Obesity: types and treatments

Obesity: types and treatments

Mervyn D. Willard

The treatment of obesity carries a high failure rate. Although temporary weight loss may not be difficult to achieve, the weight is usually regained. Patients seeking or needing medical intervention for obesity have usually lost and regained weight many times.

The diagnosis of obesity poses difficulties. A variety of pathophysiologic mechanisms have been identified, and obesity is now considered to be a group of disorders rather than a single clinical entity. The traditional terms “exogenous” and “endogenous” obesity are vague. It is now possible to describe the types of obesity more precisely and in many instances to identify etiologic processes that act singly or in combination to alter energy homeostasis and produce obesity.

Although types of obesity are in the process of being differentiated, these conditions are not yet fully understood. The advantage of classifying the causes of obesity, even if classification cannot yet be done definitively, is that it allows for individualization of treatment based on pathologic processes, which may vary considerably among individuals. Some of the recognized causes of obesity are listed in Table 1.

Types and Causes of Obesity

METABOLICALLY DETERMINED OBESITY

It has long been suspected that a low resting metabolic rate predisposes a person to obesity. Only recently, however, have prospective studies confirmed that a low metabolic rate can predict future adiposity in young adults’ and infants.(2)

The resting metabolic rate traditionally has been calculated using formulas based on body build, age and gender. However, calculated resting metabolic rates are not precise; there can be considerable variation due to genetic differences. Actual resting metabolic rate can be determined by indirect calorimetry, using respiratory gas analysis techniques similar to those employed years ago to determine basal metabolic rate. Modern instruments for this purpose are available in many pulmonary function laboratories. Clinically, a low resting metabolic rate can be suspected when a patient follows a calorie-controlled diet but still has difficulty preventing weight gain. The diagnosis is best confirmed and quantified by indirect calorimetry.

Other causes of a low resting metabolic rate include recent starvation, semistarvation and rigorous dieting. In these instances, short-term suppression of the resting metabolic rate is an adaptive response to dietary restriction. Suppression of the resting metabolic rate has also been noted in persons who skip meals, as compared with those who eat regular meals.(3)

Diminished adaptive thermogenesis may predispose a person to obesity. Although adaptive thermogenesis is a response to overfeeding in many individuals, it is diminished in some. Variation in adaptive thermogenesis is genetically determined. Currently, it is uncertain how much significance adaptive thermogenesis has in the development of obesity. Similarly, thermogenesis induced by meals is diminished in some persons, but the significance of such a response in the development of obesity is unknown.

Other metabolic determinants may further explain the strong genetic component of obesity. For example, a set point for adipose cell size may be metabolically determined. However, theories about adipocyte or total body fat set point require further validation before they can be accepted as mechanisms for obesity.

ENVIRONMENTALLY INDUCED OBESITY

Environmental factors associated with obesity include recreational eating, cultural and family eating patterns, job environments that provide or encourage the use of calorie-dense foods, the social role of eating (e.g., dinner parties), and sedentary patterns of employment and recreation.

Obesity in adolescents has been correlated with television viewing in an almost linear fashion figure. The meaning of this relationship is not clear. It could signify decreased exercise and increased snacking; it could also be an indicator of emotional disturbances that affect weight and television viewing time.

ENDOCRINOPATHIES

Hypercortisolism, polycystic ovaries, hyperinsulinism and growth hormone deficiency are associated with obesity.

In hypothyroidism, both resting metabolic rate and appetite are diminished. Routine thyroid testing is not necessary in obese patients if there is no clinical reason to suspect hypothyroidism.

Although some insulinomas cause obesity, a more common cause is the use of inappropriately high doses of insulin in the treatment of diabetes. In managing the diabetic patient, the physician may become caught in a vicious circle in which an increase in the insulin dosage is followed by weight gain, leading to hyperglycemia, which necessitates an increase in the insulin dosage. Mechanisms by which insulin regulates fat storage are shown in Figure 2.

APPETITE REGULATION ABNORMALITIES

The physiologic regulation of appetite is accomplished by a complex system of checks and balances controlled by the hypothalamus Figure 3). Insatiable hunger is the cause of obesity in rare disorders affecting the hypothalamus, such as Prader-Willi syndrome and mass lesions of the hypothalamus. Apart from hypothalamic diseases, definite and significant disorders of appetite control have not been demonstrated. Big eaters with big appetites usually are not fatter than small eaters; in both instances, the hypothalamus balances the energy equation with a remarkable degree of precision.

