Obesity: What Mental Health Professionals Need to Know

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Obesity: What Mental Health Professionals Need to Know

J. Devlin, M.D., Z. Yanovski, M.D., and G. Terence

, Ph.D.

ABSTRACT

OBJECTIVE: Obesity is a highly prevalent condition with significant

health implications. This report summarizes recent clinically

relevant findings concerning the pathogenesis and treatment of

obesity and considers their implications for psychiatric diagnosis

and management.METHOD: The authors conducted selective reviews of

the literature from the last 10 years. Topics included the

biological and behavioral factors that contribute to the onset and

maintenance of obesity, the relationship between obesity and

psychiatric illness and treatment, and the questions of whether and

how obesity should be treated.RESULTS: Genetic effects, some

mediated by eating behavior, contribute importantly to the potential

for obesity, the expression of which is promoted by environmental

factors that increase the availability of calorically dense foods

and discourage activity. There appear to be behaviorally distinct

subsets of obese persons who display particular patterns of

disordered eating and elevated rates of psychopathology. Treatment

with psychotropic medications may contribute to obesity in ways that

are only partly understood. Although successful obesity treatment is

associated with clear health benefits and available treatments offer

benefit to some, relapse remains the rule.CONCLUSIONS: Although the

presence or development of obesity is a daunting problem, it should

not be ignored by mental health professionals. Treatment should

address not only obesity per se, but also its effects on self-esteem

in a hostile cultural climate. Ongoing developments in basic and

clinical research are likely to increase the range, efficacy, and

acceptability of treatment options in the years ahead.

Obesity is among the most easy to recognize and the most difficult

to treat of medical conditions. Although most mental health

practitioners commonly treat obese individuals, there exists no

consensus on whether or how to address obesity in the patient's

overall treatment plan. This article represents the attempt of the

three authors—a psychiatrist (M.J.D.), a clinical psychologist

(G.T.W.), and a family physician (S.Z.Y.)—to identify the questions

that mental health professionals face when working with obese

patients, to address these questions to the extent that the evidence

allows, and to direct the interested reader to sources of more

detailed information on scientific and clinical aspects of obesity.

The article is based on a selective review of the literature from

the last 10 years. Recent reviews detailing the basic science of

weight regulation (1) and clinical aspects of weight management (2,

3) provide further information for interested readers. Patient-

oriented information about obesity is also available through the

Weight-Control Information Network of the National Institute of

Diabetes and Digestive and Kidney Diseases at

http://www.niddk.nih.gov/health/nutrit/nutrit.htm.

What CONSTITUTES OBESITY, AND HOW COMMON Is IT?

Obesity is defined best in terms of what is known as the body mass

index, calculated by dividing weight (in kilograms) by height (in

meters) squared. Recent clinical guidelines developed by the

National Heart, Lung, and Blood Institute define " overweight " as a

body mass index of 25–29.9 kg/m2 and obesity as a body mass index of

30 kg/m2 and greater. Body mass index of 30–34.9 kg/m2 is classified

as class I obesity, 35–39.9 kg/m2 as class II obesity, and 40 kg/m2

or more as class III or extreme obesity (2). The institute's

definition of overweight is consistent with recommendations of the

World Health Organization (3) and health agencies in most countries

outside the United States and is grounded in epidemiological data

showing increases in morbidity and mortality with body mass indexes

above 25 (2). Using this classification, it is estimated that

approximately 55% of adults in the U.S. are overweight, and about

one-half of these are considered obese (4). Obesity is inversely

associated with social class (5). Minority populations, especially

African American women, are disproportionately affected. The

percentage of individuals in the " overweight but not obese " category

(body mass index of 25.0–29.9 kg/m2) has remained relatively stable

over the past 30 years, whereas the prevalence of obesity has

increased more than 50% between 1976 and 1980 (14.5%) and 1988 and

1994 (22.5%), with a consequent reduction in those meeting criteria

for " normal weight " (4).

WHAT IS THE IMPACT OF OBESITY ON INDIVIDUALS AND ON SOCIETY?

Obesity is a chronic disorder and a serious public health problem.

The literature has presented well-documented links between obesity

and increased mortality and morbidity due to hypertension,

dyslipidemia, diabetes mellitus, coronary heart disease, congestive

heart failure, stroke, gallstones, osteoarthritis, sleep apnea,

certain types of cancer (colon, breast, endometrial, gall bladder),

menstrual abnormalities, impaired fertility, and increased pregnancy

risks (2). Overall mortality is modestly increased for overweight

individuals (body mass index of 25–29.9 kg/m2) and markedly

increased for those with body mass index over 30 kg/m2, particularly

those with severe obesity (6). Among older adults, mortality is less

strongly linked to body mass index (7), but body mass index in the

obese range remains associated with elevated mortality (8). In

addition to degree of obesity, excess fat in the abdominal region,

estimated by measuring waist circumference or waist/hip ratio, is

independently associated with increased morbidity and mortality,

particularly for overweight and class I obese individuals (2).

The adverse effects of obesity are not only medical. In Western

societies, negative attitudes toward obesity are prevalent in

society at large and among health care professionals. These

attitudes translate into tangible disadvantages in several common

endeavors, including getting into college, renting a residence, and

getting married (2). The economic impact of obesity is also

considerable. For an individual, obesity is associated not only with

increased health care expenditures but also with decreased job

earnings (9). Estimates of the total cost of obesity in the United

States, including direct (health care) and indirect (lost

productivity) costs, amount to nearly $100 billion per year (10).

