Obesity and Weight Management

From WiserWiki

[edit] Obesity and Weight Management

Louis J. Aronne

[edit] OBESITY

Obesity is an accumulation of excess adipose tissue that leads to impairment of health. This chronic disease is increasingly impacting the health of people around the world.^[1] Studies examining metabolic and genetic causes of obesity have proved that this disease arises from an excess of energy intake compared to expenditure.^[2] Each individual inherits a set of genes that control appetite and metabolism. A wide variety of environmental factors, such as food availability, level of physical activity, and individual psychology and culture, may exacerbate prevalent genetic tendencies to gain weight.^[3] Thus obesity is not simply the result of gluttony and a lack of willpower.

Data from the National Health and Nutrition Examination Survey (NHANES) suggest that more than two-thirds of individuals with a body mass index (BMI) greater than 27 (Table 58-1) have at least one additional complicating condition such as diabetes, hypertension, hyperlipidemia, sleep apnea, or arthritis of the lower extremities. Despite this positive relationship between obesity and these conditions, the treatment of obesity by physicians in the office setting has been largely ignored. As the understanding of the weight regulating mechanisms progresses, however, obesity appears to be a neuroendocrine disorder rather than a disorder of willpower.^[4][5] The successful treatment of obesity will play an important role in improving the health care of adults and children in the coming years.^[6]

Table 58-1 Calculation of Body Mass Index for Overweight/Obesity

Normal								Overweight					Obesity (class I)					Obesity (class II)					Extreme obesity (class III)
BMI	19	20	21	22	23	24	25	26	27	28	29	30	31	32	33	34	35	36	37	38	39	40	41	42	43	44	45	46	47	48	49	50
Height (inches)	Body weight (pounds)
58	91	96	100	105	110	115	119	124	129	134	138	143	148	153	158	162	167	172	177	181	186	191	196	201	205	210	215	220	224	229	234	239
59	94	99	104	109	114	119	124	128	133	138	143	148	153	158	163	168	173	178	183	188	193	198	203	208	212	217	222	227	232	237	242	247
60	97	102	107	112	118	123	128	133	138	143	148	153	158	163	168	174	179	184	189	194	199	204	209	215	220	225	230	235	240	245	250	255
61	100	106	111	116	122	127	132	137	143	148	153	158	164	169	174	180	185	190	195	201	206	211	217	222	227	232	238	243	248	254	259	264
62	104	109	115	120	126	131	136	142	147	153	158	164	169	175	180	186	191	196	202	207	213	218	224	229	235	240	246	251	256	262	267	273
63	107	113	118	124	130	135	141	146	152	158	163	169	175	180	186	191	197	203	208	214	220	225	231	237	242	248	254	259	265	270	278	282
64	110	116	122	128	134	140	145	151	157	163	169	174	180	186	192	197	204	209	215	221	227	232	238	244	250	256	262	267	273	279	285	291
65	114	120	126	132	138	144	150	156	162	168	174	180	186	192	198	204	210	216	222	228	234	240	246	252	258	264	270	276	282	288	294	300
66	118	124	130	136	142	148	155	161	167	173	179	186	192	198	204	210	216	223	229	235	241	247	253	260	266	272	278	284	291	297	303	309
67	121	127	134	140	146	153	159	166	172	178	185	191	198	204	211	217	223	230	236	242	249	255	261	268	274	280	287	293	299	306	312	319
68	125	131	138	144	151	158	164	171	177	184	190	197	203	210	216	223	230	236	243	249	256	262	269	276	282	289	295	302	308	315	322	328
69	128	135	142	149	155	162	169	176	182	189	196	203	209	216	223	230	236	243	250	257	263	270	277	284	291	297	304	311	318	324	331	338
70	132	139	146	153	160	167	174	181	188	195	202	209	216	222	229	236	243	250	257	264	271	278	285	292	299	306	313	320	327	334	341	348
71	136	143	150	157	165	172	179	186	193	200	208	215	222	229	236	243	250	257	265	272	279	286	293	301	308	315	322	329	338	343	351	358
72	140	147	154	162	169	177	184	191	199	206	213	221	228	235	242	250	258	265	272	279	287	294	302	309	316	324	331	338	346	353	361	368
73	144	151	159	166	174	182	189	197	204	212	219	227	235	242	250	257	265	272	280	288	295	302	310	318	325	333	340	348	355	363	371	378
74	148	155	163	171	179	186	194	202	210	218	225	233	241	249	256	264	272	280	287	295	303	311	319	326	334	342	350	358	365	373	381	389
75	152	160	168	176	184	192	200	208	216	224	232	240	248	256	264	272	279	287	295	303	311	319	327	335	343	351	359	367	375	383	391	399
76	156	164	172	180	189	197	205	213	221	230	238	246	254	263	271	279	287	295	304	312	320	328	336	344	353	361	369	377	385	394	402	410
Instructions:
Find the appropriate height in the left-hand column. Move across to a given weight. The number at the top of the column is the BMI at that height and weight. Pounds have been rounded off.
Calculating BMI
BMI can be calculated as follows:
If pounds and inches are used:

[edit] Epidemiology

The prevalence of overweight and obesity is increasing worldwide in adults and children at a rapid rate. The World Health Organization (WHO) is investigating the scope of the problem, which occurs in developed, as well as developing, countries.

When obesity is defined as a BMI greater than or equal to 30 (see Table 58-1), 19.9% of men and 24.9% of women are obese compared with 10.4% of men and 15.1% of women in 1960. The prevalence of overweight, which is defined as a BMI of 25 to 29.9, has increased only slightly over the same period of time (Fig. 58-1). In the United States, obesity affects minority populations more than whites. Women but not men of low socioeconomic status are more likely to be obese. Obesity is less common in the elderly, possibly because of greater mortality associated with a higher BMI or because of a decrease in BMI after age 60.

