are not technically overweight. However, in morbidly obese patients, waist circumference is always exceeded, and the measurement confers no additional risk.

The ratio of waist or abdominal circumference to hip or gluteal circumference provides an even more precise quantitative index of regional fat distribution. The hip circumference is measured at the maximal gluteal protrusion. Individuals with excess upper body fat (android obesity) are at higher risk for diabetes, atherosclerosis, and stroke than are those who have more adipose tissue in the hips, buttocks, and thighs (gynecoid obesity). In quantitative terms, individuals with waist-to-hip ratios greater than 0.8 for women and 1.0 for men have an increased risk for coronary disease.

Estimation of Disease Risk

One begins with determinations of total body fat and fat distribution, represented respectively by BMI and waist circumference. These parameters correlate well with relative risk, especially among persons younger than the age of 65 years (see Table 10.3). Relative risk from obesity is greatest among younger persons and declines somewhat with advancing age.

Determination of the absolute risk associated with obesity requires checking for underlying coronary heart disease (see Chapter 20), type 2 diabetes mellitus (see Chapter 93), noncoronary atherosclerotic disease (see Chapters 23 and 171), hypertension (see Chapter 19), and sleep apnea (see Chapter 46), in addition to the end-organ injuries that may result from them (see Chapters 26, 30, 35, 46, and 102). The cardiovascular risk assessment is enhanced by screening for principal risk factors such as hyperlipidemia (see Chapter 15), hypertension (see Chapter 14), smoking (see Chapter 54), and premature coronary disease in first-degree relatives. Calculations of absolute risk are possible from a consideration of these factors (see Chapters 26 and 27). Searches for osteoarthritis (see Chapter 146), cholelithiasis (see Chapter 69), and stress incontinence also help predict risk of weight-related consequences.

Assessment of Etiology and Consequences

As important as risk assessment is, etiologic factors and health consequences deserve attention because they are relevant to the approach to management.

History

An extensive weight history should include age of onset of obesity, weight status of parents and siblings, and any identifiable circumstances associated with the onset of obesity. Although dietary composition per se is not a risk factor for obesity, dietary composition and quantity need to be ascertained to determine total caloric intake. A high-fat diet is likely to provide excessive calories. Because physical inactivity is a major precipitant of excess weight, the patient's daily activities should be elucidated in detail to estimate daily energy requirements. Proclivity toward exercise should also be ascertained. A careful review of ongoing psychological and situational stresses is essential and should include screening for depression (see Chapter 227). Any recent attempts at smoking cessation should be reviewed for effect on weight. The social and cultural dimensions of the history should be explored for their possible contribution to weight gain.

Even in a patient without obvious medical pathology, a workup that screens for underlying endocrinologic and neurologic diseases is essential, as is a check for drug-induced causes. The history requires a thorough neuroendocrine review of symptoms: fatigue, unexplained weight gain, cold intolerance, hoarseness, change in skin and hair texture, amenorrhea, hirsutism, easy bruising, weakness, visual disturbances, and headache. Medications are reviewed for agents that may stimulate appetite or affect metabolism, such as antidepressants, oral contraceptives, corticosteroids, phenothiazines, antithyroid medications, β-blockers, and insulin.

A review of systems for the consequences of obesity should include inquiry into chest pain, shortness of breath, polyuria, polydipsia, impotence, numbness, limb pain or coldness, transient neurologic deficits, daytime sleepiness, apneic periods at night, and pain in weight-bearing joints.

The Physical Examination

The physical examination includes a check for such etiologic clues as moon facies, hirsutism, dry and thickened skin, coarse hair, truncal obesity, pigmented striae, goiter, adnexal masses, lack of secondary sex characteristics, delayed relaxation of ankle jerks, and visual field deficits. The physical examination should include a search for the consequences of obesity, including blood pressure elevation, diabetic retinopathic changes, carotid bruits, obstruction of soft tissues in the upper airway, cor pulmonale, rales, cardiac enlargement,

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degenerative changes in the hips and knees, and signs of peripheral arterial insufficiency and peripheral neuropathy.

Laboratory Testing

Laboratory testing includes two components: the diagnosis of an underlying medical etiology and the detection of metabolic consequences. A strategy of routinely testing for all possible medical causes in the absence of suggestive clinical findings adds to expenses and increases the risk of generating a high percentage of false-positive results (see Chapter 2). Nonetheless, some clinicians routinely screen for hypothyroidism with a thyrotropin determination because the test is sensitive, the condition has a relatively high frequency, and the clinical presentation of hypothyroidism can be very subtle (see Chapter 104).

