Evaluation and Treatment of Obesity
Author: Michael T. Railey, MD, Faculty Family Physician, Deaconess Health System, and Assistant Professor of the Department of Community and Family Medicine, Director of the Third Year Clerkship, Saint. Louis University School of Medicine, St. Louis, MO.
Peer Reviewer: Randall Flanery, PhD, Director, Weight Management Program, Saint Louis Behavioral Medicine Institute, St. Louis, MO.
Editor’s NoteOne of the most frustrating dilemmas of the primary care physician is the successful management and treatment of obesity.1 The problem of weight gain is intimately interwoven in the etiology and/or treatment of many major illnesses. These include diabetes, hypertension, renal disease, cardiovascular disease, dyslipidemias, and even osteoarthritis.2-5 (See Table 1.) We battle not only with the problem itself, but also with the habits, cultural mores, and genetic make-ups of the patients we see. It is estimated that $35-40 billion in economic costs was spent during the 1980s on weight reduction and obesity- related products, as America wages its "battle of the bulge."6 More than one-third of Americans are overweight, and many more children are in a greater state of physical unfitness than has been the case in recent years.7
When are drugs indicated in the treatment of obesity? Is surgery ever an option? Why are we fatter now than ever before? What portion of overweightness can be attributed to genetics? What is the most successful approach to treatment? These questions and many others will be addressed in this article as current thoughts, studies, and trends in regard to diagnosis, treatment, and long-term management are reviewed. Significant research will also be discussed in the arena of genetics, including an update on the present fund of knowledge.
Despite our increase in general medical knowledge and health care technology, America has become fatter and fatter over the last 2-3 decades.8 Obesity is a true epidemic in this country. Surveys confirm that the sedentary lifestyle combined with the great availability of tasty, rich, fatty, and cheap foods are highly contributory to the problem. Overweight prevalence increased 8% between 1976 and 1980.8 In the period 1988-1991, 33.4% of United States adults age 20 and older were estimated overweight.8 In 1995, the former Surgeon General C. Everett Koop declared obesity to be a major health problem.24 Over the last 10 years, the percentage of Americans who are overweight has increased from 25% of the population to 33%. It is important to note that certain groups in the population are at greater risk. Women have a higher prevalence of obesity than men do.4,5,8 Black women have the highest prevalence of all in the United States, with 48.6% being overweight.8 They are followed closely by Mexican-American women, with 46.7% being overweight. For all ethnic groups in the United States combined, 31% of adult men and 35% of adult women are estimated to be overweight. Data from the National Health and Nutrition Examination Survey (NHANES III) found that 21% of adolescents were overweight.8 Using the Metropolitan Life Insurance Company desirable weight tables, a 1996 Harris Poll found that 74% of respondents were overweight, compared to only 59% of respondents in 1986.9 One problem in obtaining accurate statistics regarding this problem is the variety of ways to ascertain the diagnosis. The NHANES study uses the Body Mass Index (BMI) to determine obesity. BMI = weight (kg)/height (m2) This calculation results in a standard of 27.8 or more for men and 27.3 or more for women as a cutoff point for overweight.8 Once BMI reaches 30, a status of morbid obesity is defined. (See Table 2.) Research studies have consistently identified a J-shaped relationship between BMI and overall mortality.10
Another measurement of obesity is the waist to hip ratio. An acceptably normal value of waist to hip ratio is less than 1.0 for men and less than 0.85 for women. Higher ratios indicate greater upper-body and abdominal fat, which has been associated with increased risk of obesity-related illnesses.11-14 Subcutaneous skin fold measurements are also used to measure fat distribution.25 The most common measurements for peripheral fat evaluation are triceps, biceps, and thigh. CT scans and MRI scans have recently been suggested to measure visceral fat, but these modes of evaluation are costly and impractical.
The causes of the overweight syndrome are multifactorial. In the past, a lack of will power and laziness were thought to be the primary explanations.13 We now more accurately divide causes into genetic, behavioral, and environmental arenas.
