Annu. Rev. Clin. Psychol. 2006. 2:35777 doi: 10.1146/annurev.clinpsy.2.022305.095249 Copyright c 2006 by Annual Reviews.

All rights reserved First published online as a Review in Advance on January 16, 2006

OBESITY
Anthony N. Fabricatore and Thomas A. Wadden
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University of Pennsylvania, School of Medicine, Department of Psychiatry, Weight and Eating Disorders Program, Philadelphia, Pennsylvania 19104-3309; email: fabricat@mail.med.upenn.edu; wadden@mail.med.upenn.edu

Key Words

weight loss, overweight, body mass index

Abstract The prevalence of obesity is growing at an alarming rate. Thus, investigation into the etiology, comorbidities, and treatment of obesity has burgeoned in recent years. While novel therapiesboth behavioral and pharmacologicalhave been developed and tested, the mean weight losses achieved with nonsurgical approaches have remained virtually unchanged over the past 20 years. Fortunately, the modest weight losses achieved with these methods are associated with signicant reductions in obesity-related health problems. With the most intensive available treatment (i.e., bariatric surgery), many patients achieve remission of comorbid conditions. This article denes obesity and provides an overview of the disease conditions associated with excess weight. Treatment options and outcomes are reviewed and future stepsincluding efforts to prevent obesityare identied. Finally, the literature on the relationship between obesity and depression is examined. CONTENTS
INTRODUCTION: THE OBESITY EPIDEMIC . . . . . . . . . . . . . . . . . . . . . . . . . . . . Denitions and Comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Health Effects of Weight Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Treatment Options . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . LIFESTYLE MODIFICATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Outcomes of Lifestyle Modication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Improving Weight Maintenance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The National Weight Control Registry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . What Is the Optimal Diet for Long-Term Weight Control? . . . . . . . . . . . . . . . . . . . What Is the Optimal Exercise Regimen for Long-Term Weight Control? . . . . . . . . From Efcacy to Effectiveness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . PHARMACOTHERAPY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Long-term Pharmacotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . BARIATRIC SURGERY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . MOVING TOWARD PREVENTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . OBESITY AND DEPRESSION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Obesity-Depression Relationship in Women Versus Men . . . . . . . . . . . . . . . . Extreme Obesity Increases the Risk of Depression . . . . . . . . . . . . . . . . . . . . . . . . . CONCLUSION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1548-5943/06/0427-0357$20.00 358 358 359 360 361 361 362 363 364 365 366 366 367 367 368 370 371 371 373

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INTRODUCTION: THE OBESITY EPIDEMIC

The World Health Organization (WHO) estimated that a billion adults worldwide are overweight, including 300 million who are obese (WHO 2002). Accordingly, the WHO has described obesity as a global epidemic (WHO 1998). The problem of excess weight is particularly pronounced in the United States, where the prevalence of obesity among adults doubled from 15% in 19761980 to 30.6% in 20012002 (Flegal et al. 2002, Hedley et al. 2004). The number of children and adolescents who are considered overweight (i.e., 95th percentile for age and sex) or at risk for overweight (i.e., 85th percentile) has similarly increased in recent years and suggests that the obesity crisis in the United States will only continue to grow (Ogden et al. 2002).

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Denitions and Comorbidities

The body mass index (BMI) is a ratio of weight to height that is used to estimate obesity. BMI is calculated as weight in kilograms divided by the square of height in meters. (Alternatively, BMI can be gured by multiplying weight in pounds by 703 and dividing that product by the square of height in inches.) Weight classications according to BMI are as follows: underweight, BMI < 18.5 kg/m2 ; average weight, BMI 18.524.9 kg/m2 ; overweight, BMI 25.029.9 kg/m2 ; and obesity, BMI 30 kg/m2 . Obesity is further categorized as Class I (mild, BMI 30.034.9 kg/m2 ), II (moderate, BMI 35.039.9 kg/m2 ), or III (severe/extreme, BMI 40 kg/m2 ). For reference, Table 1 displays the weights that correspond with the BMI ranges described above for individuals of three sample heights. The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health concluded that the risks of heart disease, type 2 diabetes, sleep
TABLE 1 Weights corresponding to body mass index ranges for three sample heights Height Body mass index (kg/m2 ) <18.5 kg/m2 18.524.9 kg/m2 25.029.9 kg/m2 30.034.9 kg/m2 35.039.9 kg/m2 40 kg/m2 162.6 cm (64 in.) <48.9 kg (107.8 lbs) 48.965.9 kg (107.8145.4 lbs) 66.079.2 kg (145.5174.5 lbs) 79.392.3 kg (174.6203.6 lbs) 92.4105.5 kg (203.7232.8 lbs) 105.6 kg (232.9 lbs) 172.7 cm (68 in.) <55.2 kg (121.7 lbs) 55.274.4 kg (121.7164.0 lbs) 74.589.2 kg (164.1196.9 lbs) 89.3104.2 kg (197.0229.8 lbs) 104.3119.1 kg (229.9262.6 lbs) 119.2 kg (262.7 lbs) 182.9 cm (72 in.) <61.9 kg (136.4 lbs) 61.983.4 kg (136.4183.4 lbs) 83.5100.1 kg (184.0220.8 lbs) 100.2116.8 kg (220.9257.6 lbs) 116.9133.5 kg (257.7294.5 lbs) 133.6 kg (294.6 lbs)

