User login
- Diet and exercise coupled with behavioral modification can improve both patient-related and disease-related outcomes in the short term; however, long-term efficacy is lacking (A).
- Drugs such as sibutramine or orlistat may achieve modest, short-term weight loss, but their long-term effectiveness is unproven (A).
- For patients with a BMI >40, gastric bypass procedures can lead to long-term weight loss (B).
Physician intervention to encourage and assist obese patients to lose weight is warranted, for these reasons:
- Prevention of adverse outcomes. Left untreated, obesity is clearly related to the development of many adverse health outcomes, including diabetes mellitus, hypertension, stroke, hyperlipidemia, coronary artery disease, gallstones, osteoarthritis, obstructive sleep apnea, vascular disease, depression, and certain cancers (breast, endometrial, prostate, colon).1-4
- Reduction of morbidity and mortality. A causal effect between intentional weight loss and mortality has been difficult to prove, but even modest weight loss can reduce the morbidity of obesity-related disease, such as arthritis and obstructive sleep apnea (Strength of recommendation: A).5-7 For those at increased risk of death from cardiovascular disease, such as persons with obesity and diabetes mellitus, intentional weight loss coupled with lifestyle change can significantly reduce mortality (SOR: C).8 Nearly 280,000 deaths per year are attributable to obesity.9
- Cost reduction. Nearly 25% of American adults are obese, and more than half are overweight.1,2 Obesity burdens society with significant costs, including more than $50 billion annually for direct care. With an additional $30 billion spent each year on weight-loss products and services, this disease accounts for over 5% of annual health care expenditures in the United States.5
Nature or nurture?
Excess fat is created when energy intake exceeds cellular energy consumption. The complex relationship between the human body’s environment and the development of obesity is poorly understood, but recent genetic investigations have elucidated new mechanisms in the regulation of both satiety and energy expenditure. Using data from heritability studies, some researchers have estimated that up to 70% of the variability in weight among humans can be explained by genetic influences, but it is unlikely that changes in human genes account for the recent change in obesity prevalence.10
Risk factors
Identifiable risks factors for obesity in adulthood include parental history of obesity, low socio-economic background, and a history of high birth weight.11
Prevention
Recently, factors including consumption of sugar-sweetened beverages, lack of breast-feeding, and television viewing have been identified as risk factors for childhood and adolescent obesity.12-14 Because obesity at a young age can lead to adult obesity, these factors may be targeted to prevent adult obesity.
School-based programs for diet and exercise appear to be ineffective for preventing obesity (SOR: B).15,16 However, most research has been of limited quality. In one recent randomized study, reduction of television viewing (including videotape and videogame use) through school intervention was associated with significant reduction in BMI (SOR: B).14
Screening recommendations
The United States Preventive Service Task Force recommends periodic measurement of both height and weight in adults (SOR: B). The waist-to-hip ratio is thought to have insufficient evidence for recommendation as a routine screening tool because studies identifying a benefit to screening using only the waist-to-hip ratio have not been completed (SOR: C).17
Initial determination of obesity
Although the standard for body fat measurement is densitometry, which determines the density of a body submersed in water, the cost and technical requirements prohibit routine use in the clinical setting.18-20 The waist-to-hip ratio and waist circumference are used to identify central (or android) obesity in which adipose tissue in the abdomen is associated with atherosclerosis.21,22 The waist circumference is found by measuring the circumference around the waist at the level of the iliac crest. Values above 40 inches for men and 35 inches for women are indicative of increased risk of adverse health outcomes.5,19 The waist-to-hip ratio is calculated by dividing the circumference of the waist at the level of the L3 by the hip circumference measured at the largest area of the gluteal region.19 For men, waist-to-hip ratios greater than 1.0 are associated with significantly increased risk of cardiovascular events. For women, a ratio greater than 0.85 indicates increased risk.19
Body-mass index calculation
The body-mass index (BMI), also known as the Quetelet index, is the most commonly used measure of obesity.20 BMI is a patient’s weight in kilograms divided by his or her height in meters squared (kg/m2 ).5,19 A free online BMI calculator is available through the National Heart, Lung and Blood Institute at www.nhlbisupport.com/bmi/bmicalc.htm.
Although the BMI estimates total body fat and compares well with densitometry, it may be less accurate in selected populations (eg, the elderly, certain ethnic groups, and persons with large muscle mass).19 Generally, when BMI exceeds 25, the greater the BMI, the greater the obesity-related morbidity and mortality.5,19,20,23 Table 1 shows the classification of obesity based on BMI, and Table 2 shows the BMI for combinations of height and weight in inches and pounds.5
TABLE 1
Body mass index (BMI) and degrees of obesity
| BMI | Category | Therapeutic options |
|---|---|---|
| <18.5 | Underweight | |
| 18.5–25.9 | Normal weight | Reinforce positive lifestyle |
| 25.0–29.9 | Overweight | Diet, exercise, behavior modification |
| 30.0–34.9 | Obese (Class I) | Diet, exercise, behavior modification; consider pharmacologic therapy* |
| 35.0–39.9 | Obese (Class II) | Diet, exercise, behavior modification; consider pharmacologic therapy |
| ≥40.0 | Obese (Class III or “Morbid Obesity”) | Consider surgical management |
| *For patients with multiple cardiovascular risk factors (eg, diabetes, hyperlipidemia), BMI >27 may be an indication for pharmacologic intervention at; at BMI >37, patients may be considered candidates for surgical therapy. | ||
| From the National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of obesity in adults: the Evidence Report. Bethesda, Md: US Department of Health and Human Services, 1998. | ||
Evaluation of documented obesity
In history taking and physical examination, look for reversible causes of obesity (including medications and endocrine disorders), consider the degree of obesity, and determine whether comorbid conditions are present, to help estimate prognosis. Evaluate the patient’s dietary and exercise habits, as well as willingness to modify these habits if necessary.1,5 Finally, review the patient’s weight history and any attempts at weight loss.
Medications associated with weight gain include psychotropic drugs, anticonvulsant agents, steroid hormones, insulin, and many oral hypoglycemic agents.1
Endocrine disorders such as Cushing’s syndrome and hypothyroidism may also contribute to obesity, but only rarely. Physical findings that increase the likelihood of Cushing’s syndrome, and their respective positive likelihood ratios (LR+)— the higher the value, the greater the likelihood of disease—include: hypertension (2.3), moon facies (1.6), thin skinfold (115.6), ecchymoses (4.5), and acne (2.2).19 Findings, and their likelihood ratios, associated with hypothyroidism include coarse skin (5.6), cool/dry skin (4.7), bradycardia (4.1), enlarged thyroid (2.8), and hoarse voice (5.4).19 The very high LR for skinfold thickness was determined for women of childbearing age who had elevated risk of having Cushing’s syndrome because of a history of both menstrual irregularities and hirsutism. Skinfold thickness is determined by using calipers on an area of minimal subcutaneous fat (eg, back of the hand). For women of reproductive age, skinfold thickness is normally greater than 1.8 mm.19
Laboratory assessment of the obese patient will rarely find a cause of weight gain (eg, hypothyroidism), but the addition of selected diagnostic tests will aid in the determination of prognosis. An abnormal fasting glucose level or impaired glucose tolerance is a major risk factor for cardiovascular disease. Abnormal lipid profiles heighten that risk for obese patients. All patients with documented obesity should undergo assessment for abnormal lipids and impaired glucose tolerance5 (SOR: D).
Treatment
The most important step in treating obesity is to establish a calorie deficit. The deficit can be achieved by increasing energy expenditure or by reducing energy intake or absorption. On average, a caloric deficit of 500 kilocalories per day will result in a weight loss of 1 pound per week.5 Reasonable expectations of therapy include weight loss of 1–2 pounds a week and a loss of 10% of total body weight in 5 months.5
Interventions for weight loss fall into 4 categories: lifestyle modifications (diet, exercise, and behavioral modification), drug therapy, complementary or alternative measures, and surgery. Table 3 summarizes the levels of evidence to support each intervention.
TABLE 3
Efficacy of weight-loss interventions
| Weight loss | ||||
|---|---|---|---|---|
| SOR* | Intervention | Short-term | Long-term | Comments |
| Diet, exercise, and behavioral modification | ||||
| A | Low/very-lowcalorie diet | 8% average weight loss from 3–12 months | Weight nears baseline in studies >24 months | Very-low-calorie diets may require laboratory assessment of metabolic function |
| High rate of noncompliance | ||||
| A | Low/very low fat with reduced calories | Similar to lowcalorie with moderate fat | Weight nears baseline in studies >24 months | No known side effects |
| A | Exercise | Less weight loss than diet therapy | Likely no significant weight loss | Improved cardiovascular fitness |
| May be effective in preventing weight gain | ||||
| A | Low-calorie diet + exercise | Increased weight loss vs. diet or exercise alone | Weight nears baseline in long-term studies | Improved cardiovascular fitness |
| Compliance a major problem | ||||
| B | Behavior modification | Increases effectiveness of diet, exercise | No significant effect at 5 years | No reported harms |
| Only studied when used with other methods | ||||
| C | Lowcarbohydrate diet | Not significant if calories are not reduced | No long-term data available | No known side effects, but creates nutritional imbalance and ketosis |
| Needs additional study | ||||
| Medication | ||||
| A | Sibutramine | ˜ 4 kg for trials less than 1 year | Modest weight loss when used for >1 year | Can elevate blood pressure |
| Number needed to treat (NNT) for 5% weight loss at 1 year = 3 | ||||
| NNT for 10% weight loss at 1 year = 5 | ||||
| A | Orlistat | ˜ 2–3 kg for trials less than 1 year | ˜ 3 kg at 2 years | GI side effects common, possible vitamin deficiencies |
| NNT for 5% weight loss at 1 year = 5 | ||||
| NNT for 10% weight loss at 1 year = 7 | ||||
| Surgery | ||||
| B | Roux-en-Y Gastric bypass | ˜ 50 kg (110 lbs) at 1 year | ˜ 50 kg (110 lbs) at up to 4 years | Significant operative risk and post-operative GI side effects |
| Nadir for weight loss occurs at 12–24 months | ||||
| B | Gastric banding | ˜ 30 Kg (66 lbs) at one year | 10–15% of initial weight lost may be regained long-term | Significant operative risk and post-operative GI side effects |
| Generally considered less effective that gastric bypass | ||||
| Complementary/alternative medicine | ||||
| B | Hypnosis | Minimal reduction | No statistically significant difference | Studied in combination with cognitive behavioral therapy |
| Systematic reviews reveal significant heterogeneity of low-quality randomized controlled trials | ||||
| B | Acupuncture | No significant difference | No significant difference | Systematic review reveals poor quality |
| RCTs, which limits ability to determine effect | ||||
| * Strength of recommendation | ||||
| A = Systematic review of randomized controlled trials (RCT) (with homogeneity) or individual RCT with narrow confidence interval | ||||
| B = Systematic review of cohort studies (with homogeneity), individual cohort studies or low-quality RCT, individual case-control study or SR of case-control studies (with homogeneity) | ||||
| C = Case series and poor quality cohort and case control studies | ||||
Lifestyle modifications
Management of obesity in every case should include dietary changes, exercise, and behavioral modification.