Genetic. There may be more than 30 genes associated with fat deposition. Only 12 seem to be associated with appetite.15-17 The Ob gene produces a protein called leptin, which has been demonstrated to decrease fat when given exogenously to mice.16 The Ob gene is a candidate for genetic predisposition to extreme obesity.23 Studies have shown that an individual’s body size is in part genetically coded as surely as eye color. The weight to which our bodies gravitate is like a preselected temperature on a thermostat. As we await human studies in this area, it is generally agreed that genetics plays a major role in fat deposition, probably comprising at least 40% of the total picture.25
Behavioral. Behavioral abnormalities commonly manifest themselves in eating habits. The tendency for binge eating, stress-related overeating, and participating in fad diet plans can contribute to the overweight syndrome. Learned cultural habituations and even economic status have been tied to obesity in many research projects. Kelley describes differences in physical activity of young black adults compared to whites, implying greater risk for later obesity.18-21 The number of daily hours of television watching has also been shown to correlate with the overweight syndrome.22 What is certain is that no program of weight loss will lead to permanent success without behavior modification. Self motivation and commitment is required and should be encouraged by the treating clinician.
Environmental. Evidence supports that obese people eat more food than non-obese people, and relationships have been identified associating overweight with environmental factors.25-27 This includes the type and amount of exercise, the amount and composition of the food eaten, the individual’s metabolism, and the time of day and speed with which the food is consumed. Studies have found that 60% of Americans are sedentary, and fewer than 1 in 10 Americans exercises at levels sufficient for cardiorespiratory benefits.20,21 These factors are also influenced by environment. Further, epidemiologic studies have found that the environment of obese parents can contribute to higher incidence of obesity, and 75% of obese adolescents become obese adults.28,29 Obesity during childhood is not as effective a predictor of adult obesity as is adolescent obesity.
Bray et al demonstrated that the relationship between relative weight (expressed as BMI) and mortality is a J-shaped curve.10 There is a small increase in mortality risk with BMI values between 27 and 30, a greater increase with values between 30 and 35, and a high risk with a BMI above 35. Not only is the total amount of fat important, but also where the fat is distributed. Numerous cross-sectional studies show that fat in a central or upper body (android) distribution is a health risk. The importance of regional obesity has been explored in many studies.12 Egger concludes in his review that the association between waist to hip ratios and risk indicators appears to be independent of sex, race, and age.11 Pouliot et al measured plasma glucose and insulin levels in non-obese and obese patients matched with low or high levels of visceral fat. In the presence of high visceral abdominal fat, hyperinsulinemia was found. This was important because there is suggestive evidence that high insulin levels are a risk factor for hypertension and coronary artery disease.31 In general, the larger the abdominal adipose mass, the higher the overall mortality.11,12,25,30 Physiologically, when we ingest a meal, it is more efficient for the body to convert dietary fat to body fat than it is to convert carbohydrate or protein to body fat. Knowing this, we must avoid high fat consumption. As a rule, we should ingest no more than approximately 30% of our total calories per 24 hours in fat.17,25 When we eat a fatty meal, gastric motility is reduced, and a large meal of 50 g of fat so retards emptying that five hours later fat is still found in the stomach from that meal. Obesity predisposes to development of abnormal levels of circulatory lipids. In studies involving obese high visceral fat women, compared to obese low visceral fat women, there were higher levels of total cholesterol and LDL cholesterol. HDL cholesterol type was reduced. This is associated with greater risk for atherosclerosis and coronary artery disease.2,3,31
Obesity increases risk for diabetes and hypertension.3,4,12 In the Canadian Family Survey, body mass index was correlated with systolic hypertension demonstrating increased risk with weight increase. Chan et al showed strong positive association between overall obesity and risk of diabetes. There is also an increased risk of certain kinds of cancer with increased obesity.2,3 For women, the major risk is for endometrial cancer.3 Increases in relative risk of 2.0-3.5 are reported in women with BMI of 28-30. Obesity also has other complications. Increased weight bearing can lead to exacerbation of osteoarthritis. Inadequate chest wall mobility in the morbidly obese can lead to carbon dioxide retention and pulmonary insufficiency. If these symptoms become severe enough, the sleep apnea syndrome could result.
Obesity is a complex disease and therefore must be managed on many fronts. Comprehensive treatment involves diet, exercise, behavior modification, and, in some cases, drugs and or surgery. Relapses in treatment success are common, and the physician should prepare to remain encouraging and transmit a sense of hope to the patient. It is recommended to have a realistic goal for the patient seeking to lose weight. Those in weight loss programs need to know that they are not expected to look like high school cheerleaders again. Ten percent weight loss from starting point is a good and obtainable beginning goal. If so desired, new goals can be repeatedly reset and obtained. In the few studies available following patients for longer than two years, the trend has been to regain weight by the fifth year following weight loss.25,32 Emphasis must be placed on the maintenance phase and again on having realistic expectations and short-term goals leading to that result.