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apnea, osteoarthritis, and asthma are strongly and positively associated with BMI (NHLBI 1998). Other studies have suggested that obesity increases the risk of cancer morbidity and mortality (Bergstrom et al. 2001, Calle et al. 2003). Excess weight also is associated with increased all-cause mortality. A study published by researchers at the Centers for Disease Control and Prevention estimated that poor diet and physical activity accounted for 365,000 (15.2% of total) deaths in the United States in 2000 (Mokdad et al. 2005). Although one recent study found that overweight was not associated with excess deaths (Flegal et al. 2005), another large investigation concluded that overweight women and men lived 3.3 and 3.1 fewer years, respectively, than their average-weight counterparts, controlling for the effects of smoking (Peeters et al. 2003). Obesity increased the risk of death and shortened life expectancy (by 5.8 years for women and 7.1 years for men) in those studies (Flegal et al. 2005, Peeters et al. 2003). These data run contrary to the position of some who suggest that the obesity epidemic is a myth fueled by cultural hysteria and moral panic (Campos 2004).

The Health Effects of Weight Loss

The morbidity and mortality gures cited above may be of concern to individuals who are above their recommended body weights. Fortunately, however, intentional weight loss is associated with clinically signicant improvements in health. An evidence-based report published by the NHLBI (1998) found that reductions of as little as 5%10% of initial body weight are associated with benecial reductions in blood pressure, lipids, and other metabolic abnormalities. Findings from the Diabetes Prevention Program (DPP) also support the benets of modest weight loss (DPP Research Group 2002a). In this large, multisite, randomized controlled trial, 3234 overweight and obese adults with impaired glucose tolerance (i.e., were at risk for developing type 2 diabetes) were assigned to one of three conditions: (a) placebo, (b) metformin (800 mg twice per day), or (c) a lifestyle modication program designed to induce a weight loss of 7% of initial body weight and increase physical activity to at least 150 minutes per week. Participants who received lifestyle modication (which is described in detail below) lost approximately 7% of their initial weight after six months and maintained a loss of about 4% three and a half years later. Perhaps the most important nding of the DPP, however, is shown in Figure 1; participation in lifestyle modication reduced the four-year incidence of diabetes by 31% compared with metformin and by 58% compared with placebo. Although these results are impressive, investigators still do not know whether intentional weight loss reduces mortality, as demonstrated by a randomized trial. To address this issue, the Look AHEAD (i.e., Action for Health in Diabetes) study will compare the incidence of fatal and nonfatal myocardial infarction and stroke over an average of 10 years (Look AHEAD Research Group 2003). Participants in this ongoing trial are more than 5000 overweight and obese adults with type 2

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Cumulative Incidence of Diabetes (%)

40 30 20 10 0

Placebo Metformin Lifestyle

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0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 Year

Figure 1 Cumulative incidence of diabetes according to Diabetes Prevention Program (DPP) study group. The diagnosis of diabetes was based on the criteria of the American Diabetes Association. The incidence of diabetes differed signicantly among the three groups ( p < 0.001 for each comparison). Reprinted with permission from DPP Research Group (2002a), copyright c 2002 Massachusetts Medical Society. All rights reserved.

diabetes who receive either an intensive lifestyle modication program or a limited educational program in addition to standard medical care. The ndings of this study will provide a rm basis for setting public policy concerning weight management.

Treatment Options
Broadly, three clinical weight loss options exist for overweight and obese individuals: (a) lifestyle modication (i.e., diet, exercise, and behavior therapy), (b) pharmacotherapy, and (c) bariatric surgery. Which treatment option is appropriate is a function of the patients weight, health status, previous weight loss attempts, and preferences. Table 2 summarizes the treatment algorithm published by NHLBI and the North American Association for the Study of Obesity (NAASO) in the Practical Guide: Identication, Evaluation, and Treatment of Overweight and Obesity in Adults (hereafter, Practical Guide; NHLBI & NAASO 2000). The following sections describe each of these treatments and their associated outcomes.

OBESITY TABLE 2 A guide to selecting treatmenta BMI category (kg/m2 ) Treatment Diet, physical activity, and behavior therapy
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2526.9 With comorbidities

2729.9 With comorbidities

3034.9 +b

3539.9 +

40 +

Pharmacotherapy Surgery

With comorbidities

+ With comorbidities

a Table reprinted from The Practical Guide: Identication, Evaluation, and Treatment of Overweight and Obesity in Adults (NHLBI & NAASO 2000). b

The + represents the use of indicated treatment regardless of comorbidities.

LIFESTYLE MODIFICATION
The Practical Guide recommends a program of diet, exercise, and behavior therapy for all persons with a BMI 30 kg/m2 and those with a BMI 25 kg/m2 with medical comorbidities (NHLBI & NAASO 2000). Such programs are usually offered in academic medical centers and are delivered to groups of 812 persons. Treatment also may be delivered to individuals, but group-based programs produce slightly larger weight losses, regardless of patients preferences for group or individual treatment (Renjilian et al. 2001). Sessions are frequently 6090 minutes in length and are held weekly for approximately six months. The intervention is typically delivered by professionals with expertise in psychology, nutrition, exercise physiology, or health education, who instruct patients in self-monitoring, decreasing energy intake, increasing energy expenditure, and overcoming barriers to treatment adherence (DPP Research Group 2002b, Wadden & Butryn 2003).