Dietary changes. Diets create a caloric deficit by reducing the intake of calories. Average weight loss with low-calorie diets is approximately 8% at 3–12 months (SOR: A),5 with most of the loss occurring in the first 3–5 months.24 There are many kinds of diets for weight loss, including low calorie, very-low calorie, low fat, very low fat, and low carbohydrate, but long-term compliance with all types of dietary interventions is a significant problem. When diet alone is used as therapy, between one third and one half of weight loss will not be maintained.24 Emerging strategies to help improve dietary compliance include behavioral modification (see below) and meal substitutes. Recent reports of interventions such as meal-replacement shakes indicate that long-term weight loss can be significantly improved (SOR: B).25-27
Examples of low-calorie, nutritionally balanced diets are Weight Watchers, Jenny Craig, Nutrisystem, the National Cholesterol Education Program Step I and Step II diets, and the Dietary Approaches to Stop Hypertension (DASH) diet. Low-calorie diets provide 800–1500 kilocalories per day.5,28,29 Very-low-calorie diets (400–500 kilocalories per day) may increase rates of weight loss initially, but at 1 year, results are similar to those of low-calorie diets (SOR: A).5,30
A low-fat diet (fat content 10%–19%) without a decrease in total calorie intake does not promote weight loss (SOR: A).5,31 Very-low-fat diets containing less than 10% fat have been described by such authors as Ornish and Pritikin.25 Obese patients using either the low-fat or very-low-fat diet can lose body weight and body fat, but only if calories are also decreased (SOR: A).5,28
Low-carbohydrate diets, such as Dr Atkin’s diet, are associated with modest (approximately 5 kg, or 11 lbs) weight loss (SOR: C).28,32 Improved study design is required to further evaluate the effectiveness and safety of low-carbohydrate diets in the clinical setting.
Exercise. Most studies of exercise are based on 30–50 minutes of moderately intense aerobic exercise, repeated 3–7 times per week.5 When it is the only prescribed therapy, exercise can be expected to produce modest weight loss only (SOR: A).5,33 Exercise combined with dietary intervention, however, increases weight lost (SOR: A), and exercise by itself may prevent weight gain (SOR: C).5
Behavioral Modification. Behavioral modification has been evaluated in combination with diet or exercise, and has been shown to increase compliance and weight loss for durations of 1 year or less (SOR: A).5,34 Weight gain is common when therapy is discontinued, and at 5 years, there is no difference between those who received behavioral therapy and those who were in control groups (SOR: A).5
Medications
Medications for treatment of obesity act through 1 or more of 3 mechanisms:
- Appetite suppression (eg, sibutramine, antidepressants such as fluoxetine)
- Increased metabolic activity (eg, stimulants such as ephedra with caffeine, Β-3 agonists)
- Decreased absorption of caloric load (orlistat)
For mild-to-moderate obesity (BMI >30 and <40), medications can be beneficial (SOR: A), but long-term weight loss beyond 2 years has not been studied.35 Pharmacologic intervention without lifestyle intervention actually decreases a person’s ability to lose weight (SOR: B).36
Two medications are approved by the United States Food and Drug Administration for long-term obesity management: sibutramine and orlistat. Both drugs reduce weight modestly (SOR: A).37-39 Both medications have similar indications for use: BMI >30, or BMI >27 with the presence of other cardiovascular risk factors (ie, diabetes or hyperlipidemia). Both should be used in conjunction with reduced-calorie diet and exercise (SOR: B).36
Sibutramine is usually started at 10 mg once a day, given with or without food. The dose may be titrated to a maximum of 15 mg/d after 4 weeks if weight loss has been inadequate.1 Sibutramine is known to increase pulse rate and blood pressure in a significant number of patients; because of this, regular evaluation of vital signs is required. At present, long-term use of sibutramine cannot be recommended, and safety data are unavailable beyond 1 year of use. Sibutramine should be avoided if these conditions are present: hypertension, coronary heart disease, congestive heart failure, an arrhythmic condition, pregnancy, renal impairment, concomitant use of MAOI, or a history of stroke.
Orlistat is started at 120 mg three times a day, and is taken with meals that contain fat. It may still be effective if taken up to one hour after eating. Orlistat may be avoided if the meal contains no fat. This drug may interfere with the absorption of some fat-soluble vitamins, and it is therefore recommended that patients take a multivitamin that has fat-soluble vitamins at least 2 hours before or after ingesting orlistat. Orlistat is not absorbed into the body and, at this time, no laboratory follow-up is needed. Regular evaluation of weight is needed to assess the efficacy of treatment. Orlistat should be avoided by those who have cholestasis or malabsorptive disorders or by those taking cyclosporine.40
Other medications that have been used include phentermine, ephedra, dexfenfluramine, phenyl-propanolamine (PPA), and mazindol.1,2 All of these medications produce significant weight loss in the short term (SOR: A), but they are not indicated for long-term use.2 In fact, phenylpropanolamine and dexfenfluramine are no longer available because of their severe side effects.2 Antidepressants do not yield a consistent benefit in well-designed studies of obesity management.2
Table 3 summarizes the effects of medications on weight loss.
Surgery
Surgical management of obesity is reserved for extremely obese persons because of the significant morbidity and mortality associated with the interventions. Currently, gastric bypass procedures result in less than 1% perioperative mortality and about 10% perioperative morbidity.41 Patients with a BMI >40 (or >37 with weight-related comorbidities) are candidates for surgery.42
It has been estimated that, for these patients, the cost per pound lost is less with surgery than with medications.43 In most series, the average morbidly obese patient can expect to lose 50% of excess body weight at 5 years after bypass surgery, and 50% of excess weight will be lost even 10 years post-operatively (SOR: B).44
Several options are available for surgical management of obesity. While the technical aspects of surgery are beyond the scope of this article, some generalizations can be made. Procedures may reduce the size of the stomach to decrease the volume of intake (gastroplasty), or may create a malabsorption condition (intestinal bypass) to decrease absorption of calories. The combination of a restrictive procedure with malabsorption (Rouxen-Y gastic bypass) is superior to a restrictive procedure alone (SOR: B).44
The surgical management of morbid obesity improves quality of life for patients,43 but no published studies to date have been able to evaluate the effect of the surgical management on mortality in the morbidly obese patient.
Complementary and alternative therapies
In addition to the traditional methods of weight loss, acupuncture and hypnosis have been studied in the treatment of obesity. Acupuncture does not appear to have any benefit greater than placebo (SOR: B).45 Hypnosis has also been reviewed and likely adds little, if any, benefit beyond that of placebo (SOR: B).45 Most studies of both acupuncture and hypnosis suffer from the difficulties of performing adequate control groups, and meta-analyses have demonstrated mixed results.45,46
Maintenance programs
There is significant evidence that when patients discontinue effective weight loss interventions (eg, diet or behavioral modification) they will return to their baseline weight. Because of this, it is important to consider maintenance programs as part of overall treatment and to imbue in patients the expectation that treatment will be lifelong. Examples of an approach to maintenance therapy include attendance at regular exercise or therapy sessions even after achieving weight-loss goals, or continued participation at commercial weight-loss program meetings or support groups.
ACKNOWLEDGEMENTS
The author was supported by grant 1 D45 PE 50175 -01, “Faculty Development in Family Medicine” funded by Health Resources and Services Administration (HRSA). The author wishes to thank Bill Hueston, MD, Peter Carek, MD, Arch Mainous III, PhD, and Lori Dickerson, PharmD, for their help with manuscript review. The author wishes to thank Tara Hogue for her for help with the preparation of this manuscript.
1. Dickerson L, Carek PJ. Drug therapy for obesity. Am Fam Physician 2000;51:2131-8.
2. Arterburn D, Hitchcock-Noel P. Obesity. Clinical Evidence 2001;5:512-9.
3. Mun EC, Blackburn GL, Matthews JB. Current status of medical and surgical therapy for obesity. Gastroenterology 2001;120:559-81.
4. Field AE, Coakley EH, Must A, Spandano JL, Laird N, Dietz WH, et al. Impact of overweight on the risk of developing common chronic diseases during a 10 year period. Arch Intern Med 2001;151:1581-5.
5. National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of obesity in adults: The evidence report. Bethesda, Md: US Department of Health and Human Services; 1998.
6. Messier SP, Loeser RF, Mitchell MN, Valle G, Morgan TP, Rejeski WJ, et al. Exercise and weight loss in obese older adults with knee osteoarthritis: a preliminary study. J Am Geriatr Soc 2000;48:1052-72.
7. Shneerson J, Wright J. Lifestyle modification for obstructive sleep apnoea (Cochrane Review). In: The Cochrane Library, Issue 4, 2001. Oxford: Update Software.