WHAT CAUSES AND MAINTAINS OBESITY?

Obesity is best conceptualized as a complex, multifactorial disorder

with both genetic and environmental components.

Genetics of Obesity

Single-gene animal models of obesity have led to the identification

of several gene products that are associated with obesity, including

leptin, the leptin receptor, agouti signaling protein, and

carboxypeptidase E (11). Of particular importance, the mutated gene

products in these animal models have human homologues that appear to

have similar functions, suggesting that these proteins may also play

roles in the development or maintenance of human obesity.

Numerous central and peripheral factors that increase or decrease

food intake and energy expenditure have been identified, and more

such factors are being discovered on a regular basis (1). Uncoupling

protein was described decades ago as a ubiquitous component of brown

fat, where it serves to dissipate energy as heat. Because adult

humans have little brown fat, its role in human energy regulation

was assumed to be minimal. The recent discovery of novel uncoupling

proteins that are found in many human tissues, including white

adipose tissue (uncoupling protein 2) and muscle (uncoupling protein

3) (12), offers a new pathway by which energy regulation might

occur, and the potential for therapeutic manipulation has generated

an explosion of research. Another target of human and animal

research is the ß3 adrenergic receptor. Preliminary human studies

suggested that a variant in this receptor might be associated with

lower resting metabolic rate, earlier-onset diabetes, and greater

degree of obesity (13, 14), and ß3 adrenergic agonists are an active

target of drug development.

Although recent discoveries of novel mechanisms for energy

regulation are exciting, single-gene mutations are unlikely to

account for the majority of human obesity. Cases have been reported

of humans with mutations of several of the genes involving animal

models of obesity (11). In addition, a recently described mutation

in the gene coding for peroxisome-proliferator-activated receptor 2

(a regulator of adipocyte differentiation) may be more common in

obese individuals (15). However, the vast majority of obese humans

do not show major mutations involving known pathways leading to

obesity. For example, leptin levels in most obese humans are high

and correlate extremely well with body fatness (16). Although single-

gene mutations as causal factors in obesity are probably rare, a

number of studies have implicated linkage between certain sites

housing candidate genes believed to be involved in animal models of

obesity and phenotypic characteristics such as body mass index or

percentage of body fat (17–19). Animal models that more closely

represent human obesity, such as mice that become obese only when

exposed to a high-fat diet, have also been developed (20). Although

genetic variants may not lead to major alterations in the protein

product of the gene, they may nonetheless, either singly or in

combination with other genes, have an impact on the protein

product's function.

The complexity of the genetics of obesity means that simple answers

about its causes are unlikely. However, basic research findings

identifying pathways that regulate food intake, adipocyte

differentiation, and energy expenditure are likely to assist in the

development of effective strategies for both prevention and

treatment of obesity. Drugs could be developed to block the effects

of neuropeptides and receptors stimulating food intake, to enhance

the effects on food intake or energy expenditure of factors involved

in the catabolic pathway, or to alter the pathways involved in the

differentiation or metabolism of adipocytes.

Behavioral Genetics

Often, " genetic " causes of obesity are contrasted with those seen

as " behavioral, " implying that only factors such as metabolic rate

or propensity to gain weight as fat are under genetic control.

Behavioral genetics refers to the contribution of genetic

variability to relevant behaviors (eating and physical activity).

Behavioral factors such as dietary preference for fats, choice of

interval between meals, degree of caloric compensation in response

to food restriction, or even inclination to engage in physical

activity can have strong genetic components (21–23). Genetically

determined preferences may interact with environmental factors to

yield conditioned eating patterns (24). Unfortunately, research in

this area has lagged behind investigations of some of the more

easily measured phenotypic characteristics, such as metabolic rate

or percentage of body fat (23). The recognition that certain

behaviors may have a genetic basis has important implications for

targeting behavior change. Environmentally triggered eating

behaviors should be much more responsive to environmental

modifications than those with a genetic basis. The degree to which

certain behaviors are genetically or environmentally based may vary

both between individuals and between populations.

Our " Toxic " Environment

Adoption, twin, and family studies have consistently noted that

obesity has a strong heritable component, with approximately 30%–70%

of variability in body weight or fat mass being genetically

determined (25, 26). This is considered a major genetic effect,

comparable to the genetic contribution in diseases such as

schizophrenia, coronary artery disease, and breast cancer (27).

However, it leaves a large component of variation in body weight

unexplained by genetic mechanisms. Environmental factors account for

this component. Of interest, studies have suggested that most of the

familial resemblance for body mass index in adults is due to genetic

influences rather than shared family environment (25).

Obesity has increased dramatically over the past decade in the

United States, as well as in most of the developed world. The most

likely explanation is that our population has been exposed to

dramatic environmental changes over the past 30 years and that these

changes have acted together to create what has been called an

obesity-promoting " toxic " environment (28). Throughout most of human

history, starvation, rather than obesity, has been the predominant

threat to survival, with a resulting evolution of a " thrifty "

phenotype that is energy-efficient and fat-loving (29). What serves

as a genetic advantage in a low-energy, high-physical-activity

environment can lead to obesity with the ready availability of high-

fat, high-calorie foods coupled with significant decreases in

physical activity. The case of the Pima Indians provides a good

example of environmental effects on a given genetic background (30).