Outcomes of Lifestyle Modication

Several reviews have shown that standard lifestyle modication programs yield weight losses of 7%10% of initial body weight with four to six months of treatment (Wadden & Butryn 2003, Wing 2002). Foster and colleagues (1997), however, found that persons entering lifestyle modication would like to lose two to three times this amount. Counseling patients on the average reductions achieved with lifestyle modication does not appear to alter patients great expectations for weight loss (Wadden et al. 2003) and may not even be necessary. Linde and colleagues (2004) reported no adverse psychological consequences of having unrealistically high expectations and suggested that higher goals may even be positively associated with long-term weight loss.

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Clinicians and researchers have attempted to improve the outcomes of lifestyle modication by making a number of alterations to standard programs. Two methods for enhancing weight loss, both of which involve increasing dietary structure, have been identied. First is the use of specic, structured meal plans. Wing and colleagues (1996) found that participants who were given meal plans (i.e., menus, recipes, and grocery lists) to facilitate adherence to a diet of 12001500 calories per day lost signicantly more weight (12 kg) than those who were instructed to consume the same number of calories but were provided with no additional structure (8 kg). Ditschuneit and associates (1999) found that meal replacement products (i.e., portion- and calorie-controlled shakes with an appropriate nutritional balance) are another means of enhancing dietary adherence and, thus, weight loss. Participants in their study were instructed to consume a self-selected low-calorie diet of 12001500 calories per day (i.e., the conventional foods group) or an isocaloric diet in which two meals and two snacks each day were replaced with portioncontrolled, formulated products (i.e., the meal replacement group). Participants in the meal replacement group lost more than ve times as much weight as those in the conventional foods group (7.1 kg and 1.3 kg, respectively) after three months of treatment. A recent meta-analysis conrmed the benets of meal replacement products (Heymseld et al. 2003).

Improving Weight Maintenance

The added structure of using meal plans and meal replacements is likely benecial because it limits food choices and the potential for error in calculating calorie intake. In addition to optimizing weight loss, these strategies also appear to facilitate the maintenance of weight loss. Wing and colleagues (1996) found that participants who were provided with meal plans not only lost more weight at six months than those who were not given meal plans, but also maintained signicantly greater reductions after 12 months of follow-up (6.9 kg and 3.3 kg, respectively). Similarly, the meal replacement study by Ditschuneit et al. (1999), described above, included a second phase in which all participants, regardless of original group assignment, were encouraged to replace one meal and one snack with formulated products each day beginning at month three and continuing for the next four years (Flechtner-Mors et al. 2000). As can be seen in Figure 2, the added structure of meal/snack replacements appeared to induce weight loss in the group originally assigned to conventional foods and to facilitate the maintenance of weight loss in the group that used meal replacements in the rst phase of the study. Randomized controlled trials are now needed to evaluate the long-term benets of meal replacement products used for two or more years. Another means of improving the maintenance of weight loss is to offer extended contact with the treatment provider. As stated above, the mean weight loss achieved with four to six months of lifestyle modication is approximately 7%10% of initial body weight. Without further treatment, however, participants

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Figure 2 Mean ( SEM) percentage change from initial body weight in patients during 51 months of treatment with an energy-restricted diet (1200 to 1500 kcal/day). Patients received either a conventional energy-restricted diet (control group A) or a diet with two meal and snack replacements (group B) for three months. During the remaining four years, all patients received one meal and snack replacement daily. Reprinted with permission from Flechtner-Mors et al. (2000), copyright c 2000 North American Association for the Study of Obesity. All rights reserved.

typically regain about one-third of their lost weight in the following year, and many patients return to their baseline weights over ve years (Wadden & Butryn 2003). A study by Perri and colleagues (1988) revealed that participants who continued to meet with their provider twice a month for a year after completing the initial 20-week treatment maintained a weight loss of 11.4 kg, compared with 3.6 kg among patients who did not receive continued contact. Thus, most lifestyle modication programs now include a maintenance phase of treatment, in which contact continues on a monthly or twice-monthly interval after the initial weightloss phase. Extended contact with a treatment provider likely engenders a feeling of accountability that motivates long-term adherence for persons who have lost weight.

The National Weight Control Registry

Investigators potentially can identify strategies to facilitate weight maintenance by studying individuals who have been successful in this regard. The National

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Weight Control Registry is a database of such individuals, who have achieved and maintained a weight loss of at least 13.6 kg (30 lbs) for at least one year. The average registrant has lost 33 kg and has maintained at least a 13.6 kg reduction for more than ve years (Klem et al. 1997). Participants report that they continue to follow a low-calorie diet, regularly monitor their body weight, and expend approximately 25003300 calories per week in physical activity (Wing & Phelan 2005). Thus, it appears that the strategies necessary for weight maintenance are quite similar to those required for weight loss.
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What Is the Optimal Diet for Long-Term Weight Control?