8. Williamson DF, Thompson TS, Thun M, Flanders D, Pamuk E, Byers T. Intentional weight loss and mortality among overweight individuals with diabetes. Diabetes Care 2000;10:1499-1504.
9. Allison DB, Fontaine KR, Manson JE, Stevens J, Van Itallie TB. Annual deaths attributable to obesity in the United States. JAMA 1999;282:1530-8.
10. Yanovski J, Yanovski S. Recent advances in basic obesity research. JAMA 1999;282:1504-6.
11. Parsons TJ, Power C, Logan S, Summerbell CD. Childhood predictors of adult obesity: a systematic review. Int J Obes Relat Metab Disord 1999;8 (suppl):S1-107.
12. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001;357:505-8.
13. Gillman MW, Rifas-Shiman SL, Camargo CA, Berkey CS, Frazier AL, Rocket HRH, et al. Risk of overweight among adolescents who were breastfed as infants. JAMA 2001;285:2451-7.
14. Robinson T. Reducing children’s television viewing to prevent obesity. JAMA 1999;282:1551-7.
15. Campbell K, Waters E, O’Meara S, Summerbell C. Interventions for preventing obesity in children (Cochrane Review). In: The Cochrane Library, Issue 5, 2001. Oxford: Update Software.
16. Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. Randomized controlled trial of primary school based intervention to reduce risk factors for obesity. BMJ 2001;323:1029-32.
17. US Preventive Services Task Force. Screening for obesity. In: US Preventive Services Task Force: Guide to Clinical Preventative Services: Report of the US Preventive Services Task Force. 2nd ed. Baltimore, Md: Williams and Wilkins; 1995;219-29.
18. Flier JS, Foster DW. Eating Disorders: Obesity, anorexia nervosa, and bullemia nervosa. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, Pa: WB Saunders; 1998;1051-97.
19. McGee S. Evidence-based physical diagnosis. Philadelphia, Pa: WB Saunders; 2001.
20. Willett WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999;351:527-35.
21. Rexrode KM, Carey VJ, Hennekens CH, Walters EE, Colditz GA, Stampfer MJ, et al. Abdominal adiposity and coronary heart disease in women. JAMA 1998;280:1843-8.
22. Iwao S, Iwao N, Muller DC, Elahi D, Shimokata H, Andres R. Does waist circumference add to the predictive power of the body mass index for coronary risk? Obesity Research. 2001;9:585-95.
23. Toriano RP, Frongillo EA, Sobal J, Levitsky DA. The relationship between body weight and mortality: a quantitative analysis of combined information from existing studies. Int J Obes Relat Metab Disord 1996;20:63-75.
24. Hensrud DD. Dietary treatment and long-term weight loss and maintenance in type 2 diabetes. Obesity Research 2001;9:348S-353S.
25. Ditschuneit HH, Flechtner-Mors M. Value of structured meals for weight management: risk factors and long-term weight maintenance. Obesity Research 2001;9(suppl 4):284S-289S.
26. Ditschuneit HH, Flechtner-Mors M, Johnson TD, Adler G. Metabolic and weight-loss effects of a long-term dietary intervention in obese patients. Am J Clin Nutr 1999;69:198-204.
27. Flechtner-Mors M, Ditschuneit HH, Johnson TD, Suchard MA, Adler G. Metabolic and weight loss effects of long-term dietary interventions in obese patients: four-year results. Obesity Research 2000;8:399-402.
28. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obesity Research 2001;9(suppl 1):1S-50S.
29. Finer N. Low-calorie diets and sustained weight loss. Obesity Research 2001;9(suppl 4):290S-292S.
30. Saris W. Very-low-calorie diets and sustained weight loss. Obesity Research 2001;9(suppl 4):292S-301S.
31. Pirozzo S, Summerbell C, Cameron C, Glasziou P. Advice on low-fat diets or obesity (Cochrane Review). In: The Cochrane Library, Issue 2, 2002. Oxford: Update Software.
32. Skov AR, Toubro S, Ronn B, Holm L, Astrup A. Randomized trial on protein vs.carbohydrate in ad libi-tum reduced diet for the treatment of obesity. Int J Obes 1999;23:528-36.
33. Bray GA. Role of physical activity and exercise in obesity. Up To Date (online 9.3). Retrieval date 11/5/2001. Up To Date, Inc. Wellesley, Mass, USA.
34. Thorogood M, Hillsdon M, Summerbell C. Changing behaviour. Clinical Evidence 2000;5:25-52.
35. Weintraub M, Sundaresan PR, Schuster B, Averbuch M, Stein EC, Byrne L. Long-term weight control study V. Clin Pharmacol Ther 1992;51:615-8.
36. Wadden T. Benefits of lifestyle modification in the phar-macologic treatment of obesity: a randomized trial. Arch Intern Med 2001;151:218-27.
37. Smith MB. Randomized placebo-controlled trial of long-term treatment with sibutramine in mild to moderate obesity. J Fam Pract 2001;50:505-12.
38. Sjostrom L, Rissanen A, Anderson T, Boldrin M, Golay A, Koppeschaan HPF, et al. Randomized placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients. European Multicentre Orlistat Study Group. Lancet 1998;352:157-72.
39. O’meara S, Riemsma R, Shirran L, Mather L, ter Riet G. A rapid and systematic review of the clinical effectiveness and cost-effectiveness of orlistat in the management of obesity. Health Technology Assess 2001;5:18.
40. Physician’s Desk Reference. PGS. Montvale, NJ: Medical Economics; 2001;2809-13.
41. Balsiger BM, Kennedy FP, Abu-Lebdeh HS, Collazo-Clavell M, Jensen MD, O’Brien T, et al. Prospective evaluation of Roux-en Y gastric bypass as primary operation for medically complicated obesity. Mayo Clin Proc 2000;75:573-80.
42. Gastrointestinal Surgery for Severe Obesity. NIH Consensus Statement Online 1991; 25-27. Cited August 1, 2001;9(1):1-20.
43. Van Gemert WG, Van Dielen F, Soeters PB, Greve JW. Quality of life before and after weight-reducing surgery and cost-effectiveness analysis. In: Deitel M,†Cowan SM, eds. Update: Surgery for the Morbidly Obese Patient. Toronto: FD Communications; 2000;595-602.
44. Sugerman HJ. The epidemic of severe obesity: value of surgical treatment. Mayo Clin Proc 2000;75:559-572.
45. Ernst E. Acupuncture/acupressure for weight reduction? A systematic review. Wien Klin Wochenschr 1997;109:50-2.
46. Allison DB, Faith MS. Hypnosis as an adjunct to cogni-tive-behavioral psychotherapy for obesity: a meta-analyt-ic reappraisal. J Consult Clin Psychol 1995;54:513-5.
- Diet and exercise coupled with behavioral modification can improve both patient-related and disease-related outcomes in the short term; however, long-term efficacy is lacking (A).
- Drugs such as sibutramine or orlistat may achieve modest, short-term weight loss, but their long-term effectiveness is unproven (A).
- For patients with a BMI >40, gastric bypass procedures can lead to long-term weight loss (B).
Physician intervention to encourage and assist obese patients to lose weight is warranted, for these reasons:
- Prevention of adverse outcomes. Left untreated, obesity is clearly related to the development of many adverse health outcomes, including diabetes mellitus, hypertension, stroke, hyperlipidemia, coronary artery disease, gallstones, osteoarthritis, obstructive sleep apnea, vascular disease, depression, and certain cancers (breast, endometrial, prostate, colon).1-4
- Reduction of morbidity and mortality. A causal effect between intentional weight loss and mortality has been difficult to prove, but even modest weight loss can reduce the morbidity of obesity-related disease, such as arthritis and obstructive sleep apnea (Strength of recommendation: A).5-7 For those at increased risk of death from cardiovascular disease, such as persons with obesity and diabetes mellitus, intentional weight loss coupled with lifestyle change can significantly reduce mortality (SOR: C).8 Nearly 280,000 deaths per year are attributable to obesity.9
- Cost reduction. Nearly 25% of American adults are obese, and more than half are overweight.1,2 Obesity burdens society with significant costs, including more than $50 billion annually for direct care. With an additional $30 billion spent each year on weight-loss products and services, this disease accounts for over 5% of annual health care expenditures in the United States.5
Nature or nurture?
Excess fat is created when energy intake exceeds cellular energy consumption. The complex relationship between the human body’s environment and the development of obesity is poorly understood, but recent genetic investigations have elucidated new mechanisms in the regulation of both satiety and energy expenditure. Using data from heritability studies, some researchers have estimated that up to 70% of the variability in weight among humans can be explained by genetic influences, but it is unlikely that changes in human genes account for the recent change in obesity prevalence.10
Risk factors
Identifiable risks factors for obesity in adulthood include parental history of obesity, low socio-economic background, and a history of high birth weight.11
Prevention
Recently, factors including consumption of sugar-sweetened beverages, lack of breast-feeding, and television viewing have been identified as risk factors for childhood and adolescent obesity.12-14 Because obesity at a young age can lead to adult obesity, these factors may be targeted to prevent adult obesity.
School-based programs for diet and exercise appear to be ineffective for preventing obesity (SOR: B).15,16 However, most research has been of limited quality. In one recent randomized study, reduction of television viewing (including videotape and videogame use) through school intervention was associated with significant reduction in BMI (SOR: B).14
Screening recommendations
The United States Preventive Service Task Force recommends periodic measurement of both height and weight in adults (SOR: B). The waist-to-hip ratio is thought to have insufficient evidence for recommendation as a routine screening tool because studies identifying a benefit to screening using only the waist-to-hip ratio have not been completed (SOR: C).17
Initial determination of obesity
Although the standard for body fat measurement is densitometry, which determines the density of a body submersed in water, the cost and technical requirements prohibit routine use in the clinical setting.18-20 The waist-to-hip ratio and waist circumference are used to identify central (or android) obesity in which adipose tissue in the abdomen is associated with atherosclerosis.21,22 The waist circumference is found by measuring the circumference around the waist at the level of the iliac crest. Values above 40 inches for men and 35 inches for women are indicative of increased risk of adverse health outcomes.5,19 The waist-to-hip ratio is calculated by dividing the circumference of the waist at the level of the L3 by the hip circumference measured at the largest area of the gluteal region.19 For men, waist-to-hip ratios greater than 1.0 are associated with significantly increased risk of cardiovascular events. For women, a ratio greater than 0.85 indicates increased risk.19
Body-mass index calculation
The body-mass index (BMI), also known as the Quetelet index, is the most commonly used measure of obesity.20 BMI is a patient’s weight in kilograms divided by his or her height in meters squared (kg/m2 ).5,19 A free online BMI calculator is available through the National Heart, Lung and Blood Institute at www.nhlbisupport.com/bmi/bmicalc.htm.