Alteration of appetite control occurs as a normal physiologic process in several instances. The hypothalamus makes adjustments for the level of physical activity in a precise linear fashion, except in sedentary persons. Low or sedentary levels of activity are associated with inappropriately increased levels of food intake in animals and humans.

A physiologic alteration in appetite also occurs as a result of food deprivation. The hypothalamus appears to remember periods of deprivation, and compensatory overeating at a later time is the usual consequence.

Appetite alteration and rebound overeating provide an explanation for the “restrained eater” syndrome.(7) Chronic dieters often fail to achieve satiety and are constantly hungry and frustrated. Their self-imposed restraint is fragile; when frustration and hunger break through, rebound overeating occurs. For these persons, parties, picnics, vacations and holidays provide occasions for eating sprees during which they regain the weight they have lost.

Normally, the full complement of adipocytes is reached by puberty and then remains constant. After puberty, adipocytes can increase in mass, but they do not ordinarily increase in number. However, these cells are capable of increasing in size only up to certain limits, with their mass rarely exceeding 1.5 (micro)g. If overeating continues after adipocytes have reached their maximal size, cell proliferation can be triggered Figure 4).

Once proliferation of adipocytes has occurred it cannot be reversed. Thereafter, the only means of achieving weight reduction is to diminish individual cell size. Most diet regimens only reduce adipocyte size down to about 0.4 (micro)g per cell.” Although severe regimens, such as near fasting, temporarily induce a very small cell size and dramatic weight loss, such regimens also induce a number of adaptive mechanisms, including increased appetite, increased use of substrates for fat storage, decreased resting metabolic rate and increased lipoprotein lipase activity.(9,10)

In most types of obesity, adipocyte size enlarges from a norm of about 0.5 (micro)g per cell to 0.7 to 1.0 (micro)g per cell. In morbid obesity, there is a striking increase in the number, as well as the size, of adipocytes, from a norm of about 30 billion to approximately 120 billion.” Because of the increased number of adipocytes, there are limits to the weight loss that can be maintained. In addition, massively obese individuals usually have multiple causes of obesity that need to be addressed if even modest weight losses are to be maintained.

A form of localized adipose cell proliferation occurs in the femoral adipocytes of women. Excessive proliferation of adipocytes around the hips, thighs and buttocks has been called gynecoid, or lower body, obesity Figure 5). This form of obesity is remarkable in that it is not associated with the metabolic complications of obesity that occur in central, or android, obesity, which is the usual pattern of fat distribution(12) Figure 6). Adipose cell proliferation and fat storage in femoral adipocytes appear to be regulated hormonally for the purpose of supporting lactation. During pregnancy, lipogenesis predominates. During lactation, lipolysis predominates in the femoral adipose cells, but not in the abdominal adipocytes. (13) Femoral adipocytes may be more resistant than abdominal adipocytes to weight reduction by the usual forms of treatment; however, this remains to be clearly demonstrated.

COMPULSIVE EATING DISORDERS

When psychologic need, rather than appetite, is the driving influence on eating, overeating and obesity may result. A hallmark of psychologically compelled eating is excessive food intake in the absence of hunger. Compulsive eating disorders include secondary gain, reactive eating and bulimia.

Examples of secondary gain derived from obesity include avoidance of responsibility, using obesity as an excuse; fulfillment of dependency needs; avoidance of sexuality due to emotionally traumatic experiences, and support of a self-image of substantiality or strength. A variety of forms of secondary gain in marital situations have been described by Stuart and Jacobson.”

With reactive eating, the subject of an extensive review by Ganley, (15) eating occurs in response to stress or anxiety. The disorder has also been called emotional eating because, for these individuals, food has an unusual ability to soothe or relieve dysphoric feelings. How the disorder is acquired is not known. Reactive eating appears to be somewhat refractory to treatment, and it is associated with high treatment failure rates in weight loss programs. The disorder is frequently present in patients seeking surgical treatment for obesity.

Bulimia is characterized by binges during which there is a feeling of loss of control and an inability to stop eating. Purging by vomiting is of ten employed to prevent massive weight gain. Other associated features include poor self-esteem, impulsiveness, family stress and undue concern about body image. Binges may be triggered in part by physiologic factors. Dietary restriction and failure to achieve satiety precede binges and probably help drive binges in a cyclic pattern.(16)

PHARMACOLOGICALLY INDUCED OBESITY

Certain drugs are known to affect appetite and metabolic rate. Smoking causes an acute increase in metabolic rate, (17) increased 24-hour energy expenditure and changes in lipogenesis. Whether smoking cessation has a direct effect on appetite is uncertain. The average weight gain in the initial period of smoking cessation is the equivalent of 200 or 300 kcal per day.