Pimas living in Arizona have been compared with distant relatives

living in Mexico who are much more physically active and eat a diet

50% lower in fat. The Mexican Pimas averaged 57 pounds lighter than

their Arizona counterparts, and few had diabetes (30).

Another more salutary environmental trend contributing to increased

rates of overweight and obesity in the United States is the decline

in the prevalence of smoking in recent years. Smoking cessation is

often accompanied by weight gain that reflects a combination of

decreased metabolic rate and increased caloric intake. Possible

mediators of the effect of smoking and smoking cessation on weight

include 1) elevation of plasma leptin levels due to smoking (31); 2)

nicotine-associated increase in hypothalamic leptin receptor

sensitivity, which reverses after smoking cessation (32); and 3)

compensatory increase in the activity of adipose tissue lipoprotein

lipase among smokers, which persists in the short term after

quitting (33). One-quarter of the increase in prevalence of

overweight for men in the past 10 years and one-sixth of the

increase for women is attributable to smoking cessation (34).

Nonetheless, the health benefits of smoking cessation far outweigh

the negative consequences of weight gain, and weight gain can be

minimized if smoking cessation is accompanied by a moderate increase

in exercise (35).

DO OBESE PEOPLE EAT MORE OR ARE THEY MORE METABOLICALLY EFFICIENT?

Although genetic differences in metabolic efficiency are likely to

exist, there is little evidence that low metabolic rate plays a

major role in the development or maintenance of obesity for the vast

majority of overweight persons, suggesting that the development and

maintenance of obesity is indeed mediated by the consumption of a

greater than normal amount of food.

Eating Behavior and Metabolism

The study of human eating behavior is methodologically difficult.

Less intrusive methods, such as patient self-report or 24-hour

dietary recall, rely on subjects' often inaccurate estimates, and

more objective methods, such as observed eating in a laboratory

setting, run the risk of being unrepresentative of the subject's

unobserved eating. Early studies that relied on these methods

suggested that many overweight individuals ate very little (36).

This " diet resistance " was often attributed to slowed metabolism due

to frequent dieting or weight cycling (37). Studies using the highly

accurate doubly labeled water method in adolescents (38) and in

adults (39) confirm that overweight individuals tend to underreport

their food intake and overreport their physical activity, reporting

only 60%–80% of actual caloric intake, in contrast to normal weight

subjects, who report 80%–100% (39, 40).

Overweight people generally consume more calories than people of

normal weight, but this does not mean they are overeating, as they

are consuming an appropriate amount of calories for their higher

body weight (assuming weight stability). This distinction is

important, as the idea that obese individuals bring about or

maintain their obesity by inappropriate overeating underlies many of

our culture's negative stereotypes about obesity.

Apart from the amount of food consumed, patterns of food consumption

are abnormal in subgroups of obese persons. Stunkard (41) first

described a distinctive subgroup of obese patients who reported

recurrent uncontrolled binge eating. Many of these patients would

meet the criteria for binge eating disorder found in Appendix B

(Criteria Sets and Axes Provided for Further Study) of DSM-IV in

that they displayed regular binge eating in the absence of the

extreme weight loss behaviors characteristic of bulimia nervosa.

Compared with non-binge-eaters, obese binge eaters eat significantly

more food in laboratory studies when instructed to binge or eat

normally, report an earlier onset of obesity and greater percentage

of lifetime on a diet, overeat more in response to negative

emotional states, report lower levels of self-esteem, and display

significantly greater levels of psychopathology, especially

depression and personality disorders (42–46).

Another abnormal eating pattern that exists most commonly in obese

individuals has become known as the " night-eating syndrome. " First

described in 1955, its key features are morning anorexia, evening

hyperphagia, and insomnia (47). More recent clinical reports have

suggested that many of these patients suffer from sleep disorders

such as somnambulism, restless legs syndrome, and obstructive sleep

apnea (48) and that most patients report some degree of amnesia for

the eating episode (49). In addition, night-eating syndrome is

associated with neuroendocrine abnormalities including attenuated

nocturnal rise in leptin and melatonin and increased plasma cortisol

(50). Further research is needed to better characterize the clinical

features and treatment responses of these individuals.

Metabolic Factors

Energy regulation in persons who are already obese is not

necessarily the same as energy regulation in those who are

developing obesity. There is some evidence that certain individuals

in a given population may be more metabolically efficient than

others, which could lead, in time, to weight gain. Twin studies have

shown a strong familial response to overfeeding and underfeeding,

both in the amount of weight gained as fat and in distribution of

body fat (51, 52). Thus, there are clear metabolic differences in

propensity for weight gain in response to caloric excess or deficit.

A recent study, in which volunteers were overfed by about 1000

kcal/day, suggested that differences in propensity to gain weight in

the presence of caloric excess could be due, in part, to increases

in energy expenditure from everyday activities, such as walking,

maintenance of posture, and fidgeting (53).