Although the BMI estimates total body fat and compares well with densitometry, it may be less accurate in selected populations (eg, the elderly, certain ethnic groups, and persons with large muscle mass).19 Generally, when BMI exceeds 25, the greater the BMI, the greater the obesity-related morbidity and mortality.5,19,20,23 Table 1 shows the classification of obesity based on BMI, and Table 2 shows the BMI for combinations of height and weight in inches and pounds.5
TABLE 1
Body mass index (BMI) and degrees of obesity
| BMI | Category | Therapeutic options |
|---|---|---|
| <18.5 | Underweight | |
| 18.5–25.9 | Normal weight | Reinforce positive lifestyle |
| 25.0–29.9 | Overweight | Diet, exercise, behavior modification |
| 30.0–34.9 | Obese (Class I) | Diet, exercise, behavior modification; consider pharmacologic therapy* |
| 35.0–39.9 | Obese (Class II) | Diet, exercise, behavior modification; consider pharmacologic therapy |
| ≥40.0 | Obese (Class III or “Morbid Obesity”) | Consider surgical management |
| *For patients with multiple cardiovascular risk factors (eg, diabetes, hyperlipidemia), BMI >27 may be an indication for pharmacologic intervention at; at BMI >37, patients may be considered candidates for surgical therapy. | ||
| From the National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of obesity in adults: the Evidence Report. Bethesda, Md: US Department of Health and Human Services, 1998. | ||
Evaluation of documented obesity
In history taking and physical examination, look for reversible causes of obesity (including medications and endocrine disorders), consider the degree of obesity, and determine whether comorbid conditions are present, to help estimate prognosis. Evaluate the patient’s dietary and exercise habits, as well as willingness to modify these habits if necessary.1,5 Finally, review the patient’s weight history and any attempts at weight loss.
Medications associated with weight gain include psychotropic drugs, anticonvulsant agents, steroid hormones, insulin, and many oral hypoglycemic agents.1
Endocrine disorders such as Cushing’s syndrome and hypothyroidism may also contribute to obesity, but only rarely. Physical findings that increase the likelihood of Cushing’s syndrome, and their respective positive likelihood ratios (LR+)— the higher the value, the greater the likelihood of disease—include: hypertension (2.3), moon facies (1.6), thin skinfold (115.6), ecchymoses (4.5), and acne (2.2).19 Findings, and their likelihood ratios, associated with hypothyroidism include coarse skin (5.6), cool/dry skin (4.7), bradycardia (4.1), enlarged thyroid (2.8), and hoarse voice (5.4).19 The very high LR for skinfold thickness was determined for women of childbearing age who had elevated risk of having Cushing’s syndrome because of a history of both menstrual irregularities and hirsutism. Skinfold thickness is determined by using calipers on an area of minimal subcutaneous fat (eg, back of the hand). For women of reproductive age, skinfold thickness is normally greater than 1.8 mm.19
Laboratory assessment of the obese patient will rarely find a cause of weight gain (eg, hypothyroidism), but the addition of selected diagnostic tests will aid in the determination of prognosis. An abnormal fasting glucose level or impaired glucose tolerance is a major risk factor for cardiovascular disease. Abnormal lipid profiles heighten that risk for obese patients. All patients with documented obesity should undergo assessment for abnormal lipids and impaired glucose tolerance5 (SOR: D).
Treatment
The most important step in treating obesity is to establish a calorie deficit. The deficit can be achieved by increasing energy expenditure or by reducing energy intake or absorption. On average, a caloric deficit of 500 kilocalories per day will result in a weight loss of 1 pound per week.5 Reasonable expectations of therapy include weight loss of 1–2 pounds a week and a loss of 10% of total body weight in 5 months.5
Interventions for weight loss fall into 4 categories: lifestyle modifications (diet, exercise, and behavioral modification), drug therapy, complementary or alternative measures, and surgery. Table 3 summarizes the levels of evidence to support each intervention.
TABLE 3
Efficacy of weight-loss interventions
| Weight loss | ||||
|---|---|---|---|---|
| SOR* | Intervention | Short-term | Long-term | Comments |
| Diet, exercise, and behavioral modification | ||||
| A | Low/very-lowcalorie diet | 8% average weight loss from 3–12 months | Weight nears baseline in studies >24 months | Very-low-calorie diets may require laboratory assessment of metabolic function |
| High rate of noncompliance | ||||
| A | Low/very low fat with reduced calories | Similar to lowcalorie with moderate fat | Weight nears baseline in studies >24 months | No known side effects |
| A | Exercise | Less weight loss than diet therapy | Likely no significant weight loss | Improved cardiovascular fitness |
| May be effective in preventing weight gain | ||||
| A | Low-calorie diet + exercise | Increased weight loss vs. diet or exercise alone | Weight nears baseline in long-term studies | Improved cardiovascular fitness |
| Compliance a major problem | ||||
| B | Behavior modification | Increases effectiveness of diet, exercise | No significant effect at 5 years | No reported harms |
| Only studied when used with other methods | ||||
| C | Lowcarbohydrate diet | Not significant if calories are not reduced | No long-term data available | No known side effects, but creates nutritional imbalance and ketosis |
| Needs additional study | ||||
| Medication | ||||
| A | Sibutramine | ˜ 4 kg for trials less than 1 year | Modest weight loss when used for >1 year | Can elevate blood pressure |
| Number needed to treat (NNT) for 5% weight loss at 1 year = 3 | ||||
| NNT for 10% weight loss at 1 year = 5 | ||||
| A | Orlistat | ˜ 2–3 kg for trials less than 1 year | ˜ 3 kg at 2 years | GI side effects common, possible vitamin deficiencies |
| NNT for 5% weight loss at 1 year = 5 | ||||
| NNT for 10% weight loss at 1 year = 7 | ||||
| Surgery | ||||
| B | Roux-en-Y Gastric bypass | ˜ 50 kg (110 lbs) at 1 year | ˜ 50 kg (110 lbs) at up to 4 years | Significant operative risk and post-operative GI side effects |
| Nadir for weight loss occurs at 12–24 months | ||||
| B | Gastric banding | ˜ 30 Kg (66 lbs) at one year | 10–15% of initial weight lost may be regained long-term | Significant operative risk and post-operative GI side effects |
| Generally considered less effective that gastric bypass | ||||
| Complementary/alternative medicine | ||||
| B | Hypnosis | Minimal reduction | No statistically significant difference | Studied in combination with cognitive behavioral therapy |
| Systematic reviews reveal significant heterogeneity of low-quality randomized controlled trials | ||||
| B | Acupuncture | No significant difference | No significant difference | Systematic review reveals poor quality |
| RCTs, which limits ability to determine effect | ||||
| * Strength of recommendation | ||||
| A = Systematic review of randomized controlled trials (RCT) (with homogeneity) or individual RCT with narrow confidence interval | ||||
| B = Systematic review of cohort studies (with homogeneity), individual cohort studies or low-quality RCT, individual case-control study or SR of case-control studies (with homogeneity) | ||||
| C = Case series and poor quality cohort and case control studies | ||||
Lifestyle modifications
Management of obesity in every case should include dietary changes, exercise, and behavioral modification.
Dietary changes. Diets create a caloric deficit by reducing the intake of calories. Average weight loss with low-calorie diets is approximately 8% at 3–12 months (SOR: A),5 with most of the loss occurring in the first 3–5 months.24 There are many kinds of diets for weight loss, including low calorie, very-low calorie, low fat, very low fat, and low carbohydrate, but long-term compliance with all types of dietary interventions is a significant problem. When diet alone is used as therapy, between one third and one half of weight loss will not be maintained.24 Emerging strategies to help improve dietary compliance include behavioral modification (see below) and meal substitutes. Recent reports of interventions such as meal-replacement shakes indicate that long-term weight loss can be significantly improved (SOR: B).25-27
Examples of low-calorie, nutritionally balanced diets are Weight Watchers, Jenny Craig, Nutrisystem, the National Cholesterol Education Program Step I and Step II diets, and the Dietary Approaches to Stop Hypertension (DASH) diet. Low-calorie diets provide 800–1500 kilocalories per day.5,28,29 Very-low-calorie diets (400–500 kilocalories per day) may increase rates of weight loss initially, but at 1 year, results are similar to those of low-calorie diets (SOR: A).5,30
A low-fat diet (fat content 10%–19%) without a decrease in total calorie intake does not promote weight loss (SOR: A).5,31 Very-low-fat diets containing less than 10% fat have been described by such authors as Ornish and Pritikin.25 Obese patients using either the low-fat or very-low-fat diet can lose body weight and body fat, but only if calories are also decreased (SOR: A).5,28
Low-carbohydrate diets, such as Dr Atkin’s diet, are associated with modest (approximately 5 kg, or 11 lbs) weight loss (SOR: C).28,32 Improved study design is required to further evaluate the effectiveness and safety of low-carbohydrate diets in the clinical setting.