Figure 58-1 Age-adjusted prevalence of overweight (BMI 25-29.9) and obesity (BMI >30). CDC/NCHS, United States, 1960-1994 (ages 20 to 74 years). (From Obes Res 6(S2)51S-210S, 1998.)

The direct health care cost of treating the proportion of diseases (such as diabetes, hypertension, and cardiovascular disease) directly attributable to obesity was estimated at $51.6 billion, representing 5.7% of the national health care expenditure in 1995. The indirect cost of obesity, which includes lost productivity as a result of these comorbidities and other associated disabilities, is $47.6 billion; this iscomparable with the economic losses due to cigarette smoking.^[6][1]

[edit] Pathophysiology

Like essential hypertension, obesity results from a genetic predisposition combined with environmental factors. Both are necessary for obesity to occur, but the genetic predisposition seems to be quite common based on the high prevalence of the disorder. The increasing prevalence of obesity around the world is likely the result of a changing environment, which now requires less physical activity and favors overconsumption of food.^[6][3][1]

Enormous strides have been made in our understanding of the weight regulating mechanisms of the body over the past few years. The discovery of the ob gene in 1994 and its product, leptin, a 146-amino acid protein hormone produced primarily by adipose tissue, galvanized the field of obesity research by providing concrete evidence that the body contains a classic negative feedback system that regulates body weight^[7][4][5] (Fig. 58-2). Mice with a homozygous mutation of the ob gene develop massive obesity as a result of increased food intake and decreased metabolic rate leading to diabetes. The syndrome, which includes impaired reproduction, is rapidly reversed by administration of recombinant leptin. While several extremely obese children around the world have been found to have similar mutations (and are now losing weight on leptin replacement therapy), defects in leptin and its production appear to be a rare cause of obesity. While not as rare, defects of the leptin receptor and other single gene defects of receptors and other components of the weight-regulating mechanism have not proved to be common causes of obesity thus far.

Figure 58-2 Model of the weight control feedback system. The weight regulating mechanism appears to resemble a highly integrated and redundant homeostatic mechanism for defending body weight. (Adapted from Campfield LA et al: Science 280:1383-1387, 1998; Porte D et al: Diabetologia 41:863-881, 1998.)

Obesity seems to result from minor gains in energy, which lead to gradual weight gain over a long period of time. External factors leading to the increase in obesity are the ready availability of inexpensive, high-fat, calorie-dense, good-tasting food, and a reduction in the need to exercise combined with a weight-regulating mechanism designed to prevent weight loss more forcefully than weight gain. Once weight is gained, physiologic mechanisms that developed over time to prevent starvation defend the new, higher body weight. The result is a “ratcheting up” of body weight—it can be gained easily but not easily lost. The body must “allow” this weight gain to occur; short-term experiments in which volunteers are overfed the same number of calories demonstrate wide variability in the amount of weight gained. This process appears to be controlled by the energy expended by muscle. However, the weight gained during these experiments is invariably lost soon after the experiment ends, in marked contrast to what the average obese patient experiences; this indicates that those who gain weight have some inherent tendency to do so. Box 58-1 contains eight key points about the energy balance system.

[edit] Regional Distribution of Fat.

The regional distribution of fat plays an important role in determining the risk of a given level of obesity.^[6][8][1] Abdominal or “apple-shaped” obesity is more common in men and is associated with a greater risk of most of the complications of obesity. An accumulation of excess intraabdominal or visceral fat is believed to account for most of the increased risk. Intraabdominal adipose tissue is more cellular, has greater blood flow, has more cortisol and testosterone receptors, and has greater lipolysis in response to catecholamines when compared with subcutaneous adipose tissue. Most importantly, intraabdominal adipose tissue is in the portal circulation; as a result, the liver is exposed to more free fatty acids, which may contribute to insulin resistance and other manifestations of “the metabolic syndrome.” Metabolic abnormalities associated with abdominal obesity include insulin resistance, hyperinsulinemia, glucose intolerance, adult-onset diabetes mellitus, hypertension, high very low-density lipoprotein (VLDL), high low-density lipoprotein (LDL), with an increase in small dense LDL particles reflected in an increased level of Apo B, low high-density lipoprotein (HDL), high fibrinogen, arthritis, menstrual irregularities, and gallbladder disease (Box 58-2).

Premenopausal women tend to accumulate more fat in the gluteofemoral region. This “pear-shaped” distribution may explain why women are at proportionately less risk than men of the same degree of obesity. While the tendency to develop abdominal obesity is genetically determined, as with total body weight, external factors play a role. For example, women who develop abdominal obesity are more likely to smoke cigarettes and use alcoholic beverages, have socioeconomic disadvantages, psychosomatic diseases, and more psychiatric and psychologic problems than women with a gluteofemoral predominance. They may be anovulatory and hyperandrogenic, with increased cortisol and insulin secretion.

[edit] Assessment of Fat Distribution.

The most precise methods of measuring fat distribution are computed tomography (CT) scanning and magnetic resonance imaging (MRI), but these are too expensive and cumbersome for routine use. Waist measurement is useful in estimating abdominal adiposity, although it obviously cannot distinguish visceral adipose tissue from overlying subcutaneous adiposity. However, measurement of waist circumference has become the accepted form of risk assessment for the regional distribution of obesity (Box 58-3 and Table 58-2).

Table 58-2 Classification of Overweight and Obesity by BMI and Waist Circumference and the Associated Disease Risk

✢Disease risk for type 2 diabetes mellitus, hypertension, and cardiovascular disease.

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

[edit] Complications

[edit] Diabetes Mellitus.