Weight Regain

Why is long-term weight loss so difficult to achieve? The degree to

which obese individuals who lose weight become more metabolically

efficient remains unresolved. The concept of a " set point for energy

balance, " first described by Keesey and Hirvonen (54), as a

predetermined point at which a given individual's body weight is

regulated, is an attractive one. Caloric restriction clearly

increases energy efficiency over the short term, decreasing leptin

and thyroid hormone levels as well as resting metabolic rate to a

level lower than that predicted by decreases in lean body mass (55,

56). Differences may also exist in physical activity-related energy

expenditure after weight reduction (57). Over the longer term,

however, most evidence of increased conservation of energy

dissipates, with resting energy expenditure levels appropriate for

the new (lower) level of body weight (58).

Thus, although metabolic factors that promote weight regain may

exist, they do not seem to explain satisfactorily the almost

inevitable weight regain observed clinically (59). The observed 5%–

10% change in energy expenditure (57) is relatively small, and

compensation either by caloric restriction or increases in physical

activity should be possible. Moreover, it should be noted that

increases in feeding lead to increases in energy expenditure, which

would be expected to assist in the overfed subjects' return to a

lower body weight. Thus, any " set point " is frequently overcome—at

least in the direction of allowing weight gain.

It has been suggested that postobese persons—those who have lost

weight—are metabolically different from never-obese persons.

Potential contributors to weight regain include the presence of fat

cell hyperplasia, leading to an increased number of small fat cells

(60), increases in lipoprotein lipase (61), which tends to promote

fat storage, and other as yet unidentified factors. Some postobese

individuals may be more sensitive to the macronutrient composition

of their diet than are never-obese persons, and thus they must

consistently eat a low-fat diet to maintain their body weight (62).

High levels of physical activity have also been found to correlate

with successful weight maintenance in a registry of long-term weight

maintainers (63), and evidence suggests that the level of physical

activity must be substantial to have an impact on weight regain

(64). In addition, food intake and physical activity may interact,

such that physical activity can mitigate against some effects of a

higher-fat diet (65). Combining a lower-fat, lower-energy-density

diet with increased physical activity may allow previously obese

individuals to decrease the dietary restraint necessary to maintain

weight loss in the face of physiologic pressures for regain. It

appears that those who have been significantly obese (i.e., body

mass index >30 kg/m2) need to persist with long-term changes in

their diet and physical activity in order to overcome the tendency

to regain their lost weight.

DO PSYCHOTROPIC MEDICATIONS PLAY A ROLE IN OBESITY?

Weight gain is among the most problematic side effects of

psychotropic agents and is one of the most frequent reasons for

nonadherence to prescribed medication regimens, particularly when

treatment extends beyond the short term (66, 67). Several classes of

psychotropic medications are associated with unwanted weight gain,

including antipsychotics, antidepressants, mood stabilizers, and, to

a lesser degree, anxiolytics (68–70). Weight gain could

theoretically be due to increased energy intake, decreased energy

expenditure, or a combination of the two; in most cases, we have too

little information to distinguish among these possibilities. In

general, medications that block histamine H1, serotonin 5-HT2C, and

dopamine D2 receptors tend to be associated with weight gain (71).

Antipsychotics

Weight gain has been noted as a concomitant of antipsychotic

treatment for the past several decades. Among currently available

antipsychotics, the low-potency phenothiazines (e.g.,

chlorpromazine, thioridazine, mesoridazine) and novel antipsychotics

(e.g., clozapine, olanzapine, risperidone, quetiapine) are most

often associated with clinically problematic weight gain. Molindone

is relatively unique in its lack of association with weight gain and

its association with weight loss in several studies (70). In terms

of relative effects on weight, the novel antipsychotics appear to be

the most potent; they are followed by phenothiazines, which have

large effects, haloperidol, which has a relatively small effect, and

finally drugs that do not promote weight gain, including molindone

and possibly loxapine and pimozide (68, 70). When weight gain

occurs, it is usually most rapid in the acute phase of treatment and

generally plateaus after 1–2 years (70). Although there are some

indications of increased appetite in patients treated with

antipsychotics (72), no systematic studies of energy intake or

expenditure involving such patients have been done.

Mood Stabilizers

Weight gain of at least 5% (and much more in some cases) occurs in

an estimated one-third to two-thirds of patients treated with

lithium and in one-quarter to one-half of patients treated with

anticonvulsants, including valproic acid and carbamazepine (68). In

the case of lithium, weight gain appears to be dose-related (73), to

occur primarily in the first 2 years of treatment, and to occur more

frequently in patients who are already overweight at the onset of

treatment (74). Among mood stabilizers that have come into use more

recently, gabapentin appears to be associated with weight gain in a

substantial minority of patients (75), lamotrigine is not typically

associated with weight change, and topiramate is associated with

mild, dose-related weight loss (76). The effect of lithium on weight

may be mediated by increased intake of calorically dense fluids due

to drug-induced thirst, increased carbohydrate and/or lipid storage,

or lithium-induced hypothyroidism, but it is as yet unclear which if

any of these factors is most clinically relevant (68). The mechanism

of anticonvulsant-induced weight gain remains poorly understood.