Diet. In prescribing a dietary program, the first step is a complete dietary history to determine the types of food digested and the circumstances surrounding daily eating. Many of the patients in my practice eat excessively in direct relationship to chronic frustrations over life issues. This is often only brought out by a skillfully executed history. After the thorough history is completed, it is very important to establish what the basal energy requirement is and base the new dietary intake upon a reduction from this level. There are many ways of determining this value, but the most useful formula is listed in Table 3. Requirements are different for men and women, and an activity factor is used. Once the daily energy requirement is obtained, it follows that weight loss should occur when a 500-1000 calorie reduction per 24 hours of intake is maintained. Reducing intake by 3500 calories results in approximately one pound of fat loss. Therefore, a person taking in 2500 calories per day should be counseled to take in only 1500-2000 calories per day. Over a period of seven days, a 500 calorie reduction per day results in approximately one pound of adipose tissue lost. The patient must be educated in regard to selection of high- and low-fat foods, with reduction of daily fat intake to no more than 30% of total calories.25 Fiber should be increased to 20-30 g/d. This approach would be acceptable with the Recommended Dietary Guidelines provided by the Departments of Agriculture and Health and Human Services. The goal is to produce no more than 1-2 pounds per week weight loss. Remember that more weight may come off from fluid loss the first few days. Adequate protein, vitamins, and minerals should be maintained. Very-low-calorie diets are not recommended as a rule.
Exercise. Studies show that 66% of Americans do not exercise on a regular basis.14,20,21 Time- and energy-saving devices that have become a part of everyday life have contributed greatly to this sedentary lifestyle. Along with the many positive contributions exercise makes in improving cardiovascular function and diminishing dyslipidemias, exercise promotes a sense of well-being and a feeling of being in control over a portion of the environment. This is helpful in staving off and even treating some forms of milder depressions. It should be noted that activity on the job may not be sufficient to burn adequate calories. One study revealed that patients’ perceptions of how much they exercise and eat are usually far off from actual reality. Once again, a careful and detailed history of both routine and structured exercise activities must be obtained.
It is known that to improve cardiovascular fitness it is necessary to exercise with enough intensity to reach 60-70% of maximum heart rate (see Table 4) and sustain this for 30 minutes at least 4-5 days per week.25,28,29,35 Many are miseducated to believe that their "weekend warrior" activity should be sufficient for adequate exercise. Consistency is the key, and long-term maintenance of modifications of routine activity is a necessity. Walking to the mailbox instead of driving, taking stairs instead of elevators, and commuting by walking to a bus or rail station, are examples of just a few modifications that need to be made. Selecting an exercise that is fun is very helpful, and, if possible, that activity should be performed outside of work. We must emphasize again the need to structure activities for long-term maintenance. Patients with physical disabilities and/or arthritis may need to select different types of exercise such as water aerobics, cycling, or swimming.
Behavior Modification. Successful long-term weight loss cannot be accomplished without behavior modification. The literature is replete with information bearing witness to the critical need for permanent changes in habits, the gradual shifting of food preferences, and the substitution of behaviors that are calorie-burning and not calorie-consuming. Investigators have studied behavioral correlates, and, in black females, Kumanyika et al demonstrated that attitudes can also affect body mass index, in that some cultures do not have the same stigma for overweight as others.33,34 This could have an effect on motivation to cut fat intake and calories. Greater than 90% of patients seen in my practice who are obese skip breakfast or eat irregularly. High-calorie and high-fat/high-salt containing fast foods need to be markedly reduced.
Group treatment of obesity is very helpful in regard to behavior modification. Small focus groups headed by a physician, a dietician, or an informed provider serve the purpose of offering an arena to encourage lifestyle modifications that can result in permanent changes. Areas that need to be addressed include stress management techniques, portions of food, nutritional education, exercise programs, handling emotional issues, cooking, shopping routines, and family matters. (See Table 5.) These groups should be long-term (4-6 months) and consistently attended. More serious eating disorders such as forms of anorexia, bulimia, and binge eating should have appropriate referral.