Lifestyle interventions typically recommend a low-calorie diet in which 55% of calories come from carbohydrate, 25%30% from fat, and the remainder from protein (e.g., Brownell 2000, DPP Research Group 2002b). This macronutrient content is consistent with the recommendations of the NHLBI Practical Guide (NHLBI & NAASO 2000) and with the reported diet of successful weight-maintainers enrolled in the National Weight Control Registry (Klem et al. 1997). The optimal macronutrient content, however, for weight loss and improvements in health is a topic of lively debate. Investigators, for example, have now compared high-protein, low-carbohydrate diets to low-fat diets in at least six randomized controlled trials (Brehm et al. 2003, Foster et al. 2003, Golay et al. 1996, Meckling et al. 2004, Samaha et al. 2003, Stern et al. 2004, Yancy et al. 2004). In both self-help and lifestyle modication programs, the prescription of a high-protein, low-carbohydrate diet induced greater weight losses at three and six months than a low-fat diet (e.g., Brehm et al. 2003, Foster et al. 2003, Samaha et al. 2003). At one year, however, the differences in weight reductions were no longer signicant (Foster et al. 2003, Stern et al. 2004). More studies of longer duration are required to evaluate the long-term safety and efcacy of these diets. A recent randomized controlled trial compared weight losses and health improvements across several popular diets (Dansinger et al. 2005). One hundred sixty overweight or obese adults were assigned to one of four groups. The four diets emphasized calorie restriction (i.e., the Weight Watchers group), carbohydrate restriction (i.e., the Atkins group), fat restriction (i.e., the Ornish group), or macronutrient balance (i.e., the Zone group). All participants, regardless of dietary condition, received four one-hour sessions with a dietitian and physician over the rst two months of the study. All groups achieved and maintained signicant weight losses at two, six, and twelve months. There were, however, no differences between groups at any time. Similarly, there were no between-groups differences in cholesterol (total, high-density lipoprotein, and low-density lipoprotein), triglycerides, blood pressure, glucose, insulin, or C-reactive protein at 12 months. Dansinger and associates (2005) concluded that the magnitude of the weight reductions and health improvements are a function not of the macronutrient composition of the diet, but of the extent to which the diet is followed. For a given

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individual, therefore, it appears that the optimal diet for enduring weight control is the one that he or she can most easily adhere to long-term.

What Is the Optimal Exercise Regimen for Long-Term Weight Control?

Instructions and strategies to increase physical activity are integral components of lifestyle modication. Exercise not only carries cardiovascular and psychological benets (Wood et al. 1991, Poirier & Despres 2001), but also contributes to energy decit and, thus, weight loss. Maintaining a high level of physical activity also appears to be an important factor in long-term weight control, as suggested by data from the National Weight Control Registry. Walking, cycling, strength training, and aerobics are the activities most commonly reported by Registry members (Klem et al. 1997), but the type of exercise is probably less crucial to long-term weight control than the amount of exercise in which a person engages. A study by Jeffery and colleagues (2003) found that lifestyle modication participants who were given an energy expenditure goal of 2500 calories per week maintained signicantly greater weight losses than did their counterparts who were given a standard, yet more modest, goal of expending 1000 calories per week in physical activity (8.5 and 6.1 kg, respectively, at 12 months; 6.7 and 4.1 kg, respectively, at 18 months). As is the case with dietary recommendations, the optimal exercise prescription is likely that which can be maintained long-term. In contrast to dietary adherence, however, it appears that less structure is benecial for facilitating adherence to physical activity recommendations. Persons instructed to exercise at home or in multiple short bouts accumulate more physical activity than do those instructed to exercise in supervised groups or in one long bout, respectively (Jakicic et al. 1995, Perri et al. 1997). Decreasing the structure of physical activity reduces barriers, such as lack of time, that may prevent regular activity. Lifestyle activity represents another means of increasing energy expenditure. Methods of increasing lifestyle activity might include walking (instead of driving) to complete errands, choosing a distant parking spot, or opting for the stairs instead of the escalator or elevator. Programmed activity, on the other hand, is what may be referred to as a workout. It typically requires a discrete period of time (i.e., 3060 minutes) and is completed at a relatively high intensity (i.e., 60%80% of maximal heart rate). Andersen and colleagues (1999) compared the effects of programmed and lifestyle activity among women who were participating in a lifestyle modication program. They found that both types of activity, when combined with a low-calorie diet, produced a weight loss of approximately 8 kg in 16 weeks. Those who were instructed to increase their lifestyle activity regained marginally ( p = 0.06) less weight after one year of treatment than did those who completed programmed exercise (0.1 kg versus 1.6 kg, respectively). Thus, lifestyle activity appears to be just as effective for weight lossand may be even more effective for weight maintenancethan structured, programmed activity.