Antidepressants

According to conventional wisdom about the relationship between

antidepressants and weight gain, treatment with tricyclic

antidepressants or with monoamine oxidase inhibitors (MAOIs) is

associated with marked weight gain, particularly during the

continuation and maintenance phases of treatment. However, as

reviewed by Ackerman and Nolan (68), more recent studies have

reported relatively modest mean weight gains, even over the long

term, and much larger increases in a relatively small number of

patients. Of the tricyclics, amitriptyline is thought to induce the

most weight gain (67, 69). The mechanism of tricyclic antidepressant-

induced weight gain appears to involve decreased basal metabolic

energy expenditure and diet-induced thermogenesis. Shifts in food

preference toward calorically dense foods occur in a minority of

patients but do not seem to be associated with significant weight

gain (69). Among the MAOIs, the reversible inhibitors of MAOA such

as moclobemide (not yet available in this country) appear to be

least likely to induce weight gain (77). Newer antidepressants,

including bupropion, venlafaxine, and nefazodone, are generally not

associated with weight gain (68). An exception is mirtazapine,

which, like the tricyclic antidepressants, is associated with weight

increase (78).

The selective serotonin reuptake inhibitors (SSRIs), including

fluoxetine, sertraline, paroxetine, fluvoxamine, and citalopram,

have generally been thought not to be associated with weight gain.

In fact, in a large multicenter trial, patients treated with 60

mg/day of fluoxetine lost a significant amount of weight, with

maximum weight loss occurring at week 20, but on average had

regained most of their lost weight by the end of 1 year of treatment

(79). Why do SSRIs differ from tricyclic antidepressants and MAOIs

in their effects on weight? Proposed mechanisms include SSRI-induced

increases in metabolic rate (69) or serotonin-mediated effects on

appetite and food intake. However, although the SSRI fluoxetine is

known to decrease binge eating in patients with bulimia nervosa (80)

and to decrease meal size but not frequency in overweight women

(81), the effects of SSRIs on food intake have not yet been well

characterized.

Recent observations of patients receiving long-term treatment with

SSRIs have suggested that the effect on weight may vary over time.

Clinicians have reported that long-term treatment with SSRIs (i.e.,

several months) is associated with regain of lost weight and

overshoot to higher-than-baseline weight in certain patients, an

effect which may be mediated by serotonin 5-HT2C receptors (82).

However, a recent large-scale study found that patients receiving

continuation treatment with fluoxetine gained no more weight over 1

year than those receiving placebo (83). Systematic studies are

needed to determine whether the pattern of weight regain in patients

who have lost weight during fluoxetine treatment differs from the

general pattern of weight regain in patients who lose weight

intentionally.

SHOULD OBESE INDIVIDUALS ATTEMPT TO LOSE WEIGHT?

Does Weight Loss Reduce Medical Risks?

Most successful weight loss treatments yield reduced blood pressure,

reduced serum triglycerides, increased HDL cholesterol, reduced

total cholesterol and LDL cholesterol, and reduced blood glucose and

hemoglobin A1c in some patients with type 2 diabetes. Medical

benefits begin to accrue with weight losses of as little as 5%–10%

of initial weight (84, 85), and successful weight loss may play an

important role in prevention of these illnesses among those at risk

(2, 86). These findings suggest that physicians should treat not

just the complications of obesity, but obesity itself, even in the

absence of recognized sequelae. NIH guidelines recommend weight loss

for individuals with a body mass index >30 kg/m2 and for individuals

with a body mass index >25 kg/m2 and two or more obesity-related

risk factors (2). For those with a body mass index between 25 and 30

kg/m2, but without additional risk factors, prevention of further

weight gain, rather than weight loss, is the goal.

Critiques of Weight Loss

Critics have called for a moratorium on weight loss programs,

arguing that dieting is not only ineffective but harmful. According

to this view, the pattern of recurrent weight loss followed by

regain—so-called " yo-yo dieting " —demoralizes patients, makes future

weight loss even more difficult, and even increases the risk of

disease (37).

Available evidence provides little empirical support for these

objections. Weight cycling has been found to be associated with

increased morbidity and mortality in several studies. However, these

studies have not looked specifically at the effects of intentional

weight loss among obese individuals. A review examining weight

cycling concluded that concerns about its adverse health effects

should not preclude efforts at sensible, moderate weight loss by

obese persons, but stressed the need for further research in this

area (87). The authors also underscored the importance of commitment

to long-term behavioral change in enhancing the likelihood of weight

stability.

Critics have also argued that the dietary treatment of obesity may

trigger or exacerbate binge eating in obese patients. This concern

is based on the link between dieting and the onset of bulimia

nervosa. However, it is important to distinguish between normal or

underweight women with bulimia nervosa and obese binge eaters. The

latter show significantly less dietary restraint than the former

(88). In contrast to patients with bulimia nervosa in whom the onset

of dieting almost always precedes the onset of binge eating (89),

obese binge eaters are just as likely to diet after the onset of

binge eating as before it (90–92). Studies have indicated that

behavioral treatments of obesity using either moderate or severe

caloric restriction appear to be effective in reducing binge eating

disorder (93–95).

Even modest weight loss can reduce health risks in obese patients in

the short term at least. The long-term effects of weight loss have

yet to be systematically evaluated. Nevertheless, although obese

individuals must be evaluated for their specific risks and

likelihood of success, for most, weight loss would be beneficial.

Clearly, the patient's motivation must be assessed, and

interventions must be geared to his or her readiness to undertake

the difficult tasks involved in losing weight.

HOW WELL DO CURRENTLY EXISTING TREATMENTS WORK?