There are many options to be used in the treatment of obesity. Most authorities agree that dietary changes coupled with behavioral modification and exercise is preferred. But, there are cases in which drug intervention becomes useful and even necessary. Twenty-five years ago, amphetamines were still in use as anorexiants, but the drug abuse potentials were so great that their usage became frowned upon. Practice habits vary among physicians, but those who deal with obesity often try to only consider the use of medications when the BMI is greater than 30 or greater than 27 with at least one co-morbidity factor such as diabetes or hypertension. Even then, the patient should have documented some legitimate effort at diet and exercise with close supervision. When drugs are prescribed, the combined management approaches discussed earlier should be encouraged and put into place.
The lipostatic theory, which is currently highly regarded by investigators, holds that signals from the body’s fat depots are transmitted to the central nervous system, then to hypothalamic areas that regulate satiety. There are approximately 40 neurotransmitters discovered so far. There are 12 thought to be associated with eating behavior. Most treatments involve three neurotransmitters: dopamine, norepinephrine, and serotonin. Two classes of drugs are currently most commonly used in the treatment of obesity. They are the noradrenergics and the serotoninergics. There is a current renewal of interest in using drug intervention that has been triggered by the long-term study of Weintraub and colleagues.38,39 In this study, phentermine, a noradrenergic agent, was combined with a serotonergic drug, fenfluramine. This trial has been used as evidence of the efficacy of medications to treat obesity. Patients did lose modest amounts of weight, but in order for weight loss to be maintained, continued use was required. In April of 1996, for the first time in 23 years, the FDA approved dexfenfluramine, another antiobesity drug. It is indicated for use in persons with a BMI of 30 or greater, or a BMI of 27 with at least one comorbid factor.36,37 Dexfenfluramine is currently the only FDA-approved antiobesity drug for long-term use. I recommend the use of the "fen-phen" regime only in rare cases and then for a short term period of time, no longer than three months, while intensive behavioral modification is being used, along with exercise and diet retraining. Table 6 lists currently approved and classified anorexiants and their doses. Side effects associated with dexfenfluramine include diarrhea, dry mouth, and lethargy. As with other anorectic agents, there is an extremely rare chance of primary pulmonary hypertension (usage of drug changes incidence to 23-46 per million compared to 1 or 2 per million in general population). Recently, some evidence has emerged regarding the possibility of valvular heart disease associated with the use of the combination of phentermine and fenfluramine. This further emphasizes the need for great caution in using these drugs until more definitive studies are completed. Currently, the use of "fen-phen" is not approved by the FDA. In cases where the drug is indicated, it appears the benefit seems to outweigh the risks.
Newer Drugs. One drug currently awaiting FDA approval is sibutramine. It is a serotonin reuptake inhibitor like dexfenfluramine; but it also increases energy expenditure by inhibiting noradrenaline reuptake. In clinical trials, the drug has demonstrated a side effect of increased heart rate, irritability, sleep disturbances, and headache. Its use concomitant with hypertension may be questionable.9,37
Orlistat or tetrahydrolipostatin has been in development by Hoffman LaRoche. It is classified as a lipase inhibitor and reduces fat absorption from the gastrointestinal tract.9,37
BRL 26380A is one of the first selective beta adrenergic agonists. The problem with this drug in development is that it has been shown to not be completely selective for the B-3 receptor and causes side effects such as tachycardia and nervousness.37
There is sufficient evidence in the literature to suggest that there are some drugs that are effective in weight loss and chronic maintenance. For now, the best approach appears to be the combination of fenfluramine and phentermine for short term only and dexfenfluramine for long term (no more than 12 months).37-39 Perceived effectiveness of these agents varies among practitioners. Some find them helpful while others see no place for drug supplementation. In my practice, it is the rare patient who qualifies for drug treatment. Patients who are eligible for consideration to be given medications must have first failed legitimate attempts at exercise, behavioral modification, and dietary adjustments. I am more comfortable with attempting drug therapy if there is a concurrent illness or medical condition that is preventing the patient from attempting the above-listed criteria. The one patient I have on dexfenfluramine has severe bilateral knee damage preventing her from doing as much calorie-burning exercise as she would like. As weight was dropped, she began a walking program. In general, the potential benefit of drug therapy must outweigh the risks of any side effects. In my practice, I never even consider drug therapy for anyone with BMI less than 30. The patient previously referred to had a BMI of 40. Table 7 lists contraindications to drug therapy. When the decision is made to use drugs, careful monitoring of the patient’s symptoms, side effects, vital signs, and appropriate laboratory studies associated with comorbid conditions must be closely watched. Patients selected for drug therapy should probably be seen twice the first 4-6 weeks, and then monthly thereafter.