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From Efcacy to Effectiveness

As noted previously, lifestyle modication programs are frequently provided in academic medical centers. However, there clearly are not enough programs to serve the millions of Americans who are attempting to control their weight. Thus, efforts to disseminate treatment to community centers, worksites, primary care practices, and the Internet are required to meet the growing demand for weight loss therapies, fueled by the ever-increasing prevalence of obesity. Currently, self-help and commercial programs are perhaps the largest providers of lifestyle modication. Although programs such as Weight Watchers, Jenny Craig, L.A. Weight Loss, Overeaters Anonymous, Take Off Pounds Sensibly (TOPS), and eDiets.com are widely available, data on their effectiveness are largely lacking (Womble et al. 2002). The Weight Watchers program, which has been the subject of three published controlled trials, has been the most thoroughly researched of the commercial and self-help weight loss programs (Tsai & Wadden 2005). The largest of those trials found that participants in Weight Watchers lost 4.3 kg and 2.9 kg at one and two years, respectively, compared with losses of 1.3 kg and 0.2 kg among controls who received two 20-minute sessions with a nutritionist and various self-help resources (Heshka et al. 2003). Data from competing commercial programs are not available. Clearly, there is a need for more empirical scrutiny of the most popular weight control programs.

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PHARMACOTHERAPY
The Practical Guide indicates that pharmacotherapy may be an appropriate treatment option for persons with a BMI 30 kg/m2 or 27 kg/m2 in the presence of weight-related comorbidities (NHLBI & NAASO 2000). Seven medications are currently approved by the Food and Drug Administration for the treatment of obesity, but only twosibutramine and orlistatare approved for long-term use (Kaplan 2005, Klein 2004). Sibutramine is a combined serotonin-norepinephrine reuptake inhibitor that appears to help limit food intake by decreasing hunger and increasing satiety (http://www.rxabbott.com/pdf/meridia.pdf). Orlistat, by contrast, acts within the digestive tract: It is a lipase inhibitor that effectively blocks the absorption of approximately one-third of the fat consumed in a meal (http://www.rocheusa.com/pro ducts/xenical/pi.pdf). Because the undigested fat is passed in stools, consuming a high-fat diet (e.g., >20 g of fat per meal or >70 g per day) can lead to undesirable gastrointestinal side effects. Thus, patients are negatively reinforced to eat a diet low in fat. Both drugs induce greater weight losses than placebo (Arterburn et al. 2004, Li et al. 2005). For example, sibutramine (15 mg) was associated with a 7.4% weight loss at six months, versus 1.2% for placebo in one large investigation (Bray et al. 1999). Similarly, a six-month randomized controlled trial found reductions of 9.8% and 6.5% for orlistat and placebo, respectively (Van Gaal et al. 1998).

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Long-term Pharmacotherapy
Experts currently encourage the long-term use of antiobesity agents in recognition of the chronic nature of obesity (Klein 2004). Just as antihypertensive, antidiabetic, and lipid-lowering medications are used to maintain normal blood pressure, glucose, and cholesterol values, respectively, antiobesity agents should not be discontinued after an initial satisfactory weight loss is achieved (Wadden et al. 2002). This position is supported by two-year trials in which patients lost weight with pharmacotherapy and were then randomized to continued medication or placebo for weight maintenance. In the STORM trial (i.e., Sibutramine Trial of Obesity Reduction and Maintenance), 605 obese participants were treated with 10 mg of sibutramine daily plus a limited dietary intervention for six months (James et al. 2000). Those who achieved at least a 5% weight reduction (77% of participants) received either sibutramine or placebo for the next 18 months. Participants switched from sibutramine to placebo maintained a weight loss of 4.9 kg at 24 months, whereas those who remained on medication maintained a signicantly larger reduction of 8.9 kg. Similar results have been found with orlistat. At least two studies have found signicantly less weight regain among patients treated with orlistat (120 mg three times a day) for two years than among those who received orlistat in year one and placebo in year two (Davidson et al. 1999, Sj str m et al. o o 1998). Although it is clearly effective, there are signicant barriers to the pharmacologic treatment of obesity. Most insurance plans do not reimburse the cost of these medications, which frequently exceeds $100 a month (Li et al. 2005). Thus, patients are forced to pay out-of-pocket for weight loss medications, whereas drugs for hypertension and lipid disordersoften the result of obesityare covered. Many investigators believe that weight loss medications are stigmatized in the same manner as obese individuals themselves (Wadden et al. 2002).

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BARIATRIC SURGERY
Bariatric surgery is the most intensive treatment option and is reserved for individuals with extreme obesity (i.e., BMI 40 kg/m2 ) or those who have a BMI 35 kg/m2 plus serious weight-related health problems (NHLBI & NAASO 2000). Extreme obesity has become increasingly common among American adults in recent years. From 1986 to 2000, the prevalence of persons with a BMI 40 kg/m2 quadrupled, and the prevalence of those with a BMI 50 kg/m2 increased vefold (Sturm 2003). The number of bariatric surgeries performed in the United States has increased even more rapidly, from approximately 16,000 in 1992 to about 103,000 in 2003 (Steinbrook 2004). The most commonly performed procedure in the United States is the Roux-enY gastric bypass (Buchwald & Williams 2004). The creation of a small stomach pouch (30 mL) dramatically restricts food intake, and the bypassing of up to 60 cm

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Effects of bariatric surgery on obesity-related conditionsa Median (range) preoperative prevalence 11% (3%100%) 38% (16%83%) 32% (3%65%) Median (range) percentage of patients whose condition improved or resolved postoperatively 100% (64%100%) 89% (25%100%)b 88% (60%100%)

Condition Type 2 diabetes (21 studies) Hypertension (19 studies) Dyslipidemia (11 studies)
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a b

Table created from data published in Maggard et al. (2005).