The positive relationship between obesity and type 2, or noninsulin–dependent, diabetes mellitus has been demonstrated in many studies. The duration and magnitude of increased body weight, predominance of abdominal distribution of fat, and further weight gain all increase the risk of developing type 2 diabetes. The risk begins at a BMI of about 22 and rises strikingly, about 25% for each BMI unit. For example, in the Nurses Health Study, the age-adjusted relative risk of developing diabetes in women with a BMI greater than 35 was 60 times that of the lowest risk group. In addition, a history of childhood obesity, steady weight gain as an adult, abdominal fat distribution, lack of physical activity, and poor diet are important risk factors. In some ethnic groups, abdominal fat distribution is an even greater risk factor for diabetes than BMI. Such patients may be at risk from excess accumulation of visceral fat even though their BMI is in the normal range. Weight reduction of 10% to 20% is associated with marked improvement in glucose and insulin sensitivity in obese, diabetic patients even before much weight is lost. Individuals who have been diabetic for longer and have lower insulin levels do not fare as well.

[edit] Hypertension.

Obesity is a well-established risk factor for developing hypertension. The prevalence of hypertension is at least 2 to 3 times greater in the overweight and obese population. The risk of developing hypertension is greater in younger individuals and increases with duration of obesity, particularly in women. The increase in sodium retention, blood volume, cardiac output, and systemic vascular resistance seen in the obese is believed to underlie the relationship. Blood pressure is reduced by weight reduction, probably because of a reduction in sympathetic nervous system activity and suppression of the renin-angiotensin system. About one-half of hypertension in whites and one-quarter of hypertension in blacks is weight-related.

[edit] Cardiovascular Disease and Lipid Disorders.

Obesity is an independent risk factor for cardiovascular disease, including coronary heart disease (CHD), stroke, and peripheral vascular disease. Increased body weight and abdominal obesity predispose individuals to cardiovascular risk factors, including elevated levels of total cholesterol, LDL cholesterol, triglycerides, apo-B (a marker for small dense LDL), insulin, plasminogen activator-1 (PAI-1), and a reduction in HDL cholesterol. Not uncommonly, obese individuals develop multiple cardiovascular risk factors. The cluster of hypercholesterolemia, hypertriglyceridemia, hyperuricemia, impaired glucose tolerance, diabetes, and hypertension in various combinations is known as “the metabolic syndrome” or “syndrome X.” The clustering of these disorders is related to hyperinsulinemia and insulin resistance, a result of visceral fat. Data from the Framingham Study placed obesity as the third most important risk factor for CHD in men after age and dyslipidemia. Risk is greater in younger age groups and in those with abdominal obesity. Weight gain as an adult further increases CHD risk.

[edit] Sleep Apnea.

The clinician should be alert to the possible presence of obstructive sleep apnea, which is a disorder that is often overlooked in obese patients. Proper diagnosis of this disorder is important because sleep apnea places the patient at even higher risk of cardiovascular morbidity and it improves with specific treatment. Evaluation of the patient for sleep apnea is contained in the section on medical history.

[edit] Gastrointestinal Disorders.

The prevalence of symptomatic gallstones increases sharply above a BMI of 30; for example, women with a BMI of 35 are at 4 times the risk of women with a BMI less than 24. An increased production of cholesterol by the liver with increasing body weight is a contributing cause. During weight loss, the risk of cholelithiasis increases because of an increase in cholesterol flux. A slower rate of weight loss, as well as the use of ursodiol, minimizes the possibility of stone formation. Finally, hepatic steatosis, fatty liver in nonalcoholic and nondiabetic patients, and gastroesophageal reflux are increased in the overweight and obese and respond well to weight reduction.

[edit] Osteoarthritis.

While the role of overweight and obesity in the more rapid deterioration of weight-bearing joints, such as the knees, ankles, and hips, is clearly mechanical, there is a small increase in osteoarthritis in nonweight-bearing joints as well.

[edit] Cancer.

Cancer of the prostate, colon, and rectum is more common in men who are overweight, while women are at risk for cancers associated with elevated levels of estrogen, including endometrial, breast, cervical, and ovarian cancer, as well as cancer of the gallbladder.

[edit] Gynecologic Disorders.

Irregular menstrual periods, menometrorrhagia, and reduced fertility are associated with increased body weight.

[edit] Patient Evaluation

A history, physical examination, and laboratory evaluation should be performed on an obese patient starting a weight loss regimen. The medical history and physical examination should focus on causes and complications of obesity to assess the risk of obesity in each case, guide treatment, and assist with prognosis. BMI should be calculated and waist circumference measured to assess risk, as well as to offer a measure of outcome in addition to weight loss (Box 58-4).

[edit] History.

The history is important for evaluating risk and deciding on treatment. Family history is important because of the strong heritability of obesity. Questions should address age of onset of obesity, minimum weight as an adult, events associated with weight gain, recent weight loss attempts, and previous weight loss modalities used successfully and unsuccessfully, and their complications. Loss of weight to below adult minimum weight is unusual, for example, and an earlier age of onset of obesity often but not always predicts a less successful outcome. A treatment modality that was previously unsuccessful or during which the patient experienced complications should generally be avoided. A history of eating disorders, bingeing, and purging by vomiting or laxative abuse are relative contraindications to treatment, and referral to a specialist in these areas is indicated. Alcohol and substance abuse require specific treatment that should take precedence over obesity treatment. Cigarette smoking can complicate treatment history, since weight is often gained when the patient stops smoking. While smoking cessation should be urged, implementing a diet and exercise program upon or before stopping can minimize weight gain.