Medications that can cause increased appetite, metabolic changes and weight gain include tricyclic antidepressants, phenothiazines, oral contraceptives and glucocorticoids. Habituation to caffeine or alcohol can also cause weight gain as a result of increased consumption of highcalorie cola or alcoholic beverages.

OTHER CAUSES

Cultural ideals set by fashion models are a source of major errors in weight management. Individuals who attempt to reach unrealistic weight goals are constantly on diets, and they inevitably experience hunger and frustration. Rebound overeating usually occurs, followed by more attempts to lose weight.

Frequently termed the “yo-yo” syndrome, weight cycling due to repeated crash dieting cannot be considered benign.”I Although more studies are needed to clarify the dangers of weight cycling, several harmful effects may occur. With each successive weight loss, the resting metabolic rate drops more quickly; consequently, weight comes off with greater difficult Evidence also suggests that lean tissue lost during crash dieting may not be recovered when weight is regained. Thus, body composition can be altered through a series of weight losses and regains. Even if the final weight is in the normal range, an increased percentage of body fat can cause metabolic abnormalities, resulting in the “metabolically obese” individual of normal weight.(19)

Assessment of Obesity Disorders

Numerous factors, acting singly or in combination, may produce obesity. Consequently, the assessment of obesity requires a broad range of diagnostic considerations. History, physical examination and laboratory tests are needed to thoroughly assess the etiology of obesity and to document any medical complications. Dieting history, exercise evaluation, social history, family history of obesity and its complications, and screening for psychopathology are all important aspects of evaluation.

A seven-day diet diary is a valuable source of information for assessment purposes. Even though underreporting of food intake can make quantitative assessment inaccurate, the pattern of eating helps characterize causes of obesity in the individual patient. Types of obesity suggested by diet diary findings are listed in Table 2. Treatment Strategies

The treatment goal of medically significant obesity is permanent reduction of weight to a level that reverses or minimizes medical complications. Weight loss by itself is not a worthwhile treatment goal, because weight is often regained.

Achievement of standard weights published in tables may be cosmetically desirable but may not be medically necessary to reverse complications. In many patients, moderate weight loss can reverse or control medical complications and is more easily maintained than drastic weight loss.

DIAGNOSIS-SPECIFIC INTERVENTION

The choice of treatment can be guided by characterization of the causes of obesity in the individual patient (Table 3). When underlying disease or pharmacologic effects are present, correction of these problems is the primary form of treatment. A low resting metabolic rate in a euthyroid patient with no recent episodes of rigorous dieting is treated with diet and exercise. To achieve energy equilibrium, caloric intake is matched to the resting metabolic rate, and exercise may be used to liberalize the diet or to induce weight loss.

Primary treatment for compulsive eating disorders is psychologic therapy. Long-term success cannot be expected without resolution of the psychodynamic forces that are driving the behavior. If marital issues are involved, couple therapy is appropriate.

DIETARY TREATMENT

A weight-loss diet (e.g., a 1,200-kcal diet) by itself is not an adequate form of treatment, because it does not address or correct the underlying causes of obesity. For the same r-easons, most commercial and popular diets have limited application.

The first requirement of dietary instruction is that it be individualized for each patient and family situation. A second requirement is permanence, since going on and off diets is counterproductive.

For restrained eaters, a key component is the incorporation of satiety strategies. Dietary strategies that enhance satiety include eating slowly, avoiding calorie dense foods, using soups at the beginning of meals and drinking beverages, such as tea, to terminate eating. Proteins and complex carbohydrates are emphasized, since these foods produce satiety and are stored less efficiently as fat than are high-fat foods.

The problem of satiety has not yet been solved by anorexiant drugs. At present, these drugs have little or no place in the management of obesity.

Dietary compliance is enhanced by use of the simplest regimen needed to accomplish the result, careful patient and family education, stepwise introduction of dietary change and behavior modification if available. Even with simple diets, the addition of behavior modification strikingly improves compliance.(20)

BEHAVIOR MODIFICATION

The techniques of behavior modification have wide application, but they are most commonly targeted at environmental inducements for overeating. If environmental inducement is a primary or contributory problem, behavior modification is useful.