Exercise. Most studies of exercise are based on 30–50 minutes of moderately intense aerobic exercise, repeated 3–7 times per week.5 When it is the only prescribed therapy, exercise can be expected to produce modest weight loss only (SOR: A).5,33 Exercise combined with dietary intervention, however, increases weight lost (SOR: A), and exercise by itself may prevent weight gain (SOR: C).5
Behavioral Modification. Behavioral modification has been evaluated in combination with diet or exercise, and has been shown to increase compliance and weight loss for durations of 1 year or less (SOR: A).5,34 Weight gain is common when therapy is discontinued, and at 5 years, there is no difference between those who received behavioral therapy and those who were in control groups (SOR: A).5
Medications
Medications for treatment of obesity act through 1 or more of 3 mechanisms:
- Appetite suppression (eg, sibutramine, antidepressants such as fluoxetine)
- Increased metabolic activity (eg, stimulants such as ephedra with caffeine, Β-3 agonists)
- Decreased absorption of caloric load (orlistat)
For mild-to-moderate obesity (BMI >30 and <40), medications can be beneficial (SOR: A), but long-term weight loss beyond 2 years has not been studied.35 Pharmacologic intervention without lifestyle intervention actually decreases a person’s ability to lose weight (SOR: B).36
Two medications are approved by the United States Food and Drug Administration for long-term obesity management: sibutramine and orlistat. Both drugs reduce weight modestly (SOR: A).37-39 Both medications have similar indications for use: BMI >30, or BMI >27 with the presence of other cardiovascular risk factors (ie, diabetes or hyperlipidemia). Both should be used in conjunction with reduced-calorie diet and exercise (SOR: B).36
Sibutramine is usually started at 10 mg once a day, given with or without food. The dose may be titrated to a maximum of 15 mg/d after 4 weeks if weight loss has been inadequate.1 Sibutramine is known to increase pulse rate and blood pressure in a significant number of patients; because of this, regular evaluation of vital signs is required. At present, long-term use of sibutramine cannot be recommended, and safety data are unavailable beyond 1 year of use. Sibutramine should be avoided if these conditions are present: hypertension, coronary heart disease, congestive heart failure, an arrhythmic condition, pregnancy, renal impairment, concomitant use of MAOI, or a history of stroke.
Orlistat is started at 120 mg three times a day, and is taken with meals that contain fat. It may still be effective if taken up to one hour after eating. Orlistat may be avoided if the meal contains no fat. This drug may interfere with the absorption of some fat-soluble vitamins, and it is therefore recommended that patients take a multivitamin that has fat-soluble vitamins at least 2 hours before or after ingesting orlistat. Orlistat is not absorbed into the body and, at this time, no laboratory follow-up is needed. Regular evaluation of weight is needed to assess the efficacy of treatment. Orlistat should be avoided by those who have cholestasis or malabsorptive disorders or by those taking cyclosporine.40
Other medications that have been used include phentermine, ephedra, dexfenfluramine, phenyl-propanolamine (PPA), and mazindol.1,2 All of these medications produce significant weight loss in the short term (SOR: A), but they are not indicated for long-term use.2 In fact, phenylpropanolamine and dexfenfluramine are no longer available because of their severe side effects.2 Antidepressants do not yield a consistent benefit in well-designed studies of obesity management.2
Table 3 summarizes the effects of medications on weight loss.
Surgery
Surgical management of obesity is reserved for extremely obese persons because of the significant morbidity and mortality associated with the interventions. Currently, gastric bypass procedures result in less than 1% perioperative mortality and about 10% perioperative morbidity.41 Patients with a BMI >40 (or >37 with weight-related comorbidities) are candidates for surgery.42
It has been estimated that, for these patients, the cost per pound lost is less with surgery than with medications.43 In most series, the average morbidly obese patient can expect to lose 50% of excess body weight at 5 years after bypass surgery, and 50% of excess weight will be lost even 10 years post-operatively (SOR: B).44
Several options are available for surgical management of obesity. While the technical aspects of surgery are beyond the scope of this article, some generalizations can be made. Procedures may reduce the size of the stomach to decrease the volume of intake (gastroplasty), or may create a malabsorption condition (intestinal bypass) to decrease absorption of calories. The combination of a restrictive procedure with malabsorption (Rouxen-Y gastic bypass) is superior to a restrictive procedure alone (SOR: B).44
The surgical management of morbid obesity improves quality of life for patients,43 but no published studies to date have been able to evaluate the effect of the surgical management on mortality in the morbidly obese patient.
Complementary and alternative therapies
In addition to the traditional methods of weight loss, acupuncture and hypnosis have been studied in the treatment of obesity. Acupuncture does not appear to have any benefit greater than placebo (SOR: B).45 Hypnosis has also been reviewed and likely adds little, if any, benefit beyond that of placebo (SOR: B).45 Most studies of both acupuncture and hypnosis suffer from the difficulties of performing adequate control groups, and meta-analyses have demonstrated mixed results.45,46
Maintenance programs
There is significant evidence that when patients discontinue effective weight loss interventions (eg, diet or behavioral modification) they will return to their baseline weight. Because of this, it is important to consider maintenance programs as part of overall treatment and to imbue in patients the expectation that treatment will be lifelong. Examples of an approach to maintenance therapy include attendance at regular exercise or therapy sessions even after achieving weight-loss goals, or continued participation at commercial weight-loss program meetings or support groups.
ACKNOWLEDGEMENTS
The author was supported by grant 1 D45 PE 50175 -01, “Faculty Development in Family Medicine” funded by Health Resources and Services Administration (HRSA). The author wishes to thank Bill Hueston, MD, Peter Carek, MD, Arch Mainous III, PhD, and Lori Dickerson, PharmD, for their help with manuscript review. The author wishes to thank Tara Hogue for her for help with the preparation of this manuscript.
- Diet and exercise coupled with behavioral modification can improve both patient-related and disease-related outcomes in the short term; however, long-term efficacy is lacking (A).
- Drugs such as sibutramine or orlistat may achieve modest, short-term weight loss, but their long-term effectiveness is unproven (A).
- For patients with a BMI >40, gastric bypass procedures can lead to long-term weight loss (B).
Physician intervention to encourage and assist obese patients to lose weight is warranted, for these reasons:
- Prevention of adverse outcomes. Left untreated, obesity is clearly related to the development of many adverse health outcomes, including diabetes mellitus, hypertension, stroke, hyperlipidemia, coronary artery disease, gallstones, osteoarthritis, obstructive sleep apnea, vascular disease, depression, and certain cancers (breast, endometrial, prostate, colon).1-4
- Reduction of morbidity and mortality. A causal effect between intentional weight loss and mortality has been difficult to prove, but even modest weight loss can reduce the morbidity of obesity-related disease, such as arthritis and obstructive sleep apnea (Strength of recommendation: A).5-7 For those at increased risk of death from cardiovascular disease, such as persons with obesity and diabetes mellitus, intentional weight loss coupled with lifestyle change can significantly reduce mortality (SOR: C).8 Nearly 280,000 deaths per year are attributable to obesity.9
- Cost reduction. Nearly 25% of American adults are obese, and more than half are overweight.1,2 Obesity burdens society with significant costs, including more than $50 billion annually for direct care. With an additional $30 billion spent each year on weight-loss products and services, this disease accounts for over 5% of annual health care expenditures in the United States.5
Nature or nurture?
Excess fat is created when energy intake exceeds cellular energy consumption. The complex relationship between the human body’s environment and the development of obesity is poorly understood, but recent genetic investigations have elucidated new mechanisms in the regulation of both satiety and energy expenditure. Using data from heritability studies, some researchers have estimated that up to 70% of the variability in weight among humans can be explained by genetic influences, but it is unlikely that changes in human genes account for the recent change in obesity prevalence.10
Risk factors
Identifiable risks factors for obesity in adulthood include parental history of obesity, low socio-economic background, and a history of high birth weight.11
Prevention
Recently, factors including consumption of sugar-sweetened beverages, lack of breast-feeding, and television viewing have been identified as risk factors for childhood and adolescent obesity.12-14 Because obesity at a young age can lead to adult obesity, these factors may be targeted to prevent adult obesity.
School-based programs for diet and exercise appear to be ineffective for preventing obesity (SOR: B).15,16 However, most research has been of limited quality. In one recent randomized study, reduction of television viewing (including videotape and videogame use) through school intervention was associated with significant reduction in BMI (SOR: B).14
Screening recommendations
The United States Preventive Service Task Force recommends periodic measurement of both height and weight in adults (SOR: B). The waist-to-hip ratio is thought to have insufficient evidence for recommendation as a routine screening tool because studies identifying a benefit to screening using only the waist-to-hip ratio have not been completed (SOR: C).17
Initial determination of obesity
Although the standard for body fat measurement is densitometry, which determines the density of a body submersed in water, the cost and technical requirements prohibit routine use in the clinical setting.18-20 The waist-to-hip ratio and waist circumference are used to identify central (or android) obesity in which adipose tissue in the abdomen is associated with atherosclerosis.21,22 The waist circumference is found by measuring the circumference around the waist at the level of the iliac crest. Values above 40 inches for men and 35 inches for women are indicative of increased risk of adverse health outcomes.5,19 The waist-to-hip ratio is calculated by dividing the circumference of the waist at the level of the L3 by the hip circumference measured at the largest area of the gluteal region.19 For men, waist-to-hip ratios greater than 1.0 are associated with significantly increased risk of cardiovascular events. For women, a ratio greater than 0.85 indicates increased risk.19
Body-mass index calculation
The body-mass index (BMI), also known as the Quetelet index, is the most commonly used measure of obesity.20 BMI is a patient’s weight in kilograms divided by his or her height in meters squared (kg/m2 ).5,19 A free online BMI calculator is available through the National Heart, Lung and Blood Institute at www.nhlbisupport.com/bmi/bmicalc.htm.