The patient's current level of physical activity is important to determine the starting point for exercise recommendations. Some individuals may be completely sedentary, while others are vigorously active, and the same recommendation to both would be inappropriate. Similarly, the patient's understanding of nutrition will determine whether a basic or a more sophisticated level of nutrition education should be taught. This evaluation is crucial toward helping the patient get the most out of each session. Material that is too advanced won't be retained, and material that is too basic will be boring.

Although the causes of obesity are not fully known, certain factors clearly play a role. Diseases such as polycystic ovarian disease and hypothyroidism are known causes of weight gain and require specific treatment (even though that treatment alone may not result in weight loss). Patients may also exhibit substantial weight gain in the year before developing type 2 diabetes mellitus.

The clinician should search for complications of obesity, such as hypertension, type 2 diabetes, hyperlipidemia, CHD, osteoarthritis of the lower extremities, gallbladder disease, gout, and certain cancers. As previously mentioned, obesity in men is associated with colorectal and prostate cancer; in women, it is associated with endometrial, gallbladder, cervical, ovarian, and breast cancer. Signs and symptoms of these disorders, such as vaginal or rectal bleeding, may have been overlooked by the patient and should be carefully reviewed by the physician.

The clinician should also be alert to the possible presence of obstructive sleep apnea, which is a disorder that is often overlooked in obese patients. Symptoms and signs include very loud snoring or cessation of breathing during sleep that is often followed by a loud clearing breath then brief awakening. The patient may be a restless sleeper; some persons find that they can only sleep comfortably in the sitting position. The patient's partner may best describe these symptoms. Daytime fatigue, with episodes of sleepiness at inappropriate times, and morning headaches also occur. On examination, hypertension, narrowing of the upper airway, scleral infection, and leg edema, secondary to pulmonary hypertension, may be observed. Laboratory studies may show polycythemia. If signs of sleep apnea are present, referral to a pulmonologist or sleep specialist is appropriate.

The use of medications that may cause weight gain (Box 58-5) is important. In some cases, it may be possible to change medications in favor of those that do not cause weight gain. The use of medications that may interact with planned treatment, such as monoamine oxidase (MAO) inhibitors and other antidepressants should be elicited. In addition, some patients take over-the-counter (OTC) weight control products and cold remedies that the clinician must be aware of because of side effects and possible interactions with medications that may be prescribed. Examples include pseudoephedrine and phenylpropanolamine, which may be found in cold remedies and diet products, and ephedra (ma huang), which is a nonspecific β-agonist found in diet products. Both are contraindicated if prescribing a sympathomimetic appetite suppressant.

[edit] Physical Examination.

The clinical manifestations of the complications of obesity are the major targets of the physical examination. Height and weight should be measured and the BMI calculated. Waist circumference should be assessed with a tape measure (see Box 58-3). Blood pressure should be checked with an appropriately-sized cuff. Examine the thyroid and look for manifestations of hypothyroidism (although important to find because it requires specific treatment, thyroid hormone supplementation does not result in weight loss in most patients). In addition, acanthosis nigricans, which suggests hyperinsulinemia, leg edema, cellulitis, and intertriginous rashes with signs of skin breakdown are often seen in the very obese.

Recall the other disorders associated with obesity and look for their signs and symptoms: type 2 diabetes, hyperlipidemia, CHD, osteoarthritis of the lower extremities, gallbladder disease, gout, and colorectal and prostate cancer in men and endometrial, gallbladder, cervical, ovarian, and breast cancer in women.

[edit] Laboratory Tests.

Laboratory evaluations should focus on risk assessment and the discovery of the causes and complications of obesity, such as type 2 diabetes, gout, hyperlipidemia, and hepatic steatosis. Other laboratory tests may indicate disorders, such as hypothyroidism and hyperinsulinemia, that may be involved in the induction of obesity and require specific treatment. Complete evaluation might include laboratory tests for glucose, uric acid, BUN, creatinine, uric acid, ALT, AST, total and direct bilirubin, alkaline phosphatase, total cholesterol, HDL, LDL, triglycerides, complete blood count, TSH, and urinalysis. In some cases, a 2-hour postprandial insulin level is valuable in diagnosing hyperinsulinemia. At present, serum leptin levels and genetic studies are research tools. Measurements of body composition, using bioelectrical impedance, while motivating to some patients, are not necessary for treating the average patient.

[edit] WEIGHT MANAGEMENT

[edit] Patient Selection

While healthy eating and the performance of behaviors that prevent weight gain should be encouraged in every patient, the primary target for treatment should be those individuals at risk because of their excess weight. This includes overweight and obese patients with a BMI greater than 25, particularly in the presence of comorbidities. Table 58-3 outlines a guide to selecting the appropriate treatment based on BMI.

Table 58-3 Guide to Selecting Treatment

[edit] Contraindications to Treatment

In general, obesity treatment is contraindicated during pregnancy, in patients with anorexia nervosa, or in patients in the terminal stage of an illness. Medical or psychiatric illnesses should be stable before weight reduction is initiated. Patients with cholelithiasis and osteoporosis must be warned that these conditions may be aggravated by weight loss. Weight loss during lactation is possible, provided milk production is well-established, and less aggressive treatment, such as a mildly hypocaloric diet, is utilized and monitored by a dietitian.

[edit] Assessing the Patient's Readiness to Lose Weight

The physician should assess the patient's readiness to lose weight before attempting to treat obesity, because an unwilling patient rarely if ever succeeds, which frustrates both the patient and the practitioner. If the patient does not wish to lose and is not at high risk, weight maintenance should be encouraged. If the patient is at high risk, the clinician should make an effort to motivate the patient by discussing the medical consequences related to the patient's case.