Behavior modification groups typically meet weekly for eight to 16 sessions with a skilled therapist. Multiple issues are addressed, such as shopping, scheduled and unscheduled eating, stimulus control, exercise, and dealing with lapses and reversals. Family involvement is encouraged. Growing evidence suggests that the family, not the individual, is the appropriate unit of behavior modification.(21,22)

Of the conservative forms of obesity treatment, behavior modification has had the most sustained success.(23)Nevertheless, after four or five years, most of the weight loss that occurs as a result of behavior modification is regained.(21)Improved outcomes may be achieved by ongoing or periodic review sessions and by more direct family involvement from the beginning of treatment. If environmental inducement is not the primary cause of obesity, behavior modification by itself may not be effective treatment.

Aerobic exercise builds cardiovascular fitness and regulates weight, but longterm compliance with this type of exercise In weight control, regularity of exercise is more important than intensity. For example, although daily walks may increase total energy expenditure by only 200 to 300 kcal per day, this type of regular exercise can ease dietary restrictions and help normalize appetite.

Exercise also helps preserve lean tissue during weight loss. Low-intensity exercise appears to be as effective as high-intensity exercise in preserving lean tissue.(25)

Gastroplasty is reserved for massive or morbid obesity that has been refractory to other forms of treatment. Vertical banded gastroplasty is the procedure of choice. By itself, this procedure does not produce dramatic results, and long-term success rates have been modest. If gastroplasty is to be successful, the patient still must use discretion in food choices.

Liposuction (suction lipectomy) is a cosmetic surgical procedure for removing excess lowerbody fat in gynecoid obesity. For this least malignant of all the obesities, liposuction may constitute the most effective treatment, provided continuing follow-up studies do not show recurrence. This surgical treatment can be considered specific to gynecoid obesity, since in this disorder, unlike almost all other forms of obesity, the offending tissue is truly localized. The Problem of Relapse

The tendency to relapse has been a problem of such regularity that obesity has been compared to addictive disorders, such as alcoholism and cigarette smoking. However, food does not appear to be addictive in the same manner as cigarettes and alcohol. Metabolic effects, appetite regulation and the phenomenon of rebound overeating may account for recurrence of obesity, and these problems need to be managed accordingly.

Two factors associated with relapse stand out in reviews(26,27): (1) an unwillingness to undertake regular exercise and (2) a lack of social support. Social support is a component of most behavior modification groups, but groups cannot be maintained indefinitely. Commercial diet clubs such as Weight Watchers provide social support, but this support is only temporary, since the attrition rate from diet clubs is exceedingly high.(28)

Active marital support is perhaps the strongest single predictor of long-term success reported in the literature.(29,30) Lack of such support appears to be prevalent and may partly account for high relapse rates. Weak or inactive marital support suggests the presence of secondary gain issues or deranged family dynamics. Presumably, couple therapy or family therapy, when indicated, would improve relapse rates; however, the usefulness of these forms of treatment has yet to be demonstrated in clinical trials.

Other factors that contribute to relapse or treatment failure include unrealistic goals, nonspecific interventions, insufficient knowledge about the pathophysiology and treatment of many types of obesity and, in many locales, unavailability of behavior modification groups, skilled educators and therapists.

Patient factors that contribute to relapse or treatment failure include expense, low motivation, depression and unwillingness to undertake treatment, especially psychologic treatment, when indicated. The effects of environmental factors may be relentless. Initially, obese patients may cope successfully. However, in succeeding years patients may regain weight as environmental influences continue to exert their effects.

Final Comment

A number of factors that contribute to failure in the treatment of obesity are beyond the physician’s control. Thus, the role of the family physician is to advise patients about ineffective treatments and guide them to the most effective forms of treatment presently available, based on a careful assessment of the causes of obesity in the individual patient.

REFERENCES

1. Ravussin E, Lillioja S, Knowler WC, et al.

Reduced rate of energy expenditure as a risk

factor for body-weight gain. N Engl J Med

1988;318:467-72.

2. Roberts SB, Savage J, Coward WA, Chew B,

Lucas A. Energy expenditure and intake in

infants born to lean and overweight mothers.

N Engl J Med 1988;318:461-6.

3 .Callaway CK Pemberton C. Relationship of

basal metabolic rates to meal-eating patterns.

In: Hirsch J, Van Itallie TB, eds. Recent advances

in obesity research. Proceedings of the

4th International Congress on Obesity. London:

Libbey, 1985:50A.

4. Poehlman ET, Tremblay A, Despres JP, et al.

Genotype-controlled changes in body composition

and fat morphology following overfeeding

in twins. Am J Clin Nutr 1986;43:

723-31.

5 .Dietz WH Jr, Gortmaker SL. Do we fatten our

children at the television set? Obesity and television

viewing in children and adolescents.

