Final Recommendation Statement

Obesity: Screening, 1996

January 01, 1996

Recommendations made by the USPSTF are independent of the U.S. government. They should not be construed as an official position of the Agency for Healthcare Research and Quality or the U.S. Department of Health and Human Services.

This topic is being updated. Please use the link(s) below to see the latest documents available.
  • Update in Progress for Healthy Diet, Physical Activity, and/or Weight Loss to Prevent Cardiovascular Disease in Adults: Behavioral Counseling Interventions

Recommendation Summary

Population Recommendation Grade
General population Periodic height and weight measurements are recommended for all patients. B
General population There is insufficient evidence to recommend for or against determination of the WHR (waist-hip circumference ratio) as a routine screening test for obesity. C

Full Recommendation:

Recommendations made by the USPSTF are independent of the U.S. government. They should not be construed as an official position of the Agency for Healthcare Research and Quality or the U.S. Department of Health and Human Services.

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Obesity is an excess of body fat.1 Most epidemiologic studies rely on indices of relative weight, such as body mass index (BMI), an index of body weight that is normalized for height, to estimate the prevalence of obesity.a For example, the National Center for Health Statistics currently uses the 85th percentile sex-specific values of BMI for persons aged 20-29 (≥27.8 kg/m2 for men and ≥27.3 kg/m2 for women) from the second U.S. National Health and Nutrition Examination Survey (NHANES II) as a cutoff to define overweight in adults.2

Approximately one third of adult Americans aged 20 and older are estimated to be overweight, based on data from NHANES III.3 Using 1990 census figures, this corresponds to 58 million people. The prevalence of overweight in the United States has increased dramatically during the past 15 years in men and women of all age and ethnic groups, and remains disproportionately high among black and Hispanic women.3 Other groups that have a high prevalence of obesity include Asian and Pacific Islanders, Native Americans and Alaska Natives, and Native Hawaiians.4 The prevalence of overweight among adolescents has also increased.5 Based on NHANES III data, about one fifth of adolescents aged 12-19 are overweight.5 The prevalence of obesity among younger children is uncertain, but is estimated to be between 5% and 25%,6 and may also be increasing.7

Increased mortality in adults has been clearly documented as a result of morbid obesity, weight that is at least twice the desirable weight.8,9 Less severe obesity (e.g., as low as 26.4-28.5 kg/m2) has also been associated with increased mortality in large prospective cohort studies.10-13 Although some studies have reported greater mortality among the thinnest individuals,14.a 1993 prospective cohort study that carefully controlled for smoking and illness-related weight loss found a linear relationship between BMI and mortality.15 Two cohort studies suggest that overweight children and adolescents may have increased mortality as adults.16,17 Childhood obesity may be a significant risk factor for adult obesity, with adolescent obesity being a better predictor than obesity at younger ages.8,18,19

Persons who are overweight are more likely to have adult-onset diabetes, hypertension, and risk factors for other diseases.8,20 The prevalence of diabetes and hypertension is 3 times higher in overweight adults than in those of normal weight.21 Observational studies have established a clear association between overweight and hypercholesterolemia and suggest an independent relationship between overweight and coronary artery disease.8,10,11,20-23 Being overweight has also been associated with several cardiovascular risk factors in children and adolescents, including hypercholesterolemia and hypertension.24-26 An elevated waist/hip circumference ratio (WHR), which may indicate central adiposity, has been shown to correlate with the presence of these conditions independent of BMI,27-35 and may predict the complications of obesity in adults better than BMI does.35,36 Obesity has also been associated with an increased risk of certain cancers (including those of the colon, rectum, prostate, gallbladder, biliary tract, breast, cervix, endometrium, and ovary), and with other disorders such as cholelithiasis, obstructive sleep apnea, venous thromboembolism, and osteoarthritis.8,20,37 Finally, obesity can affect the quality of life by limiting mobility, physical endurance, and other functional measures,8 as well as through social, academic, and job discrimination.38-40

a Overweight refers to an excess of body weight relative to height that includes all tissues and therefore may reflect varying degrees of adiposity. Despite the distinction between obesity and overweight, the majority of overweight persons are also obese, and these terms tend to be used interchangeably in the medical literature.

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Extremely overweight individuals can be identified easily in the clinical setting by their physical appearance. More precise methods may be necessary, however, to evaluate persons who are mildly or moderately overweight. The complications of obesity occur among those with elevated body fat composition, which is most accurately measured by underwater (hydrostatic) weighing, isotopic dilution measures, and other sophisticated techniques that are not suited to clinical practice.41 Bioelectric impedance, which provides an estimate of total body water from which the percentage of body fat can be calculated, is not widely available in clinical practice. This method has been reviewed elsewhere.42