Although the BMI estimates total body fat and compares well with densitometry, it may be less accurate in selected populations (eg, the elderly, certain ethnic groups, and persons with large muscle mass).19 Generally, when BMI exceeds 25, the greater the BMI, the greater the obesity-related morbidity and mortality.5,19,20,23 Table 1 shows the classification of obesity based on BMI, and Table 2 shows the BMI for combinations of height and weight in inches and pounds.5
TABLE 1
Body mass index (BMI) and degrees of obesity
| BMI | Category | Therapeutic options |
|---|---|---|
| <18.5 | Underweight | |
| 18.5–25.9 | Normal weight | Reinforce positive lifestyle |
| 25.0–29.9 | Overweight | Diet, exercise, behavior modification |
| 30.0–34.9 | Obese (Class I) | Diet, exercise, behavior modification; consider pharmacologic therapy* |
| 35.0–39.9 | Obese (Class II) | Diet, exercise, behavior modification; consider pharmacologic therapy |
| ≥40.0 | Obese (Class III or “Morbid Obesity”) | Consider surgical management |
| *For patients with multiple cardiovascular risk factors (eg, diabetes, hyperlipidemia), BMI >27 may be an indication for pharmacologic intervention at; at BMI >37, patients may be considered candidates for surgical therapy. | ||
| From the National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of obesity in adults: the Evidence Report. Bethesda, Md: US Department of Health and Human Services, 1998. | ||
Evaluation of documented obesity
In history taking and physical examination, look for reversible causes of obesity (including medications and endocrine disorders), consider the degree of obesity, and determine whether comorbid conditions are present, to help estimate prognosis. Evaluate the patient’s dietary and exercise habits, as well as willingness to modify these habits if necessary.1,5 Finally, review the patient’s weight history and any attempts at weight loss.
Medications associated with weight gain include psychotropic drugs, anticonvulsant agents, steroid hormones, insulin, and many oral hypoglycemic agents.1
Endocrine disorders such as Cushing’s syndrome and hypothyroidism may also contribute to obesity, but only rarely. Physical findings that increase the likelihood of Cushing’s syndrome, and their respective positive likelihood ratios (LR+)— the higher the value, the greater the likelihood of disease—include: hypertension (2.3), moon facies (1.6), thin skinfold (115.6), ecchymoses (4.5), and acne (2.2).19 Findings, and their likelihood ratios, associated with hypothyroidism include coarse skin (5.6), cool/dry skin (4.7), bradycardia (4.1), enlarged thyroid (2.8), and hoarse voice (5.4).19 The very high LR for skinfold thickness was determined for women of childbearing age who had elevated risk of having Cushing’s syndrome because of a history of both menstrual irregularities and hirsutism. Skinfold thickness is determined by using calipers on an area of minimal subcutaneous fat (eg, back of the hand). For women of reproductive age, skinfold thickness is normally greater than 1.8 mm.19
Laboratory assessment of the obese patient will rarely find a cause of weight gain (eg, hypothyroidism), but the addition of selected diagnostic tests will aid in the determination of prognosis. An abnormal fasting glucose level or impaired glucose tolerance is a major risk factor for cardiovascular disease. Abnormal lipid profiles heighten that risk for obese patients. All patients with documented obesity should undergo assessment for abnormal lipids and impaired glucose tolerance5 (SOR: D).
Treatment
The most important step in treating obesity is to establish a calorie deficit. The deficit can be achieved by increasing energy expenditure or by reducing energy intake or absorption. On average, a caloric deficit of 500 kilocalories per day will result in a weight loss of 1 pound per week.5 Reasonable expectations of therapy include weight loss of 1–2 pounds a week and a loss of 10% of total body weight in 5 months.5
Interventions for weight loss fall into 4 categories: lifestyle modifications (diet, exercise, and behavioral modification), drug therapy, complementary or alternative measures, and surgery. Table 3 summarizes the levels of evidence to support each intervention.
TABLE 3
Efficacy of weight-loss interventions
| Weight loss | ||||
|---|---|---|---|---|
| SOR* | Intervention | Short-term | Long-term | Comments |
| Diet, exercise, and behavioral modification | ||||
| A | Low/very-lowcalorie diet | 8% average weight loss from 3–12 months | Weight nears baseline in studies >24 months | Very-low-calorie diets may require laboratory assessment of metabolic function |
| High rate of noncompliance | ||||
| A | Low/very low fat with reduced calories | Similar to lowcalorie with moderate fat | Weight nears baseline in studies >24 months | No known side effects |
| A | Exercise | Less weight loss than diet therapy | Likely no significant weight loss | Improved cardiovascular fitness |
| May be effective in preventing weight gain | ||||
| A | Low-calorie diet + exercise | Increased weight loss vs. diet or exercise alone | Weight nears baseline in long-term studies | Improved cardiovascular fitness |
| Compliance a major problem | ||||
| B | Behavior modification | Increases effectiveness of diet, exercise | No significant effect at 5 years | No reported harms |
| Only studied when used with other methods | ||||
| C | Lowcarbohydrate diet | Not significant if calories are not reduced | No long-term data available | No known side effects, but creates nutritional imbalance and ketosis |
| Needs additional study | ||||
| Medication | ||||
| A | Sibutramine | ˜ 4 kg for trials less than 1 year | Modest weight loss when used for >1 year | Can elevate blood pressure |
| Number needed to treat (NNT) for 5% weight loss at 1 year = 3 | ||||
| NNT for 10% weight loss at 1 year = 5 | ||||
| A | Orlistat | ˜ 2–3 kg for trials less than 1 year | ˜ 3 kg at 2 years | GI side effects common, possible vitamin deficiencies |
| NNT for 5% weight loss at 1 year = 5 | ||||
| NNT for 10% weight loss at 1 year = 7 | ||||
| Surgery | ||||
| B | Roux-en-Y Gastric bypass | ˜ 50 kg (110 lbs) at 1 year | ˜ 50 kg (110 lbs) at up to 4 years | Significant operative risk and post-operative GI side effects |
| Nadir for weight loss occurs at 12–24 months | ||||
| B | Gastric banding | ˜ 30 Kg (66 lbs) at one year | 10–15% of initial weight lost may be regained long-term | Significant operative risk and post-operative GI side effects |
| Generally considered less effective that gastric bypass | ||||
| Complementary/alternative medicine | ||||
| B | Hypnosis | Minimal reduction | No statistically significant difference | Studied in combination with cognitive behavioral therapy |
| Systematic reviews reveal significant heterogeneity of low-quality randomized controlled trials | ||||
| B | Acupuncture | No significant difference | No significant difference | Systematic review reveals poor quality |
| RCTs, which limits ability to determine effect | ||||
| * Strength of recommendation | ||||
| A = Systematic review of randomized controlled trials (RCT) (with homogeneity) or individual RCT with narrow confidence interval | ||||
| B = Systematic review of cohort studies (with homogeneity), individual cohort studies or low-quality RCT, individual case-control study or SR of case-control studies (with homogeneity) | ||||
| C = Case series and poor quality cohort and case control studies | ||||
Lifestyle modifications
Management of obesity in every case should include dietary changes, exercise, and behavioral modification.
Dietary changes. Diets create a caloric deficit by reducing the intake of calories. Average weight loss with low-calorie diets is approximately 8% at 3–12 months (SOR: A),5 with most of the loss occurring in the first 3–5 months.24 There are many kinds of diets for weight loss, including low calorie, very-low calorie, low fat, very low fat, and low carbohydrate, but long-term compliance with all types of dietary interventions is a significant problem. When diet alone is used as therapy, between one third and one half of weight loss will not be maintained.24 Emerging strategies to help improve dietary compliance include behavioral modification (see below) and meal substitutes. Recent reports of interventions such as meal-replacement shakes indicate that long-term weight loss can be significantly improved (SOR: B).25-27
Examples of low-calorie, nutritionally balanced diets are Weight Watchers, Jenny Craig, Nutrisystem, the National Cholesterol Education Program Step I and Step II diets, and the Dietary Approaches to Stop Hypertension (DASH) diet. Low-calorie diets provide 800–1500 kilocalories per day.5,28,29 Very-low-calorie diets (400–500 kilocalories per day) may increase rates of weight loss initially, but at 1 year, results are similar to those of low-calorie diets (SOR: A).5,30
A low-fat diet (fat content 10%–19%) without a decrease in total calorie intake does not promote weight loss (SOR: A).5,31 Very-low-fat diets containing less than 10% fat have been described by such authors as Ornish and Pritikin.25 Obese patients using either the low-fat or very-low-fat diet can lose body weight and body fat, but only if calories are also decreased (SOR: A).5,28
Low-carbohydrate diets, such as Dr Atkin’s diet, are associated with modest (approximately 5 kg, or 11 lbs) weight loss (SOR: C).28,32 Improved study design is required to further evaluate the effectiveness and safety of low-carbohydrate diets in the clinical setting.
Exercise. Most studies of exercise are based on 30–50 minutes of moderately intense aerobic exercise, repeated 3–7 times per week.5 When it is the only prescribed therapy, exercise can be expected to produce modest weight loss only (SOR: A).5,33 Exercise combined with dietary intervention, however, increases weight lost (SOR: A), and exercise by itself may prevent weight gain (SOR: C).5
Behavioral Modification. Behavioral modification has been evaluated in combination with diet or exercise, and has been shown to increase compliance and weight loss for durations of 1 year or less (SOR: A).5,34 Weight gain is common when therapy is discontinued, and at 5 years, there is no difference between those who received behavioral therapy and those who were in control groups (SOR: A).5
Medications
Medications for treatment of obesity act through 1 or more of 3 mechanisms:
- Appetite suppression (eg, sibutramine, antidepressants such as fluoxetine)
- Increased metabolic activity (eg, stimulants such as ephedra with caffeine, Β-3 agonists)
- Decreased absorption of caloric load (orlistat)
For mild-to-moderate obesity (BMI >30 and <40), medications can be beneficial (SOR: A), but long-term weight loss beyond 2 years has not been studied.35 Pharmacologic intervention without lifestyle intervention actually decreases a person’s ability to lose weight (SOR: B).36
Two medications are approved by the United States Food and Drug Administration for long-term obesity management: sibutramine and orlistat. Both drugs reduce weight modestly (SOR: A).37-39 Both medications have similar indications for use: BMI >30, or BMI >27 with the presence of other cardiovascular risk factors (ie, diabetes or hyperlipidemia). Both should be used in conjunction with reduced-calorie diet and exercise (SOR: B).36
Sibutramine is usually started at 10 mg once a day, given with or without food. The dose may be titrated to a maximum of 15 mg/d after 4 weeks if weight loss has been inadequate.1 Sibutramine is known to increase pulse rate and blood pressure in a significant number of patients; because of this, regular evaluation of vital signs is required. At present, long-term use of sibutramine cannot be recommended, and safety data are unavailable beyond 1 year of use. Sibutramine should be avoided if these conditions are present: hypertension, coronary heart disease, congestive heart failure, an arrhythmic condition, pregnancy, renal impairment, concomitant use of MAOI, or a history of stroke.