These gures represent full resolution of hypertension. Improvement was reported in 95%100% (median = 100%) of patients with hypertension at baseline.

of small intestine reduces absorption of nutrients and, thus, calories (Maggard et al. 2005, Pories et al. 1995). A meta-analysis found that gastric bypass is associated with average postoperative weight losses of 43.5 kg at one year and 41.5 kg at three or more years (Maggard et al. 2005). Adjustable gastric banding, which is often performed laparoscopically and known as the lap-band procedure, has been performed routinely in Europe for at least a decade and is becoming increasingly popular in the United States (Buchwald & Williams 2004). Unlike the gastric bypass, the lap-band procedure is purely restrictive in that portion sizes are limited by reducing stomach capacity with a circumgastric band. This surgery induces mean reductions of 30.2 kg at one year and 34.8 kg at three or more years (Maggard et al. 2005). As shown in Table 3, bariatric surgery is associated with signicant improvements in obesity-related comorbidities. Surgery, however, is not without risks. Gastric bypass and adjustable gastric banding are associated with early (i.e., <30 days after surgery) mortality rates of 0.3%1.0% and 0%0.4%, respectively (Maggard et al. 2005). The risk of having surgery, however, may be less than the risk of foregoing it. Christou and colleagues (2004) examined ve-year mortality data for patients who elected to undergo bariatric surgery and controls (matched on age, sex, and age of morbid obesity onset) who did not undergo surgery. They found that <1% of the 1035 surgery patients died during that time, compared with >6% of the 5746 controls.

MOVING TOWARD PREVENTION

The research reviewed in the previous sections indicates that several obesity therapies can induce clinically signicant reductions in weight and related health complications. Despite the development and proliferation of weight loss programs, products, and procedures, however, the prevalence of excess weight continues to increase. Clearly, clinical weight loss interventions will not provide a solution to the growing obesity crisis.

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Many experts encourage targeting the culturenot the individualfor intervention (Horgen & Brownell 2002, Nestle & Jacobson 2000). They argue that the obesity epidemic will continue to escalate until public policy forces sweeping changes in our food and activity environments. Brownell and colleagues use the term toxic environment to describe a society in which energy-dense food is inexpensive, readily available, highly palatable, and heavily advertised, while physical activity is implicitly or explicitly discouraged by technological advances and the design of neighborhoods and work places (Battle & Brownell 1997, Horgen & Brownell 2002). The increasing prevalence of obesity, type 2 diabetes, and markers of heart disease among children (Cook et al. 2003, Kaufman 2002, Ogden et al. 2002) may provide the impetus for supporting broad policy measures that encourage healthy eating and physical activity. Regulating the advertising of unhealthy foods to children may prove an important step in changing the food culture. Children view an estimated 10,000 food-related commercials per year, most of which advertise calorie-dense foods of limited nutritional value (Brownell & Horgen 2004). Harrison & Marske (2005) found that convenience foods, fast foods, and sweets comprised 83% of the 725 foods advertised during 40 hours of the most popular television programs among children aged 611 years. The authors estimated that a 2000-calorie diet of the advertised foods would provide 20%30% more saturated fat and sodium, and 64% less ber, than is recommended. Furthermore, a diet of foods advertised in commercials specically intended for children would provide inadequate levels of ber, vitamin A, calcium, and iron, but would supply nearly one cup of sugar each day. Additional evidence points to an unhealthy eating environment for children. Austin and colleagues (2005), for instance, plotted the locations of all schools and fast-food restaurants within the city limits of Chicago. They found that the average distance between a school and the nearest fast-food restaurant was 600 meters and that 78% of schools had at least one such restaurant within 800 meters (0.5 miles). Additionally, there were three to four times as many fast-food restaurants within 1500 meters of a school as would be expected by chance. Studies such as those cited above suggest that parents, educators, and health care professionals who attempt to encourage or model healthy eating for children face substantial environmental barriers. Brownell & Horgen (2004) have proposed a number of policy measures that may reduce such obstacles to healthier eating and increased physical activity. Although a detailed discussion of potential changes is beyond the scope of this paper, Table 4 includes some representative recommendations. Some may argue that personal responsibility, and not policy change, should be emphasized in confronting the obesity epidemic. This stance seems to imply that reaching and maintaining a healthy weight is a simple matter of willpower and that obese persons lack self-control. Individuals with obesity, in fact, often are viewed as lazy, unmotivated, and stupid by members of the public as well as by health care professionals (Teachman & Brownell 2001). Many persons attribute excess

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TABLE 4

A selection of recommended actions for changing the toxic environmenta

Encourage political leaders to be bold and innovative in addressing the obesity crisis and to remove political barriers to taking action. Consider changing the price structure of food, rst by lowering the cost of healthy foods and perhaps by increasing the cost of unhealthy foods. Create a superfund to promote healthy eating, perhaps from assessments placed on food advertisements or small taxes on the sale of unhealthy foods. Require food labeling at restaurants.
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Support programs that teach children about nutrition and activity. Earmark transportation funding to increase activity (bike paths and walking paths, buses with bike racks, trafc calming, etc.).
a

Table created from text of Brownell & Horgen (2004), pp. 30913, with permission of The McGraw-Hill Companies.

weight not to genes or to an obesigenic environment, but to emotional distress. The following section reviews the empirical evidence regarding the relationship of obesity to mood disturbance.