According to an NIH Consensus Conference statement, clinically severe obesity is defined by a BMI of greater than 40 kg/m2. (See Table 8.) This class of patient, along with those who have moderate obesity accompanied by one or more comorbid conditions and have failed conventional medical management attempts, are candidates for bariatric surgery. These patients should have a multidisciplinary approach, including evaluations by psychiatry, medical, and nutritional staff before the procedure. Those selected must be well-informed and motivated and aware of all risks involved. Lifelong surveillance will be necessary. The two most commonly accepted procedures that seem to be safe and effective are the vertical banded gastroplasty and the Roux-en-Y gastric bypass.9,25 Surgery is considered successful if 50% of the weight is lost and that loss is maintained over time. Perioperative mortality is low at 0.1%. Treatment failures occur 33-50% of the time. Martin et al report with Roux-en-Y bypass a much better long-term maintenance result, with 85% of patients at eight years regaining less than 10% of weight loss. In my practice, surgery has been dismal, with greater than 80% of patients I have seen with history of bypass regaining most of the weight lost.
Obesity is a chronic disease with a high rate of recidivism. Its treatment must be approached in a multidisciplinary manner, dealing with behavioral, nutritional, medical, and lifestyle interventions in order to gain any measure of long-term success. While genetic influences are significant, they are not impossible to overcome with motivation to succeed and gradual permanent changes in habits. There are cases in which drug intervention and surgery are necessary, but each case must be weighed carefully and individually. This is an important disease that is affecting a major portion of our population and should not be seen as the result of laziness and a lack of will power. Often, obese persons are found to have concimitant eating disorders. The prevalence of binge eating is high in these patients (20-30%). Depression is also discovered in many of these patients, and these potentially serious and significant findings should be addressed by appropriate referral of counseling specialists. Helpful resources for patients and physicians are listed in Table 9.
References
1. Martin LF, Hunter SM, Lauve RM, et al. Severe obesity; Expensive to society, frustrating to treat, but important to confront. South Med J 1995;88.
2. Bray GA, Gray DS. Obesity pathogenesis. Western J Med 1988;149:429-441.
3. Pi Sunyer FX. Medical hazards of obesity. Ann Intern Med 1993;119:655-660.
4. The Fifth Report of the Joint National Committee on Hypertension. NIH January 1993. NIH No. 93-1088.
5. Report of the Secretary Task Force on Black and Minority Health. Vol I. Executive Summary, Washington, DC: U.S. Department of Health and Human Services. 1985 DHHS Pub. 85-487367 (Q63).
6. Wolf AM, Cubitz GA. The cost of obesity. U.S. Perspective Pharmacy Economics 1994;5(Supplement):34-37.
7. Himes JH, Dietz. Guidelines for overweight in adolescent preventative services. Recommendations from an expert committee. Am J Clin Nutrition 1994;59:307-316.
8. Kuczmarski RJ, Flegal KM, Campbell SM, et al. Increasing prevalence of overweight among U.S. adults. The National Health and Nutritional Examination Surveys, 1960-1991. JAMA 1994;2762:205-211.
9. Brunton, Pi-Sunyer FX. Evaluating and treating obesity. Monograph of the American Academy of Family Practice.
10. Bray GA, Gray DS. Treatment of obesity: An overview. Diabetes Metab Rev 1988;4:653-679.
11. Egger G. The case for using waist to hip ratio measurements in routine medical checks. Med J Austral 1992;156:280-285.
12. Chan, et al. Obesity fat distribution and weight gain as risk factors for clinical diabetes in men. Diabetes Care. 1994;17:961-969.
13. Price JH, Desmond SM, Droc FA, et al. Family practice physicians’ beliefs, attitudes, and practices regarding obesity. Am J Prevent Med 1987;3:339-345.
14. Chen, Blackburn. Helping patients reverse the health risks of obesity. J Clin Outcomes Man 1997;4 May/June.
15. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995; 332:621-628.
16. Amer P. The B 3 adrenergic receptorA cause and cure of obesity? Editorial. N Engl J Med 1995;333:382-383.
17. Patient Care Special Issue. The Practical Journal For Primary Care Physicians 1995; Nov. 15:153.
18. Kelley GA. Gender differences in the physical activity levels of young African American adults. J Natl Med Assoc 87:545-548.