The laboratory evaluation is most productive when directed at causes suggested by the history and the physical examination. For example, the obese patient suspected of having Cushing's syndrome because of truncal obesity, peripheral wasting, and pigmented striae is a reasonable candidate for an overnight 1-mg dexamethasone suppression test. If headaches accompanied by a visual field disturbance are present, then computed tomography of the sella turcica is needed to check for the possibility of a pituitary tumor (see Chapter 100). Measures of energy expenditure, thermogenesis, autonomic function, fat cell count, and metabolic set-point are relegated to the research laboratory. Similarly, genetic testing and assays for such appetite suppressant factors as leptins, alpha-MSH, MC4R, and PYY remain confined to the study setting but may be useful in the future.

Testing for insulin resistance and its metabolic consequences is essential to identifying those persons at increased cardiovascular risk. About half of obese persons will have evidence of insulin resistance. Fasting glucose and lipid profile (see Chapter 15) are essential determinations. Serum insulin levels provide a more direct measurement of hyperinsulinism, but assays are not well standardized. The plasma triglyceride level (>130 mg/dL) and triglyceride: high-density-lipoprotein (LDL) cholesterol ratio (>3.0) provide the best approximation of insulin levels and correlate with cardiovascular risk, as does the better established total cholesterol:HDL cholesterol ratio (<4.5). These results help detect metabolic syndrome and identify those persons at greatest cardiovascular risk and who are likely to benefit most from weight reduction.

Patients bothered by daytime sleepiness and a history of excessive snoring and disturbed sleep resulting from irregular breathing should be considered for a formal sleep study (see Chapter 46).

INDICATIONS FOR REFERRAL

Patients who are morbidly obese and demonstrate such adverse sequelae as marked respiratory compromise, disabling arthritis, or symptomatic coronary disease require consultation for consideration of a very low calorie diet under the supervision of persons experienced in its implementation (see Chapter 233). Referral for consideration of surgical approaches to treatment may also be indicated in such persons. Obstructive sleep apnea in patients with mild-to-moderate obesity may not require such extreme measures, but pulmonary consultation in conjunction with a weight-loss program is indicated (see Chapter 46).

PATIENT EDUCATION

Most patients come for evaluation out of concern for an underlying medical condition or a genetic determinant. The vast majority have no such cause and need to know that inactivity and caloric excess are the principal reasons for their weight gain. Although they may have genetically determined risk factors, such as a proclivity for high-fat food, reduced exercise-related energy expenditure, or a defect in appetite suppression, they will benefit when the physician reemphasizes the overwhelming importance of exercise and an active lifestyle to weight control, and modest restriction in caloric intake (see Chapter 233). The occasional patient whose obesity is driven predominantly by heredity (both parents obese, onset before age 3 years) appreciates knowing that the weight problem is not a consequence of defective character. For the vast majority, the education process begins by drawing attention away from diets, medical conditions, and “metabolism problems” and to the importance of exercise. The goals are to provide the patient with an estimate of the disease risk posed by the excessive weight and an assessment of the factors contributing to it.

RECOMMENDATIONS

Make overweight detection and early intervention an important goal of the health maintenance/prevention agenda for teenagers and young adults. Focus efforts on those at greatest risk for becoming obese, namely overweight teenagers and young adult women from minority groups.
Begin the weight assessment by determining the amount of body fat and fat distribution, which independently correlate with the relative risk associated with excess weight.
Estimate body fat content by calculating the BMI (body weight in kilograms divided by the square of the height in meters).
Determine fat distribution by measuring the waist circumference at the narrowest area above the umbilicus.
Estimate the relative risk of cardiovascular disease, type 2 diabetes, and hypertension from these determinations.
Search for major cardiovascular risk factors and for evidence of end-organ damage to determine the absolute risk of cardiovascular morbidity and mortality.
Check the history and the physical examination for etiologic factors, ranging from familial propensity and early age of onset to dietary excess, physical inactivity, and underlying medical and psychological conditions.
Restrict laboratory testing to investigating etiologic hypotheses suggested by the history and the physical examination, and to assessing cardiovascular risk associated with metabolic syndrome; include measurement of fasting triglycerides and HDL cholesterol.
Provide the patient with an assessment of the factors contributing to excessive weight and with an estimate of disease risk posed by the obesity so that a customized management plan can be formulated (see Chapter 233).