Orlistat is started at 120 mg three times a day, and is taken with meals that contain fat. It may still be effective if taken up to one hour after eating. Orlistat may be avoided if the meal contains no fat. This drug may interfere with the absorption of some fat-soluble vitamins, and it is therefore recommended that patients take a multivitamin that has fat-soluble vitamins at least 2 hours before or after ingesting orlistat. Orlistat is not absorbed into the body and, at this time, no laboratory follow-up is needed. Regular evaluation of weight is needed to assess the efficacy of treatment. Orlistat should be avoided by those who have cholestasis or malabsorptive disorders or by those taking cyclosporine.40
Other medications that have been used include phentermine, ephedra, dexfenfluramine, phenyl-propanolamine (PPA), and mazindol.1,2 All of these medications produce significant weight loss in the short term (SOR: A), but they are not indicated for long-term use.2 In fact, phenylpropanolamine and dexfenfluramine are no longer available because of their severe side effects.2 Antidepressants do not yield a consistent benefit in well-designed studies of obesity management.2
Table 3 summarizes the effects of medications on weight loss.
Surgery
Surgical management of obesity is reserved for extremely obese persons because of the significant morbidity and mortality associated with the interventions. Currently, gastric bypass procedures result in less than 1% perioperative mortality and about 10% perioperative morbidity.41 Patients with a BMI >40 (or >37 with weight-related comorbidities) are candidates for surgery.42
It has been estimated that, for these patients, the cost per pound lost is less with surgery than with medications.43 In most series, the average morbidly obese patient can expect to lose 50% of excess body weight at 5 years after bypass surgery, and 50% of excess weight will be lost even 10 years post-operatively (SOR: B).44
Several options are available for surgical management of obesity. While the technical aspects of surgery are beyond the scope of this article, some generalizations can be made. Procedures may reduce the size of the stomach to decrease the volume of intake (gastroplasty), or may create a malabsorption condition (intestinal bypass) to decrease absorption of calories. The combination of a restrictive procedure with malabsorption (Rouxen-Y gastic bypass) is superior to a restrictive procedure alone (SOR: B).44
The surgical management of morbid obesity improves quality of life for patients,43 but no published studies to date have been able to evaluate the effect of the surgical management on mortality in the morbidly obese patient.
Complementary and alternative therapies
In addition to the traditional methods of weight loss, acupuncture and hypnosis have been studied in the treatment of obesity. Acupuncture does not appear to have any benefit greater than placebo (SOR: B).45 Hypnosis has also been reviewed and likely adds little, if any, benefit beyond that of placebo (SOR: B).45 Most studies of both acupuncture and hypnosis suffer from the difficulties of performing adequate control groups, and meta-analyses have demonstrated mixed results.45,46
Maintenance programs
There is significant evidence that when patients discontinue effective weight loss interventions (eg, diet or behavioral modification) they will return to their baseline weight. Because of this, it is important to consider maintenance programs as part of overall treatment and to imbue in patients the expectation that treatment will be lifelong. Examples of an approach to maintenance therapy include attendance at regular exercise or therapy sessions even after achieving weight-loss goals, or continued participation at commercial weight-loss program meetings or support groups.
ACKNOWLEDGEMENTS
The author was supported by grant 1 D45 PE 50175 -01, “Faculty Development in Family Medicine” funded by Health Resources and Services Administration (HRSA). The author wishes to thank Bill Hueston, MD, Peter Carek, MD, Arch Mainous III, PhD, and Lori Dickerson, PharmD, for their help with manuscript review. The author wishes to thank Tara Hogue for her for help with the preparation of this manuscript.
1. Dickerson L, Carek PJ. Drug therapy for obesity. Am Fam Physician 2000;51:2131-8.
2. Arterburn D, Hitchcock-Noel P. Obesity. Clinical Evidence 2001;5:512-9.
3. Mun EC, Blackburn GL, Matthews JB. Current status of medical and surgical therapy for obesity. Gastroenterology 2001;120:559-81.
4. Field AE, Coakley EH, Must A, Spandano JL, Laird N, Dietz WH, et al. Impact of overweight on the risk of developing common chronic diseases during a 10 year period. Arch Intern Med 2001;151:1581-5.
5. National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of obesity in adults: The evidence report. Bethesda, Md: US Department of Health and Human Services; 1998.
6. Messier SP, Loeser RF, Mitchell MN, Valle G, Morgan TP, Rejeski WJ, et al. Exercise and weight loss in obese older adults with knee osteoarthritis: a preliminary study. J Am Geriatr Soc 2000;48:1052-72.
7. Shneerson J, Wright J. Lifestyle modification for obstructive sleep apnoea (Cochrane Review). In: The Cochrane Library, Issue 4, 2001. Oxford: Update Software.
8. Williamson DF, Thompson TS, Thun M, Flanders D, Pamuk E, Byers T. Intentional weight loss and mortality among overweight individuals with diabetes. Diabetes Care 2000;10:1499-1504.
9. Allison DB, Fontaine KR, Manson JE, Stevens J, Van Itallie TB. Annual deaths attributable to obesity in the United States. JAMA 1999;282:1530-8.
10. Yanovski J, Yanovski S. Recent advances in basic obesity research. JAMA 1999;282:1504-6.
11. Parsons TJ, Power C, Logan S, Summerbell CD. Childhood predictors of adult obesity: a systematic review. Int J Obes Relat Metab Disord 1999;8 (suppl):S1-107.
12. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001;357:505-8.
13. Gillman MW, Rifas-Shiman SL, Camargo CA, Berkey CS, Frazier AL, Rocket HRH, et al. Risk of overweight among adolescents who were breastfed as infants. JAMA 2001;285:2451-7.
14. Robinson T. Reducing children’s television viewing to prevent obesity. JAMA 1999;282:1551-7.
15. Campbell K, Waters E, O’Meara S, Summerbell C. Interventions for preventing obesity in children (Cochrane Review). In: The Cochrane Library, Issue 5, 2001. Oxford: Update Software.
16. Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. Randomized controlled trial of primary school based intervention to reduce risk factors for obesity. BMJ 2001;323:1029-32.
17. US Preventive Services Task Force. Screening for obesity. In: US Preventive Services Task Force: Guide to Clinical Preventative Services: Report of the US Preventive Services Task Force. 2nd ed. Baltimore, Md: Williams and Wilkins; 1995;219-29.
18. Flier JS, Foster DW. Eating Disorders: Obesity, anorexia nervosa, and bullemia nervosa. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, Pa: WB Saunders; 1998;1051-97.
19. McGee S. Evidence-based physical diagnosis. Philadelphia, Pa: WB Saunders; 2001.
20. Willett WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999;351:527-35.
21. Rexrode KM, Carey VJ, Hennekens CH, Walters EE, Colditz GA, Stampfer MJ, et al. Abdominal adiposity and coronary heart disease in women. JAMA 1998;280:1843-8.
22. Iwao S, Iwao N, Muller DC, Elahi D, Shimokata H, Andres R. Does waist circumference add to the predictive power of the body mass index for coronary risk? Obesity Research. 2001;9:585-95.
23. Toriano RP, Frongillo EA, Sobal J, Levitsky DA. The relationship between body weight and mortality: a quantitative analysis of combined information from existing studies. Int J Obes Relat Metab Disord 1996;20:63-75.
24. Hensrud DD. Dietary treatment and long-term weight loss and maintenance in type 2 diabetes. Obesity Research 2001;9:348S-353S.
25. Ditschuneit HH, Flechtner-Mors M. Value of structured meals for weight management: risk factors and long-term weight maintenance. Obesity Research 2001;9(suppl 4):284S-289S.
26. Ditschuneit HH, Flechtner-Mors M, Johnson TD, Adler G. Metabolic and weight-loss effects of a long-term dietary intervention in obese patients. Am J Clin Nutr 1999;69:198-204.
27. Flechtner-Mors M, Ditschuneit HH, Johnson TD, Suchard MA, Adler G. Metabolic and weight loss effects of long-term dietary interventions in obese patients: four-year results. Obesity Research 2000;8:399-402.
28. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obesity Research 2001;9(suppl 1):1S-50S.
29. Finer N. Low-calorie diets and sustained weight loss. Obesity Research 2001;9(suppl 4):290S-292S.
30. Saris W. Very-low-calorie diets and sustained weight loss. Obesity Research 2001;9(suppl 4):292S-301S.
31. Pirozzo S, Summerbell C, Cameron C, Glasziou P. Advice on low-fat diets or obesity (Cochrane Review). In: The Cochrane Library, Issue 2, 2002. Oxford: Update Software.
32. Skov AR, Toubro S, Ronn B, Holm L, Astrup A. Randomized trial on protein vs.carbohydrate in ad libi-tum reduced diet for the treatment of obesity. Int J Obes 1999;23:528-36.
33. Bray GA. Role of physical activity and exercise in obesity. Up To Date (online 9.3). Retrieval date 11/5/2001. Up To Date, Inc. Wellesley, Mass, USA.
34. Thorogood M, Hillsdon M, Summerbell C. Changing behaviour. Clinical Evidence 2000;5:25-52.
35. Weintraub M, Sundaresan PR, Schuster B, Averbuch M, Stein EC, Byrne L. Long-term weight control study V. Clin Pharmacol Ther 1992;51:615-8.