[edit] Goals of Obesity Treatment

Given the current state of knowledge and technology, the goal of obesity treatment should be the lowest weight the patient can comfortably maintain, which in the average patient is about 5% to 10% of total body weight or 2 BMI units. Attaining “ideal” body weight or a loss of 20% or 30% or more of total body weight is not possible for the vast majority of overweight individuals. Loss of as little as 5% to 10% of body weight can improve risk factors associated with obesity.^[9][6] Unfortunately, most patients are disappointed with not achieving their personal goal, or “dream” weight, which may contribute to the poor long-term results of obesity treatment.

To prevent disappointment, the patient should be counseled that his or her body might not allow the magnitude of weight loss sought and that cosmetic goals should be discouraged. Alternative goals may include improvement in comorbidities, mobility, and feelings of well-being, a reduction in waist circumference, and simple adherence to a diet and exercise regimen. Remind the patient that research indicates that overweight men who exercise ½-hour per day have a lower risk of dying than thin ones who are completely sedentary. These alternative goals are achievable, while a cosmetic ideal is often not achieved.

Prevention of weight gain is another important treatment goal that is often minimized, but which may have an enormous positive impact on health. Many obese patients come for treatment as a result of recent weight gain. The fact that they have gained weight puts them at risk for further weight gain, and prevention must be stressed.

[edit] TREATMENT

[edit] Calorie-Restricted Diets

To induce weight loss, a calorie deficit must be created. Dieting, or a change in eating habits that results in a reduction of body weight, is the most widely used approach and is appropriate as a first-line treatment in patients seeking an appropriate BMI.^[6][8] Caloric restriction may be achieved in one of two ways. First, general guidelines for healthy eating, such as a reduction in fat, sugar, and alcohol intake, may be emphasized without calorie guidelines. This method is recommended in patients with a BMI < 25 but may also be utilized in patients with a greater BMI. Second, intentional caloric restriction with a food or formula diet may be tried. Compliance is enhanced by structure, which may include attendance at an organized program, a daily meal plan, a regular exercise regimen, and record-keeping. Results at 6 months to 1 year show 2% to 7% mean body weight loss over this period, depending on the intensity of the program. Most weight is lost over the first 4 months with a plateau of weight loss thereafter.^[6][10]

Many primary care providers feel uncomfortable prescribing a diet because of lack of formal training and time constraints. Dietitians in the community or hospital setting can provide customized diet and support that can help the patient to succeed. Balanced diets should contain a minimum of 1000 to 1200 kcal/day and have adequate amounts of all essential nutrients. Support for the clinician treating obesity in the office, including sample diets and other patient education material, may be found in the NIH publications, Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults—The Evidence Report,^[6] the Practical Guide to the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (preprint),^[8] or on the NIH website at www.nhlbi.nih.gov/nhlbi/cardio/obes/prof/guidelns/ob_home.htm.

Sweet, fatty foods, such as ice cream, cakes, and chocolate, are highly palatable and calorie dense. Consumption of foods such as these can increase body weight over time in susceptible individuals and can be difficult to fit into a weight loss program. Calories consumed as fat are easier to overeat because they are “denser” (9 cal/gm vs. 4 cal/gm for protein and carbohydrate), easily hidden in foods, and increase food palatability. When compared with carbohydrate, fat may have a delayed effect on satiety that makes it more likely to be overeaten. Despite an apparent decrease in fat intake over the past decade, the weight of Americans continues to rise. Among other possibilities, it seems clear that total calorie intake rather than fat content alone is of primary importance and that eating too many calories of low-fat foods may prevent weight loss or lead to weight gain.

[edit] Behavioral Therapy

Behavioral techniques are not used alone but in conjunction with all other approaches, including diet and exercise, medication, or surgery.^[11][6][8] The goal of behavior therapy is to overcome barriers to compliance with a diet and physical activity regimen. Behavior therapy assumes that patterns of eating and physical activity are learned behaviors and can be modified and that the environment must be changed to change these patterns over the long term. In some cases, behavioral therapy is administered on an individual basis and in other cases as group sessions. Professionals with training in psychology or a related area who can engage a group in a cohesive manner are optimal for leading such groups. Many commercial weight loss programs and self-help groups use lay leaders or successful patients; in some cases, these individuals are not prepared for the complexity of dealing with the problems that arise. More than 100 controlled trials have been published demonstrating the effectiveness of behavioral techniques, which have become more sophisticated over time.

Although dozens of behavioral techniques are used as part of the behavioral treatment of obesity, the following have been shown to enhance compliance with a program of diet and exercise.

Self-monitoring is a component of all behavioral interventions. It involves recording behaviors, including time and place of eating, associated thoughts and feelings, feeling of control, and who else was present; food consumed, including portion sizes and calorie content; and exercise, including length of sessions and intensity. By reviewing this diary with a member of the treatment team, the patient can get specific feedback about situations that are high risk and interventions that may help. In many cases a simple food and exercise diary is effective.

Stimulus control helps the patient to identify and change cues that are associated with eating too much and exercising too little. For example, limiting exposure to food by keeping it out of sight and avoiding food handling, preparation, or purchase, particularly of problem foods, may be helpful in some individuals. Eating may be limited to specific times and places separated from other activities such as reading or watching television. Efforts are made to break routine eating, which results from a long-term and ingrained “automatic” chain of behavior.

Stress management helps the patient to cope with stressful events by developing better problem-solving skills and having outlets other than eating, like meditation, for reducing stress. Problem solving (identifying problem areas and generating solutions) is important for evaluating setbacks, determining how to do better next time, and breaking the chain of negative thinking (“I blew my diet with that donut, I may as well eat the whole box”) and self-punishment.

Reinforcement is used to enhance the perceived benefit of positive behaviors, such as dietary compliance and exercise, often in the face of physical discomfort experienced as part of that compliance. Reinforcement can come from the therapist, friends and family as part of social support, or the patient alone may utilize getting nonfood rewards for reaching goals.