Behavioral Weight Control

A comprehensive behavioral weight control program, comprising

components of improved eating habits, lifestyle change, and

increased exercise, is widely viewed as the treatment of choice for

overweight and moderately obese individuals. With 5 months of

treatment, behavioral treatment combined with moderate dietary

restriction (e.g., 1000–1500 kcal/day of self-selected foods)

results in a mean weight loss of 15–20 pounds (96). Behavioral

weight loss programs are also associated with significant decreases

in depression and body image dissatisfaction, together with

increases in self-esteem and interpersonal functioning (97). The

problem is that these treatment effects are not maintained over

time.

At 1-year follow-up, patients who have received behavioral treatment

with dietary restriction regain 35%–50% of their weight loss, both

in research clinics and in the general population. Five-year follow-

ups have revealed that the vast majority of patients regained all of

the weight they had lost. A large and diverse literature is

strikingly consistent in showing the same inexorable pattern,

namely, gradual regain of weight over time (98). Viewing obesity as

a chronic condition, it is not surprising that improvement recedes

once treatment has stopped. Accordingly, a continuous care model has

been proposed (2). Extended maintenance sessions have improved

persistence of weight loss, but attendance declines after 6 months

(99).

Behavioral treatment combined with a very low calorie diet of up to

800 kcal/day, often in the form of a liquid nutritional supplement,

was highly touted and widely used several years ago. Typical

programs used a very low calorie diet for 12–16 weeks, followed by

reintroduction of a self-selected 1000–1500 kcal/day diet. This

approach produces more rapid weight loss initially, but relapse

occurs more quickly, so that treated individuals, after 1 year, show

similar weight regain to those on more moderate calorie restriction

(100).

A notable contrast to the high relapse rate among obese adults is

the outcome in children. Weight loss has been maintained over a 10-

year follow-up in children, even though their parents showed the

predictable relapse rate (101). It may be easier to teach children

healthy eating and activity habits. Moreover, the parents in these

studies provided a structured environment that supported weight

control by regulating access to food (102). This structure had the

effect of lessening reliance on self-control that may be

insufficient in the long term to cope with the pressures of a toxic

environment (28).

Predictors of weight loss have proven elusive. Personality traits,

measures of psychopathology, presence of binge eating, dietary

restraint, and history of weight cycling have all proven unreliable

(103). The process variables of early weight loss and compliance

with self-monitoring are the most useful predictors (103, 104).

Patients who do neither present very poor risk for treatment.

Adherence to an exercise regimen is a reliable correlate of

maintenance of weight loss (105, 106).

Pharmacotherapy

Adding weight loss medications to the behavioral treatment of

obesity results in weight loss 5–20 lbs. greater than that seen with

behavioral treatment alone (107). The majority of weight loss occurs

over the initial 6 months, with most studies showing relative

stability of weight over the ensuing 6 months of medication

treatment. There is little information on the safety or efficacy of

drug treatment for more than 1 year, but studies of longer treatment

indicate that gradual regain occurs in many patients (108, 109).

Weight loss medications are similar to medications used to treat

other chronic medical conditions; that is, they don't work when they

are not taken. The vast majority of studies have found that weight

is quickly regained when medication is discontinued (107).

Therefore, it makes little sense to use obesity medications short

term, in the hope that they will provide a " jump start " for patient

motivation.

After the 1992 publication of the Weintraub study (110), showing the

efficacy of long-term use of fenfluramine/phentermine therapy, an

exponential increase in the use of these agents occurred (111). The

subsequent finding that the serotonergic reuptake and releasing

agents fenfluramine and dexfenfluramine were associated with

valvular insufficiency led to their withdrawal from the market

(112). The lesson learned is that treatments have potential risks.

Where the risk-to-benefit ratio of longer-term treatment is largely

unknown, as is the case with many weight loss drugs, the prescribing

physician should have a high threshold for instituting treatment.

For obesity, current recommendations include prescription of weight

loss medications only for patients with a body mass index >30 kg/m2

without or >27 kg/m2 with associated comorbid conditions such as

type 2 diabetes (2). Two medications are currently approved for long-

term use. Sibutramine is a selective serotonin and norepinephrine

reuptake inhibitor whose efficacy is similar to that of other single-

drug treatments (113). In short-term studies, it has not been

associated with valvular heart disease (114). The primary limiting

factors for its use are elevations in pulse and blood pressure,

which are usually modest, but can be significant in some patients

(115). Another new weight-loss medication, orlistat, is a

gastrointestinal lipase inhibitor, which leads to approximately one-

third of ingested dietary fat being excreted in the stool (116). Its

efficacy for weight loss and weight maintenance is similar to that

of other obesity drugs, and it appears to have favorable impact on

obesity-related comorbidity (109). Side effects are

gastrointestinal, such as loose stools and oily spotting, and are

related to the amount of dietary fat ingested, which may aid in

adherence to a low-fat diet. Fat-soluble vitamin absorption is also

decreased, and multivitamin supplementation is recommended. Other

medications, including leptin, are in earlier stages of development,

and are likely to be years away from approval.

Older medications used to treat obesity, including phentermine (half

of the " fen/phen " combination), phendimetrazine, mazindol, and other

adrenergic agents are not approved for long-term use. The use of

SSRIs as weight control agents has shown disappointing results.