A. H. G.

ANNOTATED BIBLIOGRAPHY

1. Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among US adults, 1999–2000. JAMA 2002;288:1723. (Documents the epidemic proportions of the problem.)

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2. Peeters A, Barendregt JJ, Willendens F, et al. Obesity in adulthood and its consequences for life expectancy: a life table analysis. Ann Intern Med 2003;138:24. (A prospective cohort study from the Framingham Study; finds large decreases in life expectancy and increases in early mortality.)

3. Calle EE, Rodriguez C, Walker-Thurmond, et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 2003;348:1625. (Large prospective population study; increased weight was associated with an increase in death from all cancers.)

4. Wilson PWF, D'Agostina RB, Sullivan L, et al. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med 2002;162:1867. (Prospective cohort study from the Framingham Study; cardiovascular risk was strongly associated with overweight status.)

5. Kurth T, Gaziano JM, Berger K, et al. Body mass index and the risk of stroke in men. Arch Intern Med 2002;162:2557. (Prospective cohort study from the Physicians' Health Study; there was a significant increase in stroke risk with increasing body mass index [BMI].)

6. Kenchaiah S, Evans JC, Levy D, et al. Obesity and the risk of heart failure. N Engl J Med 2003;347:305. (Prospective cohort study from the Framingham Heart Study; an increased BMI was associated with an increased risk of heart failure.)

7. Manson JE, Willett WC, Stampfer MJ, et al. Body weight and mortality among women. N Engl J Med 1995;333:677. (Follow-up data at 16 years from the prospective Nurses' Health Study showing a striking relation between all-cause mortality and excess weight in middle-aged women.)

8. Rosenbaum M, Leibel RL, Hirsch J. Obesity. N Engl J Med 1997;337:396. (Review of the physiology and pathophysiology of weight control.)

9. Liebel RL, Hirsch J, Appel BE, et al. Energy intake required to maintain body weight is not affected by wide variation in diet composition. Am J Clin Nutr 1992;55:350. (Best evidence that what a person eats is less important than the total number of calories.).

10. Silva JE. The thermogenic effect of thyroid hormone and its clinical implications. Ann Intern Med 2003;139:205. (Review of physiology of thyroid hormone and its contribution to energy homeostasis.)

11. Weinsier RL, Hunter GR, Heini AF, et al. The etiology of obesity: relative contributions of metabolic factors, diet, and physical activity. Am J Med 1998;105:145. (An analysis of data arguing that physical activity appears to be the most important determinant of obesity in postindustrial societies.)

12. Korner J, Leibel RL. To eat or not to eat—how the gut talks to the brain. N Engl J Med 2003;349:926. (Succinct discussion of appetite control mechanisms and their potential roles in obesity.)

13. List JF, Habener JF. Defective melanocortin 4 receptors in hyperphagia and morbid obesity. N Engl J Med 2003;348:1160. (An editorial summarizing new studies on genetic causes of obesity.)

14. Hu FB, Li TY, Colditz GA, et al. Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women. JAMA 2003;289:1785. (Prospective cohort study from the Nurses' Health Study; sedentary behavior was found to be a major risk factor.)

15. McTigue KM, Garrett JM, Popkin BM. The natural history of the development of obesity in a cohort of young U.S. adults between 1981 and 1998. Ann Intern Med 2002;136:857. (A long-term prospective cohort study finding that the risk of frank obesity was greatest in overweight young persons.)

16. Expert Panel on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998;158:1855. (Evidence-based consensus panel recommendations.)

17. Janssen I, Katzmarzyk PT, Ross R. Body mass index, waist circumference, and health risk: evidence in support of current National Institutes of Health guidelines. Arch Intern Med 2002;162:2074. (Finds waist circumference correlates well with risk.)

18. Rexrode KM, Carey VJ, Hennekens CH, et al. Abdominal adiposity and coronary heart disease in women. JAMA 1998;280:1843. (Data from the Nurses' Health Study showing increased waist circumference to be an independent risk factor for coronary disease, even in persons who have a normal BMI.)

19. McLaughlin T, Abbasi F, Cheal K, et al. Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med 2003;139:802. (A cross-sectional study identifying fasting triglyceride level and ratio of triglycerides to high-density-lipoprotein cholesterol as the best proxies for insulin determination and detection of insulin resistance.)