OBESITY AND DEPRESSION

Early investigations of the psychological and psychiatric correlates of obesity were frequently comparisons of the personalities and symptom proles of obese versus nonobese persons. Results of those studies were mixed; some found that obesity was related to increased psychopathology, while others reported a protective effect of obesity (e.g., Moore et al. 1962, Stewart & Brook 1983, Wadden & Stunkard 1985). Regardless of the direction of the relationship, however, the observed differences between obese and nonobese individuals were not clinically meaningful. This rst generation of studies that examined the relationship between obesity and psychopathology was criticized for its methodological aws (Friedman & Brownell 1995). Namely, these investigations typically lacked large, representative samples and did not employ clinically validated measures of psychopathology. The quality of research in this area has improved considerably. In addition to addressing the limitations of the early studies cited above, recent investigations have sought to identify risk factors for psychopathology (particularly for depression) among obese individuals. This shift in focus signals researchers recognition that people with obesity are a heterogeneous group and that there is likely greater variability in psychological functioning among obese persons than between persons with and without this condition. Large epidemiological investigations and clinical trials have identied two obese subgroupswomen and those with extreme obesitythat are at increased risk of depression.

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The Obesity-Depression Relationship in Women Versus Men

Three population studies found that the relationship of body weight to depression differs between the sexes. The rst study examined data from the rst National Health and Nutrition Examination Survey, which was conducted from 19711975 and compared rates of depression across BMI quintiles for women and men (Istvan et al. 1992). Depression was 38% more common [odds ratio (OR) = 1.38, 95% condence interval (CI): 1.071.69] among women in the highest BMI quintile (>28.96 kg/m2 ) than in women in the lower four quintiles. Men in the highest BMI quintile (>28.7 kg/m2 ), however, were no more likely to be depressed than were their counterparts with lower BMIs (OR = 0.97, 95% CI: 0.48 1.47). Carpenter et al. (2000) similarly found that obese women were 37% more likely to report a history of depression in the past year than were women with a BMI of 20.829.9 kg/m2 . Suicidal ideation and past-year suicide attempts also were more common among obese versus nonobese women, but those increases were not statistically signicant. In the same study, excess weight was found to have a protective effect for men such that past-year depression and suicide attempts were both 37% less likely (95% CIs: 0.600.67 and 0.480.83, respectively) among obese versus nonobese men. Finally, Onyike et al. (2003) analyzed data collected from 19881994 as part of the third National Health and Nutrition Examination Survey. Similar to the two previous epidemiological studies cited above, this investigation found that obesity was signicantly related to depression for obese women (OR = 1.82, 95% CI: 1.013.30) but not for obese men (OR = 1.73, 95% CI: 0.565.37). It is well documented that the prevalence of depression is higher among women than among men in the general population (Am. Psychiatr. Assoc. 2000, Kessler et al. 1993). It is not surprising, therefore, that the relationship between obesity and depression is moderated by gender. Some researchers have posited that females not only have a greater biological and psychological vulnerability to depression than do males, but also are more likely to experience acute and chronic stressors that would activate a predisposition to depression (Nolen-Hoeksema 2002). Consistent with this idea, research has found that women experience greater dissatisfaction with weight and shape than men do, and that dissatisfaction increases with BMI (Cash 2002). Women also are subject to greater degrees of weight-related stigma and discrimination than are men (Puhl & Brownell 2001). These factors may not fully account for, but almost certainly contribute to, the differential relationship between obesity and depression across genders.

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Extreme Obesity Increases the Risk of Depression

Onyike and colleagues (2003) discovered that only the most obese individuals are at increased risk of depression. These researchers separated their sample of 8410 persons according to weight class (i.e., underweight, average weight, overweight, and class I, II, and III obesity) and found that the risk of depression was not

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WADDEN

5 4.5 4 3.5
Odds Ratio

4.63

3 2.5 2 1.5 1 0.5 0 < 18.5 18.5 - 24.9 25 - 29.9 30 - 34.9 (kg/m2) 35 - 39.9 >/= 40 Body Mass Index
1.33 1.13 1 0.96 1.9

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Figure 3 Odds ratios of past-month depression across BMI categories, adjusted for age, race/ethnicity, education, marital status, physicians health rating, dieting for medical reasons, use of psychiatric medicines, cigarette smoking, and use of alcohol, marijuana, and cocaine. Data from Onyike et al. (2003).

signicantly greater for overweight, class I obese, or class II obese men or women than for their average-weight counterparts. Individuals with class III (i.e., extreme) obesity, however, were more than four times as likely as persons of average weight to meet criteria for major depression (OR = 4.63, 95% CI: 2.0610.42). Figure 3 depicts the odds of depression across BMI categories, adjusted for age, education, marital status, and several health-related variables. The ndings cited above are consistent with those of smaller, clinical studies. As compared with less-obese individuals who sought behavioral and pharmacological weight loss interventions, extremely obese persons who sought bariatric surgery were found to have lower self-esteem and higher depression scores (Berkowitz & Fabricatore 2005). Extremely obese persons also have greater impairments in health-related quality of life than do their less obese peers (Kolotkin et al. 2002). Some evidence suggests that the relationship between BMI and depression may be mediated by impairments in health-related quality of life. Several studies have found that BMI, impaired quality of life, and symptoms of depression are all positively associated (Dixon et al. 2003, Doll et al. 2000, Kolotkin et al. 2002). Fabricatore and colleagues (2005), however, found that BMI was unrelated to depression after impairments in health-related quality of life were included in multivariate models. Results from this cross-sectional study await replication in a longitudinal investigation.