Regarding combination therapy, there have been few controlled

studies demonstrating the safety or efficacy of any drug combination

for the treatment of obesity, including fluoxetine/phentermine,

orlistat/phentermine, or others. The combined use of medications,

except in the context of clinical studies with full informed

consent, should be discouraged (107).

The NIH Clinical Guidelines on the Identification, Evaluation, and

Treatment of Overweight and Obesity in Adults provides guidance on

acceptable use of weight loss medications in the treatment of

obesity. The guidelines may be downloaded from

http://www.nhlbi.nih.gov/guidelines/obesity/ob_home.htm.

Surgery

Gastrointestinal surgery appears to be the most effective treatment

for some severely obese individuals with class III obesity (body

mass index of 40 kg/m2 or more) or class II obesity (body mass index

of 35–39.9 kg/m2) with comorbid medical conditions such as sleep

apnea or type 2 diabetes. The most commonly used procedures are

gastric bypass (e.g., Roux-en-Y gastrojejunostomy) and gastric

restriction (e.g., vertical banded gastroplasty). On average,

patients maintain a weight loss of 25%–40% of their preoperative

body weight after these procedures (117). Lipectomy and liposuction

are cosmetic procedures that do not yield medically significant

weight loss (118).

It is important for prospective patients to realize a number of

things. As with any major surgery, there are operative mortality

risks estimated at 0.3%–1.6% in specialized centers, short-term

complications such as peritonitis and anastomotic leaks in 1.6%–2.3%

of patients, and long-term complications such as cholelithiasis and

vitamin and mineral deficiencies, which can be minimized with

careful management (119). In addition, after surgery, patients are

no longer able to eat in the way they were accustomed to. Those who

have undergone gastric bypass experience " dumping syndrome "

(sweating, palpitations, lightheadedness, nausea) if they ingest

significant amounts of calorically and osmotically dense food, and

therefore become conditioned not to eat these foods. Patients who

have had gastric restriction surgery are unable to eat more than a

limited amount of food at a single sitting without vomiting, and

thus must eat several small meals per day to maintain adequate

nutrition. Patients also must understand that following surgery,

lifelong medical surveillance is a necessity (2).

The Swedish Obese Subjects study, a large-scale nonrandomized study

of surgery versus conventional treatment, provided the most

compelling evidence for the benefits of surgery. In that study,

1,600 patients followed for a mean duration of 4 years after surgery

experienced much greater sustained weight loss and a lower incidence

of diabetes mellitus compared to control subjects. Unlike patients

receiving conventional treatment, the surgical patients also

reported dramatic short-term and sometimes long-term improvements in

health-related quality of life (86). However, most reports suggest

that 20%–30% of the patients were unimproved in the long term (119,

120). It is possible for patients to eat in a way that maintains

their preoperative weight or to be unable to adapt to the

limitations imposed by surgery, e.g., to repeatedly eat to the point

of vomiting. We cannot yet predict with confidence which patients

are likely to have poor outcomes, although some evidence has

suggested that the presence of an eating disorder before surgery

(121, 122) or history of inpatient psychiatric treatment (123)

predict less favorable outcome.

Psychotherapy

Psychotherapy should not be considered a primary treatment for

obesity. However, this does not mean that psychotherapy has no role.

Both cognitive behavioral therapy and interpersonal therapy have

been found to be effective in normalizing eating and reducing

distress in obese patients with binge eating disorder, although

neither intervention is associated with significant weight loss

(124). Psychotherapy may be helpful in enhancing self-acceptance in

obese patients who have learned to feel ashamed about their weight

and may help patients to cope with the effects of prejudice

and " weightism " that are pervasive in our culture. Often, greater

self-acceptance and the resulting increase in overall self-esteem

are key steps in developing motivation for working toward a

healthier lifestyle and/or for undertaking weight control treatment

(125). Body image therapy programs have been developed to help obese

individuals alter the way they perceive and evaluate their bodies

(126). These interventions are crucial for many obese patients,

because most such patients, even after successful weight loss

treatment, remain at a higher-than-normal weight. Self-help

organizations that promote size acceptance provide recognition and

support for obese individuals and serve as a forum for addressing

discrimination and altering harmful cultural stereotypes.

Integrated Treatment

Behavioral treatment to improve diet and increase physical activity

is the cornerstone of any weight loss treatment program regardless

of the degree of obesity. If additional treatment is indicated,

because of more severe obesity, medical complications, or lack of

response to behavioral treatment, other modalities, such as

medications or surgery, may be added. Effective treatment may be

provided in various settings. Although university and hospital-based

programs often provide the most comprehensive care, commercial, work-

site, and self-help programs that incorporate behavioral principles

may also be appropriate for many individuals. It is likely that

there will be increasing use of brief physician or nurse visits to

manage obesity, using materials developed by federal agencies and

other organizations (2).

DO STRATEGIES EXIST FOR EVALUATION AND TREATMENT OF PSYCHIATRICALLY

ILL OBESE PATIENTS?