Cognitive change addresses potentially self-defeating negative thoughts, beliefs, and attitudes to increase the chances of success.

Relapse prevention skills recognize that obesity is a chronic disease requiring chronic treatment and are aimed at teaching patients coping skills so that when lapses occur (an almost predictable sequence of events leading to “collapse”), the patient's willful discontinuation of efforts at weight control can be averted.

Crisis intervention, a more intensive, structured program than is usually utilized in weight maintenance might be indicated at such a point.

A summary of recent studies^[10] combining behavioral treatment with moderate dietary restriction and exercise as part of a comprehensive program showed 8.5 kg average weight loss from an initial average weight of 91.9 kg over 21 weeks of treatment with a 22% rate of attrition. A 5.6 kg loss was maintained after 1 year of follow-up. Behavior therapy, a structured diet, nutrition education, and increased physical activity constitute the first-line approach for the vast majority of patients, and perhaps the only approach suggested for those with a BMI less than 30 who have no comorbid conditions. Longer periods of treatment yield better results, and continued intermittent treatment is appropriate.

[edit] Exercise

Physical activity plays an important role in increasing energy expenditure and is a key component of any weight maintenance program.^[12][8] Weight loss is accompanied by a striking reduction in total energy expenditure, seemingly as part of the body's effort to halt weight loss and facilitate the regain of lost weight. Recent evidence suggests that variations in energy expenditure during daily activities aside from exercise (Non-Exercise Activity Thermogenesis [NEAT]) determines how much weight is gained during a prolonged period of experimental overeating in humans. This result may be due to an increase in “fidgeting” or an intrinsic property of muscle. Clinical studies, however, suggest that the effect of exercise appears to be greater on preventing weight regain than it is in facilitating weight loss. In effect, it is possible that exercise prevents a compensatory mechanism that reduces energy expenditure with weight loss from functioning as effectively.

Cardiovascular training, or aerobic activity, is most often utilized for weight management because of the large number of calories expended during its performance and because fat is burned once a certain threshold is reached. Anaerobic strength training, or resistance exercise such as circuit weight training, is now being recommended as well because it builds lean body mass and may induce changes in body composition that favor a lower body fat mass. Most importantly, the overweight patient can achieve health benefits from regular exercise even if he or she remains overweight, mainly by improving cardiovascular risk factors. Regular adherence to an exercise program may also promote dietary compliance or be a marker of better dietary compliance and improve quality of life by enhancing self-esteem, reducing stress, and relieving depression.

Any physical activity that the patient enjoys and is willing to perform is recommended. For the completely sedentary patient, walking is often the best way to get started. Patients with physical limitations secondary to arthritis or size may start with water exercises, bedside stretching, seated activities, or a program designed by an exercise physiologist or physical therapist. In general, 30 to 45 minutes of exercise 3 to 5 days per week is recommended, although more is better and greater intensity may be better. No maximum has been suggested, but generally up to 1 hour daily, with 1 day off is reasonable. Three 10-minute periods of activity yield about the same benefit as a single 30-minute period, and compliance with such a program is better. Increasing physical activity during daily life, such as climbing stairs instead of taking an elevator; walking or cycling rather than taking a car; and parking further away from the entrance to the mall, can be simple ways to add small periods of physical activity to a busy lifestyle.

[edit] Formula Diets

Liquid formula diets of 800 calories given as 4 or 5 (or more) “shakes” per day are also known as supplemented fasts. At present, there is no evidence that using less than 800 calories per day is of any benefit, and the use of such a diet is not recommended. Starvation diets or “water fasting” is not recommended because of the excessive loss of lean body mass and the risk of cardiac arrhythmias. Examples of liquid formula diets include Optifast, HMR, and Medifast.

These diets are only appropriate for well-informed patients with a BMI greater than 30 who have not been successful with other methods. They are contraindicated during pregnancy and breastfeeding and in patients with bulimia and anorexia nervosa and relatively contraindicated in patients with type 1 diabetes, renal or liver disease, unstable angina, and malignant dysrhythmias and in patients with systemic infections and protein-wasting disorders that include use of corticosteroids. Formula diets provide superior weight loss (1.5 to 2.5 kg/week) and rapidly reduce the severity of a number of complications of obesity, including diabetes, hypertension, hyperlipidemia, and sleep apnea. Under careful medical supervision, a 90-day formula diet has been shown to be safe in patients with more than 50 lbs to lose. Common side effects include fatigue, weakness, dizziness, constipation or diarrhea, dry skin, irregular menses, brittle nails, and nausea. Electrolyte abnormalities are rare with modern, properly-used formula diets, but hyperuricemia and gout, which respond to liberalization of calories and carbohydrate, can occur. Gallstones develop in about 11% of patients and 25% become symptomatic, although patients on traditional diets have also been noted to develop gallstones. The use of ursodiol can prevent gallstone formation. Cardiac risk, initially a concern in the late 1970s, has been shown to be as low as expected in similarly obese individuals not dieting.

These diets must be combined with support and behavior, nutrition, and exercise education.^[11][6][10] If used alone, rapid weight regain is almost certain, even if the diet is “medically supervised.” Even if a comprehensive program is used, long-term follow-up shows no difference when compared with a balanced diet. In the short-term, however, since compliance is higher and if losing weight is medically important, formula diets can be considered.

[edit] Fad Diets

Fad diets and other diet methods often promise a quick, easy way to lose weight. Unfortunately, these methods distract the patient from the real task at hand. While many methods of unhealthy dieting can reduce weight in the short run, the true test comes in long-term weight loss. Diets that are too drastic are difficult to follow long-term: unfortunately, the patient too often bears the blame for the lack of success, adding to a vicious cycle of failure.