36. Wadden T. Benefits of lifestyle modification in the phar-macologic treatment of obesity: a randomized trial. Arch Intern Med 2001;151:218-27.
37. Smith MB. Randomized placebo-controlled trial of long-term treatment with sibutramine in mild to moderate obesity. J Fam Pract 2001;50:505-12.
38. Sjostrom L, Rissanen A, Anderson T, Boldrin M, Golay A, Koppeschaan HPF, et al. Randomized placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients. European Multicentre Orlistat Study Group. Lancet 1998;352:157-72.
39. O’meara S, Riemsma R, Shirran L, Mather L, ter Riet G. A rapid and systematic review of the clinical effectiveness and cost-effectiveness of orlistat in the management of obesity. Health Technology Assess 2001;5:18.
40. Physician’s Desk Reference. PGS. Montvale, NJ: Medical Economics; 2001;2809-13.
41. Balsiger BM, Kennedy FP, Abu-Lebdeh HS, Collazo-Clavell M, Jensen MD, O’Brien T, et al. Prospective evaluation of Roux-en Y gastric bypass as primary operation for medically complicated obesity. Mayo Clin Proc 2000;75:573-80.
42. Gastrointestinal Surgery for Severe Obesity. NIH Consensus Statement Online 1991; 25-27. Cited August 1, 2001;9(1):1-20.
43. Van Gemert WG, Van Dielen F, Soeters PB, Greve JW. Quality of life before and after weight-reducing surgery and cost-effectiveness analysis. In: Deitel M,†Cowan SM, eds. Update: Surgery for the Morbidly Obese Patient. Toronto: FD Communications; 2000;595-602.
44. Sugerman HJ. The epidemic of severe obesity: value of surgical treatment. Mayo Clin Proc 2000;75:559-572.
45. Ernst E. Acupuncture/acupressure for weight reduction? A systematic review. Wien Klin Wochenschr 1997;109:50-2.
46. Allison DB, Faith MS. Hypnosis as an adjunct to cogni-tive-behavioral psychotherapy for obesity: a meta-analyt-ic reappraisal. J Consult Clin Psychol 1995;54:513-5.
1. Dickerson L, Carek PJ. Drug therapy for obesity. Am Fam Physician 2000;51:2131-8.
2. Arterburn D, Hitchcock-Noel P. Obesity. Clinical Evidence 2001;5:512-9.
3. Mun EC, Blackburn GL, Matthews JB. Current status of medical and surgical therapy for obesity. Gastroenterology 2001;120:559-81.
4. Field AE, Coakley EH, Must A, Spandano JL, Laird N, Dietz WH, et al. Impact of overweight on the risk of developing common chronic diseases during a 10 year period. Arch Intern Med 2001;151:1581-5.
5. National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of obesity in adults: The evidence report. Bethesda, Md: US Department of Health and Human Services; 1998.
6. Messier SP, Loeser RF, Mitchell MN, Valle G, Morgan TP, Rejeski WJ, et al. Exercise and weight loss in obese older adults with knee osteoarthritis: a preliminary study. J Am Geriatr Soc 2000;48:1052-72.
7. Shneerson J, Wright J. Lifestyle modification for obstructive sleep apnoea (Cochrane Review). In: The Cochrane Library, Issue 4, 2001. Oxford: Update Software.
8. Williamson DF, Thompson TS, Thun M, Flanders D, Pamuk E, Byers T. Intentional weight loss and mortality among overweight individuals with diabetes. Diabetes Care 2000;10:1499-1504.
9. Allison DB, Fontaine KR, Manson JE, Stevens J, Van Itallie TB. Annual deaths attributable to obesity in the United States. JAMA 1999;282:1530-8.
10. Yanovski J, Yanovski S. Recent advances in basic obesity research. JAMA 1999;282:1504-6.
11. Parsons TJ, Power C, Logan S, Summerbell CD. Childhood predictors of adult obesity: a systematic review. Int J Obes Relat Metab Disord 1999;8 (suppl):S1-107.
12. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001;357:505-8.
13. Gillman MW, Rifas-Shiman SL, Camargo CA, Berkey CS, Frazier AL, Rocket HRH, et al. Risk of overweight among adolescents who were breastfed as infants. JAMA 2001;285:2451-7.
14. Robinson T. Reducing children’s television viewing to prevent obesity. JAMA 1999;282:1551-7.
15. Campbell K, Waters E, O’Meara S, Summerbell C. Interventions for preventing obesity in children (Cochrane Review). In: The Cochrane Library, Issue 5, 2001. Oxford: Update Software.
16. Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. Randomized controlled trial of primary school based intervention to reduce risk factors for obesity. BMJ 2001;323:1029-32.
17. US Preventive Services Task Force. Screening for obesity. In: US Preventive Services Task Force: Guide to Clinical Preventative Services: Report of the US Preventive Services Task Force. 2nd ed. Baltimore, Md: Williams and Wilkins; 1995;219-29.
18. Flier JS, Foster DW. Eating Disorders: Obesity, anorexia nervosa, and bullemia nervosa. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, Pa: WB Saunders; 1998;1051-97.
19. McGee S. Evidence-based physical diagnosis. Philadelphia, Pa: WB Saunders; 2001.
20. Willett WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999;351:527-35.
21. Rexrode KM, Carey VJ, Hennekens CH, Walters EE, Colditz GA, Stampfer MJ, et al. Abdominal adiposity and coronary heart disease in women. JAMA 1998;280:1843-8.
22. Iwao S, Iwao N, Muller DC, Elahi D, Shimokata H, Andres R. Does waist circumference add to the predictive power of the body mass index for coronary risk? Obesity Research. 2001;9:585-95.
23. Toriano RP, Frongillo EA, Sobal J, Levitsky DA. The relationship between body weight and mortality: a quantitative analysis of combined information from existing studies. Int J Obes Relat Metab Disord 1996;20:63-75.
24. Hensrud DD. Dietary treatment and long-term weight loss and maintenance in type 2 diabetes. Obesity Research 2001;9:348S-353S.
25. Ditschuneit HH, Flechtner-Mors M. Value of structured meals for weight management: risk factors and long-term weight maintenance. Obesity Research 2001;9(suppl 4):284S-289S.
26. Ditschuneit HH, Flechtner-Mors M, Johnson TD, Adler G. Metabolic and weight-loss effects of a long-term dietary intervention in obese patients. Am J Clin Nutr 1999;69:198-204.
27. Flechtner-Mors M, Ditschuneit HH, Johnson TD, Suchard MA, Adler G. Metabolic and weight loss effects of long-term dietary interventions in obese patients: four-year results. Obesity Research 2000;8:399-402.
28. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obesity Research 2001;9(suppl 1):1S-50S.
29. Finer N. Low-calorie diets and sustained weight loss. Obesity Research 2001;9(suppl 4):290S-292S.
30. Saris W. Very-low-calorie diets and sustained weight loss. Obesity Research 2001;9(suppl 4):292S-301S.
31. Pirozzo S, Summerbell C, Cameron C, Glasziou P. Advice on low-fat diets or obesity (Cochrane Review). In: The Cochrane Library, Issue 2, 2002. Oxford: Update Software.
32. Skov AR, Toubro S, Ronn B, Holm L, Astrup A. Randomized trial on protein vs.carbohydrate in ad libi-tum reduced diet for the treatment of obesity. Int J Obes 1999;23:528-36.
33. Bray GA. Role of physical activity and exercise in obesity. Up To Date (online 9.3). Retrieval date 11/5/2001. Up To Date, Inc. Wellesley, Mass, USA.
34. Thorogood M, Hillsdon M, Summerbell C. Changing behaviour. Clinical Evidence 2000;5:25-52.
35. Weintraub M, Sundaresan PR, Schuster B, Averbuch M, Stein EC, Byrne L. Long-term weight control study V. Clin Pharmacol Ther 1992;51:615-8.
36. Wadden T. Benefits of lifestyle modification in the phar-macologic treatment of obesity: a randomized trial. Arch Intern Med 2001;151:218-27.
37. Smith MB. Randomized placebo-controlled trial of long-term treatment with sibutramine in mild to moderate obesity. J Fam Pract 2001;50:505-12.
38. Sjostrom L, Rissanen A, Anderson T, Boldrin M, Golay A, Koppeschaan HPF, et al. Randomized placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients. European Multicentre Orlistat Study Group. Lancet 1998;352:157-72.
39. O’meara S, Riemsma R, Shirran L, Mather L, ter Riet G. A rapid and systematic review of the clinical effectiveness and cost-effectiveness of orlistat in the management of obesity. Health Technology Assess 2001;5:18.
40. Physician’s Desk Reference. PGS. Montvale, NJ: Medical Economics; 2001;2809-13.
41. Balsiger BM, Kennedy FP, Abu-Lebdeh HS, Collazo-Clavell M, Jensen MD, O’Brien T, et al. Prospective evaluation of Roux-en Y gastric bypass as primary operation for medically complicated obesity. Mayo Clin Proc 2000;75:573-80.
42. Gastrointestinal Surgery for Severe Obesity. NIH Consensus Statement Online 1991; 25-27. Cited August 1, 2001;9(1):1-20.
43. Van Gemert WG, Van Dielen F, Soeters PB, Greve JW. Quality of life before and after weight-reducing surgery and cost-effectiveness analysis. In: Deitel M,†Cowan SM, eds. Update: Surgery for the Morbidly Obese Patient. Toronto: FD Communications; 2000;595-602.
44. Sugerman HJ. The epidemic of severe obesity: value of surgical treatment. Mayo Clin Proc 2000;75:559-572.
45. Ernst E. Acupuncture/acupressure for weight reduction? A systematic review. Wien Klin Wochenschr 1997;109:50-2.
46. Allison DB, Faith MS. Hypnosis as an adjunct to cogni-tive-behavioral psychotherapy for obesity: a meta-analyt-ic reappraisal. J Consult Clin Psychol 1995;54:513-5.