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CONCLUSION
Obesitywhich is increasingly prevalent in the United States and throughout the worldis a serious medical condition that is associated with increased morbidity (e.g., diabetes, cardiovascular disease, sleep apnea, osteoarthritis) and mortality. Additionally, some obese persons (i.e., women and those with a BMI 40 kg/m2 ) are at elevated risk of depression. Many available treatments result in clinically signicant weight losses and improvements in weight-related comorbidities. Facilitating the long-term maintenance of such losses, however, remains a challenge to clinicians and researchers. Thus, obesity must be considered a refractory condition that requires chronic care. Barriers to obesity treatment include lack of or limited third-party payment for weight loss therapies and an environment that is not conducive to weight control. As long as societal norms include overconsumption of calorie-dense foods and the built environment implicitly discourages energy expenditure, even the bestdesigned and most powerful treatments will be insufcient to curb the epidemic of excess weight. Prevention efforts must be undertaken on a grand scale in order to reverse the increasing prevalence of obesity and related disorders. DISCLOSURE TW is a consultant to Abbott Laboratories, which produces the weigh-loss medication sibutramine (Meridia). The Annual Review of Clinical Psychology is online at http://clinpsy.annualreviews.org LITERATURE CITED
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Annual Review of Clinical Psychology Volume 2, 2006

CONTENTS
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THE HISTORY AND EMPIRICAL STATUS OF KEY PSYCHOANALYTIC CONCEPTS, Lester Luborsky and Marna S. Barrett DOCTORAL TRAINING IN CLINICAL PSYCHOLOGY, Richard M. McFall METHODOLOGICAL AND CONCEPTUAL ISSUES IN FUNCTIONAL MAGNETIC RESONANCE IMAGING: APPLICATIONS TO SCHIZOPHRENIA RESEARCH, Gregory G. Brown and Lisa T. Eyler THE USE OF STRUCTURAL ANALYSIS OF SOCIAL BEHAVIOR (SASB) AS AN ASSESSMENT TOOL, Lorna Smith Benjamin, Jeffrey Conrad
Rothweiler, and Kenneth L. Critcheld

1 21

51

83

REINTERPRETING COMORBIDITY: A MODEL-BASED APPROACH TO UNDERSTANDING AND CLASSIFYING PSYCHOPATHOLOGY,

Robert F. Krueger and Kristian E. Markon 111 135

WOMENS MENTAL HEALTH RESEARCH: THE EMERGENCE OF A BIOMEDICAL FIELD, Mary C. Blehar POSTTRAUMATIC STRESS DISORDER: ETIOLOGY, EPIDEMIOLOGY, AND TREATMENT OUTCOME, Terence M. Keane, Amy D. Marshall,
and Casey T. Taft

161 199 237 267 291 327 357 379

THE PSYCHOPATHOLOGY AND TREATMENT OF BIPOLAR DISORDER,

David J. Miklowitz and Sheri L. Johnson

ATTEMPTED AND COMPLETED SUICIDE IN ADOLESCENCE,

Anthony Spirito and Christianne Esposito-Smythers

ENDOPHENOTYPES IN THE GENETIC ANALYSES OF MENTAL DISORDERS, Tyrone D. Cannon and Matthew C. Keller SCHIZOTYPAL PERSONALITY: NEURODEVELOPMENTAL AND PSYCHOSOCIAL TRAJECTORIES, Adrian Raine AUTISM FROM DEVELOPMENTAL AND NEUROPSYCHOLOGICAL PERSPECTIVES, Marian Sigman, Sarah J. Spence, and A. Ting Wang OBESITY, Anthony N. Fabricatore and Thomas A. Wadden MILD COGNITIVE IMPAIRMENT AND DEMENTIA,
Marilyn S. Albert and Deborah Blacker

vii

viii

CONTENTS

COGNITION AND AGING IN PSYCHOPATHOLOGY: FOCUS ON SCHIZOPHRENIA AND DEPRESSION, Philip D. Harvey, Abraham
Reichenberg, and Christopher R. Bowie 389 411 435 469

CONTINGENCY MANAGEMENT FOR TREATMENT OF SUBSTANCE ABUSE, Maxine Stitzer and Nancy Petry PERSONALITY AND RISK OF PHYSICAL ILLNESS, Timothy W. Smith and
Justin MacKenzie

RECOVERED MEMORIES, Elizabeth F. Loftus and Deborah Davis

Annu. Rev. Clin. Psychol. 2006.2:357-377. Downloaded from arjournals.annualreviews.org by University of California - Los Angeles on 07/20/06. For personal use only.

INDEX
Subject Index 499

ERRATA
An online log of corrections to Annual Review of Clinical Psychology chapters (if any) may be found at http://www.AnnualReviews.org