Pediatrics 1985; 75:807-12.

6 .Brownell KD, Stunkard Aj. Physical activity

in the development and control of obesity. In:

Stunkard AJ, ed. Obesity. Philadelphia: Saunders,

1980:300-24.

7. Herman CP, Polivy J. Restrained eating. In:

Stunkard Aj, ed. Obesity. Philadelphia: Saunders,

1980:208-25.

8. Bjorntorp P, Carlgren G, Isaksson B, Krotkiewski

M, Larsson B, Sjostrom L. Effect of

an energy-reduced dietary regimen in relation

to adipose tissue cellularity in obese women.

Am J Clin Nutr 1975;28:445-52.

9. Callaway CW. Biologic adaptations to starvation

and semistarvation. In: Frankle RT, Yang

MU, eds. Obesity and weight control: the

health professional’s guide to understanding

and treatment. Rockville, Md.: Aspen, 1988:

97-108.

10. Eckel RH, Yost Tj. Weight reduction increases

adipose tissue lipoprotein lipase responsiveness

in obese women. J Clin Invest 1987;80:

992-7.

11. Van Itallie TB, Kral JG. The dilemma of morbid

obesity. JAMA 1981;246:999-1003.

12. Kissebah AH, Vydelingum N, Murray R, et

al. Relation of body fat distribution to metabolic

complications of obesity. J Clin Endocrinol

Metab 1982;54:254-60.

13. Rebuffe-Scrive M, Enk L, Crona N, et al. Fat

cell metabolism in different regions in women.

Effects of menstrual cycle, pregnancy, and lactation.

J Clin Invest 1985;75:1973-6.

14. Stuart RB, Jacobson G. Weight, sex, and marriage:

a delicate balance. New York: Simon &

Schuster, 1987.

15. Ganley RM. Emotion and eating in obesity: a

review of the literature. Int J Eating Disord

1989;8:343-61.

16. Polivy J, Herman CP. Dieting and binging. A

causal analysis. Am Psychol 1985;40:193-201.

17. Perkins KA, Epstein LH, Stiller RL, Marks

BL, Jacob RG. Acute effects of nicotine on

resting metabolic rate in cigarette smokers.

Am J Clin Nutr 1989;50:545-50.

18. Blackburn GL, Wilson GT, Kanders BS, et al.

Weight cycling: the experience of human dieters.

Am J Clin Nutr 1989;49(5 Suppl): 1105-9.

19. Ruderman NB, Schneider SH, Berchtold P.

The metabolically-obese,” normal-weight

individual. Am J Clin Nutr 1981;34:1617-21.

20. Nugent CA, Carnahan JE, Sheehan ET, Myers

C. Salt restriction in hypertensive patients.

Comparison of advice, education, and group

management. Arch Intem Med 1984;144:

1415-7.

21. McVoy JH. Family fat: assessing and treating

obesity within a family context. In: Harkaway

JE, ed. Eating disorders. Rockville, Md.:

Aspen, 1987:71-83.

22. Epstein LH, Valoski A, Wing RR, McCurley

J. Ten-year follow-up of behavioral, family based

treatment for obese children. JAMA

1990;264:2519-23.

23. Stunkard Aj. Conservative treatments for

obesity. Am J Clin Nutr 1987;45(5 Suppl):

1142-54.

24. Kramer FM, Jeffery RW, Forster JL, Snell MK.

Long-term follow-up of behavioral treatment

for obesity: patterns of weight regain among

men and women. Int J Obesity 1989; 13:123-36.

25. Ballor DL, McCarthy JP, Wilterdink Ej. Exercise

intensity does not affect the composition

of diet- and exercise-induced body mass loss.

Am J Clin Nutr 1990;51:142-6.

26. Brownell KD, Marlatt GA, Lichtenstein E,

Wilson GT. Understanding and preventing

relapse. Am Psychol 1986;41:765-82.

27. Foyeyt JP. Issues in the assessment and treatment

of obesity. J Consult Clin Psychol 1987;

55:677-84.

28. Volkmar FR, Stunkard Aj, Woolston J, Bailey

BA. High attrition rates in commercial weight

reduction programs. Arch Intern Med 1981;

141:426-8.

29. Fischmann-Havstad L, Marston AR. Weight

loss maintenance as an aspect of family emotion

and process. Br J Clin Psychol 1984;23(Pt

4):265-71.

30. Pearce JK LeBow MD, Orchard J. Role of

spouse involvement in behavioral treatment of

overweight women. J Consult Clin Psychol

1981;49:236-44.

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