[edit] Medication

The concept of using medication for the treatment of obesity has undergone radical changes over the past few years.^[13][14] The new understanding of obesity makes it appear as much a metabolic, endocrine disorder as diabetes; therefore obesity also deserves a medical treatment when indicated. The side effect profile of early amphetamine-based appetite suppressants was severe, and their use led to addiction and habituation because escalating doses were often needed to maintain lost weight. As a result, medications were used in the short-term to induce weight loss and were then discontinued, leaving the patient to maintain the weight loss. When patients inevitably regained weight, they were blamed for not having enough motivation. Later appetite suppressants, such as phentermine, diethylpropion, and phendimetrazine, had fewer side effects but had limited impact since only short-term studies were performed in which weight loss, rather than improvement in comorbidity, was usually the only outcome measured. As a result, most states limited prescriptions to a maximum of 3 months.

In 1992, the publication of a small 4 year-long trial of phentermine and fenfluramine by Weintraub popularized the notion of chronic treatment. Dexfenfluramine was approved for long-term use in 1996 after 10 years of use around the world. However, concerns about unacceptable side effects, primarily regurgitant valvular lesions of the heart and pulmonary hypertension, led to the withdrawal of fenfluramine and dexfenfluramine in September 1997. In November 1997, the FDA approved sibutramine for long-term use in obesity, and in April 1999, orlistat was approved for long-term use.

In general, medication helps patients to comply with a reduced calorie regimen (Table 58-4). Not every patient responds to a given medicine. If a patient loses more than 4 pounds during the first month, the prognosis for losing more than 5% of body weight is good. If not, consideration should be given to changing medication after another month of treatment.

Table 58-4 Weight Loss Drugs

✢Short-term use is 3 months or less.

[edit] Drugs Approved for Long-term Use.

Sibutramine (Meridia), a norepinephrine and serotonin reuptake inhibitor (SNRI), was originally developed as an antidepressant but was more effective at reducing weight.^[14] Although a schedule IV compound, sibutramine demonstrated little or no evidence for abuse or habituation like the other drugs in the SNRI category. A 1-year placebo-controlled trial demonstrated that 65% of patients who received 15 mg sibutramine daily lost more than 5% of body weight compared with only 29% of patients taking placebo; and 39% lost more than 10% of their body weight compared with 8% reaching the same mean weight loss in the placebo-treated group. Health benefits demonstrated with the use of sibutramine include reductions in triglycerides, uric acid, total cholesterol, and LDL cholesterol and an increase in HDL cholesterol. Adverse events seen during randomized trials included dry mouth, constipation, insomnia, increased appetite, dizziness, and nausea. A mean increase in blood pressure of 4 mm Hg was also seen in trials. The increase is less in patients who lose more than 5% of body weight and who would be most likely to continue treatment. About 12% of patients have an increase in systolic blood pressure of 15 mm Hg or more; however, less than 1% of patients treated had to be withdrawn from trials as a result of an increase in blood pressure. Blood pressure and pulse should be checked 2 to 4 weeks after starting the drug and then monthly for the first 6 months, then every 2 months or more often if indicated. If a patient with hypertension is getting good weight loss, you may consider treating the blood pressure more aggressively for a period to see if it drops with continued weight loss. The majority of patients who lose weight experience a drop in blood pressure.

Orlistat (Xenical), an inhibitor of pancreatic lipases, prevents the absorption of 30% of fat consumed, thus reducing caloric intake.^[15] Analysis of patients completing a 1-year placebo-controlled trial demonstrated that 55% of patients treated with orlistat lost more than 5%, and 25% lost more than 10% of their body weight compared with 33% and 15%, respectively, achieving the same mean weight loss in the placebo-treated group. In addition, orlistat slowed down the rate of weight regain in the second year of treatment. Health benefits demonstrated in clinical trials of orlistat include a reduction in LDL and increase in HDL cholesterol, reduction in blood pressure and fasting insulin levels, improvement in oral glucose tolerance test outcomes, and improved glycemic control in obese diabetics. The gastrointestinal side effects associated with orlistat use were usually mild in intensity and occurred early in treatment. Dropout rates due to side effects have been low in controlled trials. No effect on mineral balance, gallstone, or renal stone formation was seen. A mild reduction in the levels of vitamin D and beta-carotene was noted in some treated patients during trials. Supplementation with a multivitamin taken remotely from a dose of orlistat has been recommended.

[edit] Drugs Approved for Short-term Use.

Noradrenergic agents, such as the schedule IV drugs phentermine (Ionamin, Fastin, Adipex) and diethylpropion (Tenuate), and the over-the-counter (OTC) drug phenylpropanolamine (Dexatrim, Accutrim) have been shown to be better than placebo in short-term studies. No long-term studies of weight loss or health benefit have been performed. As a result, if these drugs are used for longer than 3 months, the patient must be informed that such use is “off-label” and has not been studied.

[edit] Drugs Not Approved for Obesity Treatment.

Selective serotonin reuptake inhibitors (SSRI), such as fluoxetine and sertraline, have not been found to be useful in long-term obesity treatment. Studies suggest that weight regain may occur after 6 months of treatment despite ongoing use of the drugs. These drugs have, however, been shown to be beneficial as an adjunct to the behavioral management of binge eating disorder.

[edit] Over-the-counter Products.