19. Bungum V. Determinants of physical activity among female adolescents. Am J Prevent Med 1997;13.
20. Prevalence of sedentary LifestylesBehavioral Risk Factor Surveillance System, U.S. 1991. MMWR Morb Mortal Wkly Rep 1993;42:576-579.
21. Prevalence of Physical Inactivity During Leisure Time Among Overweight PersonsBehavioral Risk Factor Surveillance System, 1994. 1996;45 (9).
22. Robinson TN, Hammer LD, Killer JD, et al. Does TV viewing increase obesity and reduce physical activity? Pediatrics 1983; 91:273-280.
23. Clement K, et al. Indication for linkage of the human OB gene region with extreme obesity. Diabetes 1996;45:687-690.
24. Flanery RF. Should obesity be treated? Behav Med Consult 1995;4 (4).
25. Pi-Sunyer FX. Current approaches to the management of obesity. Dannemiller Memorial Educational Foundation; 1996.
26. Croft JB, et al. Socioeconomic and behavioral correlated of BMI in black adults; The Pitt Study. Am J Pub Health 1992;82 (6).
27. Stunkard AJ. The Salmon Lecture. Some perspectives on human obesity: Its cause. Bull NY Acad Med 1988;64:902-923.
28. Himes JH, Dietz WH. Guidelines for overweight in adolescent preventative services: Recommendations from an expert committee. Am J Clin Nutr 1994;59:307-316.
29. NIH Consensus Statement. Physical Activity and Cardiovascular Health. 1995;13 (3).
30. Higgins M, Kannel W, Garrison R, et al. Hazards of obesityThe Framingham Experience. Acta Med Scand 1988;723 (Suppl):23-36.
31. Pouliot MC, Despres JP, Nadeau A, et al. Visceral obesity in men; Associations with glucose tolerance, plasma insulin, and lipoprotein levels. Diabetes 1992;41:826-834.
32. Wing R. Handbook of Obesity. Bray G, Bouchard C. James P. eds. In press.
33. Kumanyika, et al. Weight-related attitudes and behaviors of black women. J Am Dietetic Assoc 1993;93 (4).
34. Allen DA, Mayo K, Michel Y. Body size values of white and black women. Res Nursing Health 1993;16:323-333.
35. McHenry PL, Ellestod NH, Gletcher GF, et al. Statement on exercise: A positive statement for health professional by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology. Circulation 1990;81:396-398.
36. Elks. Appetite suppressants as adjuncts in the treatment of obesity. J Fam Pract 1996;42 (3).
37. Sherer, Wilson. Pharmacologic options in the treatment of obesity. Prim Care Therapeutics 1995;1 (4).
38. Weintraub M, Sundareson DR, Madam M, et al. Long-term weight control study I (Weeks 0-34). Clin Pharmacol Therapeutics 1992;51:586-594.
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Physician CME Questions
1. The most practical and reliable means of determining the diagnosis of obesity in the office setting is by the measurement of:
a. the C-T Scan or MRI of abdominal visceral fat.
b. morning weight from two separate occasions.
c. Metropolitan Life Insurance Table.
d. body mass index.
e. biceps skin fold measurement.
2. The amount of abdominal visceral fat in men has been shown to correlate positively with:
a. hyperinsulinemia and increased risk of coronary artery disease.
b. successful bypass surgery for morbid obesity.
c. chronic liver disease.
d. clotting disorders.
e. nothing. Visceral fat does not have significant metabolic significance.
3. Concerning the use of drug intervention in the treatment of morbid obesity, select from the following the statement that is true.
a. Drugs are not useful in the treatment of morbid obesity.
b. Drug intervention is appropriate as long as there are no comorbid conditions.
c. Drugs for obesity are approved by the FDA for only short treatments of three months.
d. Drugs must be used in combination with exercise, behavioral modification, and dietary changes.
e. Drug intervention is only considered when the body mass index is greater than 40 kg/m2.
4. In regard to the treatment obesity, permanent weight changes only result when:
a. surgical intervention such as gastric bypass is performed.
b. drugs are prescribed for a for minimum of six months.
c. the patients exercise regularly.
d. behavior modification is successfully carried out.
e. patients join a professional weight loss program.
5. The drug dexfenfluramine is classified as:
a. noradrenergic.
b. catecholaminergic.
c. an amphetamine-related drug.
d. thermogenic (increases metabolism).
e. serotonergic.
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