Initial Evaluation

Because some studies of clinical groups of obese patients report

unexpectedly high rates of depressive and anxiety disorders (127,

128), the clinician should be particularly careful to screen for

these disorders, even if they are not suggested by the initial

complaint. Obese individuals, even those who are seen for treatment

of a condition unrelated to their weight, are at increased risk of

suffering from binge eating disorder. Therefore, it is important to

inquire about problematic eating patterns, loss of control related

to eating, and weight control practices, including dieting,

exercise, diet pills (prescribed, over-the-counter, and illicit), or

various forms of purging after eating. Is the patient caught in a

cycle of " crash dieting " followed by weight regain and further

demoralization? If the patient is exercising, is the need to

exercise interfering in any way with occupational or interpersonal

functioning? It is crucial to assess the patient's attitudes toward

his or her weight and shape. Is the patient's obesity a source of

shame, and does the patient avoid particular activities (e.g.,

parties, shopping for clothes)? Has the patient experienced

discrimination in social or occupational settings? Finally, it is

important to ascertain whether the patient is receiving adequate

medical care (129). Obese patients may avoid doctors because of fear

of being criticized or humiliated about their weight. It is

particularly important to inquire about gynecological care; obese

women may experience particular anxiety related to gynecological

exams and may therefore avoid routine care. A discussion of the

patient's anxiety and referral to an understanding practitioner may

be invaluable.

Cognitively Impaired Patients

Although weight control strategies have not been systematically

evaluated in obese patients with impaired cognition and/or

psychosis, a small number of open studies and case reports suggest

that weight-reducing diets (130), behavioral programs (131–134), and

even surgery (135) can be successful in some individuals. The

risk/benefit calculation of weight loss treatment in this population

is even more complex than for psychiatrically well persons, but

these studies make the important point that the possibility of

weight loss in cognitively impaired individuals should not be

dismissed out of hand.

Patients Receiving Psychotropic Agents

An open discussion of the possibility of weight gain and, should

significant weight gain occur, a discussion of the pros and cons of

continued treatment and the options for management are crucial in

promoting collaboration rather than treatment nonadherence. Overall

strategies include dose adjustment or a switch to an alternative

medication in the same class that is less associated with weight

gain. If these maneuvers are impossible or ineffective, the stepped-

care approach to obesity management outlined above should be

considered, and the clinician should take into account the patient's

ability to adhere to recommendations, e.g., exercise or dietary

regimens. Education and consciousness raising, e.g., the importance

of drinking noncaloric or low-calorie rather than high-calorie

fluids, is a relatively simple and potentially helpful intervention.

For patients with antidepressant-induced weight gain, some

clinicians report success with adding SSRIs, bupropion, or

psychostimulants to the primary antidepressant. This addition may

serve as an antidepressant augmentation strategy as well as a weight

control maneuver (136).

OBESITY TREATMENT: WHERE ARE WE HEADED?

Given the lack of effective treatments for adults, prevention is all

the more a priority. Primary prevention of obesity is likely to

require significant environmental manipulations that could be

brought about only through changes in public policy (137). If we

cannot do this, we must intervene as early as possible. In striking

contrast to the discouraging long-term results of treatment studies

with adults, studies have shown lasting maintenance of weight loss

in the treatment of obese children (101). Care must be taken,

however, to ensure that obese children receive adequate nutrition

and do not engage in the dysfunctional type of dieting that has been

linked to the development of bulimia nervosa. It will be important

to encourage sensible eating habits, increased physical activity,

and development of healthy body-related attitudes (102).

Another response to the poor long-term outcome of treatment has been

the call to reassess therapy goals. Brownell and Wadden (138) have

proposed that we abandon traditional weight loss goals based on

weight tables in favor of what they describe as " reasonable weight. "

Significant health benefits are associated with relatively modest

weight losses that fall far short of the healthy ideal and patients'

own aesthetic ideals (84). Unfortunately, many if not most patients

will find such modest weight loss goals unsatisfying, even

unacceptable (139). Appearance-driven concerns, rather than health

needs, continue to motivate obese individuals to lose weight.

Societal pressures reinforce these appearance-driven concerns by

portraying obese individuals in a negative manner. In addition, some

patients believe that they need to lose far more than 10% of their

weight to attain significant health benefits.

The challenge to health care providers, particularly mental health

professionals, is clear. It is important to help obese people build

self-esteem and encourage them to lead as full a life as possible,

regardless of their weight and of whether they succeed in efforts at

weight control. " Nondieting " programs have demonstrated that

significant gains in self-acceptance are possible even in the

absence of weight loss (T.A. Wadden, personal communication, 1998).

Enhancing self-acceptance may not only provide a more compassionate

approach to what has proved a refractory problem, but might also

lead to more lasting reductions in weight by virtue of helping

patients to accept only modest weight loss and improve compliance

with health-relevant eating and exercise behaviors (125, 140, 141).

FOOTNOTES

Received Jan. 14, 1999; revisions received June 21 and Oct. 6, 1999;

accepted Oct. 18, 1999. From the New York State Psychiatric

Institute and the Department of Psychiatry, Columbia University

College of Physicians and Surgeons; the Obesity and Eating Disorders

Program, National Institute of Diabetes and Digestive and Kidney

Diseases, Bethesda, Md.; and the Rutgers Eating Disorder Clinic,

Rutgers University, Piscataway, NJ. Address reprint requests to Dr.

Devlin, New York State Psychiatric Institute, Unit 116, 1051

Riverside Dr., New York, NY 10032; mjd5@... (e-mail).

Supported by NIMH grant MH-54612 to Dr. Devlin. The authors thank

Yager, M.D., for help in the conception of this article and for

many helpful comments.