A wide variety of products are available to the public. Some, like chromium picolinate, which is a trace mineral, and chitosan, which is a fiber product, L-carnitine, and hydroxycitric acid, show insufficient efficacy to recommend their use. These products are marketed as “nutritional supplements” with insufficient testing or proof that they work as advertised. Others, like the combination of ephedrine (ephedra, ma huang, herbal “fen/phen”) and caffeine (guarana, kola nut) often seen in “fat burning products,” have been shown to be effective but are not safe for unsupervised use because of the risk of side effects like tachycardia and hypertension and are not approved for treatment of obesity. Phenylpropanolamine, a sympathomimetic also used widely in OTC decongestants, is also available as an OTC appetite suppressant for short-term use only.

[edit] Future Pharmacologic Treatment.

The future of the pharmacologic treatment of obesity is particularly promising, with more than fifty new drugs in the early stages of development.^[16] Human trials of recombinant leptin are currently underway. Like insulin, leptin and its analogs will be administered either subcutaneously or intravenously, thus limiting its use. Preliminary clinical trials have shown only modest weight loss in a subset of patients.

Other drugs under development include compounds that activate central melanocortin receptors, unbind corticotropin-releasing factor from its binding protein, and β-agonists, which act selectively on skeletal muscle or adipose tissue to increase metabolic rate and lipolysis.

[edit] Medical Management of the Obese Diabetic

Drugs that do not cause weight gain should be considered as first-line therapy in the treatment of the obese type 2 diabetic. Metformin (Glucophage), which inhibits intestinal glucose transport, reduces hepatic gluconeogenesis, enhances peripheral glucose uptake by muscle and adipose tissue, and tends to cause weight loss rather the weight gain usually seen with the use of insulin and sulfonylureas. In addition, an increase in HDL, reduction in triglycerides, and even a reduction in blood pressure have been reported. Despite the rare but potentially serious side effect of lactic acidosis, metformin should be considered first-line treatment for overweight type 2 diabetics. Acarbose (Precose), an α-glucosidase inhibitor that slows down the absorption of carbohydrate, is also valuable in minimizing the demand for insulin in an obese type 2 diabetic.

[edit] Surgery

Surgery should be considered in obese patients with a BMI greater than 40 or between 35 and 40 who fail other methods of treatment if serious obesity-related complications are present.^[6][17] Careful screening of candidates is required if the patient is to benefit from the procedure. Surgical candidates must be motivated and well-informed about the risks of the procedure, as well as the change in their lives that will occur as a result of the procedure and its long-term effects. These changes may be relatively minor, such as the need for long-term treatment with vitamin and mineral supplements, or may include chronic vomiting or diarrhea after meals. In general, weight loss of 60% to 80% of the excess is achieved. Weight loss reaches a maximum at 18 months to 2 years, with some weight regain up to the fifth year postoperatively and weight stability thereafter. Unfortunately, in some surgical series up to 20% of patients ultimately regain all lost weight.

The vertical-banded gastroplasty (gastric stapling) is the most commonly performed procedure. A 30 cc pouch with a restricted outlet is constructed along the lesser curvature of the stomach. A Silastic ring or band of Marlex mesh restricts the outlet size, and four rows of staples reinforce the free wall to prevent breakdown. The amount of weight lost is correlated with the volume of the pouch and diameter of the outlet, with larger volume and diameter yielding less weight loss, but fewer side effects. In general, 70% of patients maintain a loss of 20% of total body weight on 5-year follow-up. It is not as effective as the gastric bypass in carbohydrate cravers because of the “soft-calorie syndrome,” in which highly caloric liquid or meltable foods are consumed to excess, leading to weight regain.

The gastric bypass involves constructing a small proximal gastric pouch as with the gastroplasty, whose outlet is a limb of small bowel of varying lengths, as in a Roux-en-Y gastrojejunostomy. Increasing the length of the loop increases weight loss, as well as long-term side effects and nutrient malabsorption. The procedure produces malabsorption of food and the dumping syndrome; it is effective in patients who might not respond to gastroplasty because of carbohydrate craving. Because of the malabsorption of vitamins and minerals, these patients need careful nutritional instruction and follow-up, as well as behavioral training. More weight is lost with this procedure than with gastroplasty, but the risk of complications is greater.

Mortality associated with obesity surgery is about 1% in the hands of surgeons experienced with these procedures and the perioperative management of the severely obese patient. Early morbidity of both procedures that occur in about 10% of cases include perioperative complications such as wound infection, dehiscence, leaks from staple-line breakdown, stomal stenosis, marginal ulcers, deep vein thrombophlebitis, and other pulmonary problems. Longer-term complications, which occur with both procedures, include cholecystitis and failure to lose weight. Complications of the gastroplasty include pouch and distal esophageal dilation with esophageal reflux and persistent vomiting, with or without stomal obstruction. Additional complications that may occur with the bypass include vitamin and mineral deficiencies, including calcium, B-12, folate, and iron, and dumping syndrome, in which meals are followed by gastrointestinal discomfort, diarrhea, and other symptoms.

In women of childbearing age, the effects of the particular nutrient deficiencies noted with gastric bypass are of concern because of the risk of their known association with fetal damage. In general, women who have had either procedure should be on birth control during the weight loss phase because of the uncertainty and the risks of fetal development in the setting of weight loss and maternal undernutrition. Women who have had these procedures and are at a stable weight may become pregnant, but they must be carefully monitored during pregnancy to prevent such deficiencies. The increased calorie, protein, and nutrient demands must be emphasized along with the usual weight gain of pregnancy.

Despite these risks and complications a large, multicenter study comparing surgery with diet alone has been ongoing in Sweden. The Swedish Obese Subjects (SOS) trial enrolled approximately 4000 patients considered appropriate for obesity surgery. Obesity surgery was performed on 2000 and 2000 have been treated with diet alone. After 4 years of follow-up, surgery has produced substantial weight loss and an improvement in all variables monitored, including new cases of diabetes and hypertension, mortality, time lost from work, mood, and disability, in both men and women.

[edit] REFERENCES