The most common clinical method for detecting obesity is the evaluation of body weight and height based on a table of suggested or "desirable" weights. e.g.,43-45 These tables generally reflect the weight at which mortality is minimized, and they only approximate the extent of fatness. The criteria for healthy body weight are a matter of controversy among experts and vary considerably as presented in different weight-for-height tables.46,47 Weights for children and adolescents are typically evaluated in relation to average weight for age, height, and gender. This information can be obtained from growth charts that are based on percentile distributions of body size attained at specific ages.2 An alternative measure to using weight-for-height tables or growth charts is the BMI, a weight-height index that is calculated by dividing the body weight in kilograms by the square of the height in meters (kg/m2). The BMI is easily performed, is highly reliable,48 and has a correlation of 0.7-0.8 with body fat content in adults.49-52 BMI also correlates with body fat content in children and adolescents.50,51,53 In adults, overweight has been defined by the National Center for Health Statistics as a BMI ≥ 27.8 for men and ≥ 27.3 for women (the 85th percentile values for persons aged 20-29 in NHANES II)2 a BMI at this level has been associated with increased risk of morbidity and mortality.8 In adolescents, a BMI exceeding the 85th percentile for age and gender has been suggested as one definition for overweight2 or for those at risk of overweight.54

Other anthropometric methods that may be useful in the clinical setting include the measurement of skinfold thickness and the indirect assessment of body fat distribution. Skinfold thickness is a more direct measure of adiposity than BMI and correlates well with body fat content in both adults and children, but this technique requires training and has lower intra- and interobserver reliability than height and weight measurements used to calculate BMI.55,56 The WHR, the circumference of the waist divided by the circumference of the hips, which may be a better predictor of the sequelae associated with adult obesity than BMI, can also be measured in the clinical setting. The reliability of the WHR is comparable to that of BMI.57 A WHR greater than 1.0 in men and 0.8 in women has been shown to predict complications from obesity, independent of BMI,36 although the WHR has not been evaluated in all ethnic groups. 

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The purpose of screening for obesity is to assist the obese individual to lose or at least maintain weight and thereby prevent the complications of obesity. Such screening may also assist with counseling other patients regarding maintaining a healthy weight. Most studies of interventions for obesity involve subjects who are overweight we found no studies evaluating interventions for persons identified solely on the basis of an elevated WHR. Although there is little evidence from prospective studies that weight loss by obese individuals improves their longevity, there is evidence that obesity is associated with increased mortality8-13 and that weight loss in obese persons reduces important risk factors for disease and mortality.8,58 Prospective cohort studies59,60 and randomized clinical trials61-64,66 have demonstrated that caloric restriction or weight loss reduces systolic and diastolic blood pressures as well as the requirements for antihypertensive medication in obese adults with hypertension. These effects were independent of sodium restriction. In controlled67 and uncontrolled trials68,69 of low-calorie diets in obese diabetic patients, weight reduction was associated with improved glycemic control and reduced need for oral hypoglycemic agents and insulin. Weight loss generally improves the blood lipid profile70-72 and can reduce symptoms related to obstructive sleep apnea.73,74 To benefit from the detection of obesity, however, patients must be motivated to lose weight, must have access to an efficacious method of reducing body weight, and must maintain the resulting weight loss.

Various weight-reducing regimens are available, but many have only short-term efficacy and fail to achieve long-term weight loss.6,9,75,76 Research to explain the difficulty in achieving long-term weight loss is ongoing. One theory is that obesity is related to an internal "set-point" that maintains excess body fat in certain individuals.77 Some evidence suggests that energy expenditure decreases to compensate for reduced body weight,78 which would tend to return body weight to the usual weight. Such a decrease in energy expenditure could contribute to the failure of most weight-reducing regimens to achieve long-term benefits.

Dietary modification is the most commonly used weight-loss strategy, and can achieve weight reduction over the short-term in both adults and children.6,76,79 Very-low-calorie diets (<800 kcal/day), which have been used for moderately to severely obese adults who have failed more conservative approaches,80 produce greater short-term weight loss than standard low-calorie diets of 1,000-1,500 kcal/day.76,79,80 Long-term results, however, are similar with both types of programs: the majority of participants eventually return to their pre-treatment weight within 5 years,76,79 although sustained weight loss may be achieved by some patients.81-85 Cohort studies and randomized controlled trials of behavioral modification, often combined with dietary therapy, have shown modest long-term benefits in adults86-88 and children.89,90 The results of the intensive dietary and behavioral interventions evaluated in these studies may not necessarily be applicable to the type of counseling likely to be given in a busy clinical primary care practice, and referral to other qualified providers or to qualified weight-management programs1 may be necessary to achieve similar results. The amount of weight loss that can be achieved with exercise, either alone or in combination with other methods, is relatively limited in adults76,91-93 and children,94-96 but physical activity may be beneficial in maintaining weight loss76,92,97,98 and reducing the WHR92,99 in adults. Numerous randomized clinical trials have shown that various appetite-suppressant drugs can be effective in producing short-term weight loss in adults.100-109 The effects, however, are limited to periods when the drug is taken, and some studies have shown a plateauing or gradual regain of weight with prolonged use.76,100,101,104,105,107,110,111 Surgical techniques such as vertical band gastroplasty and gastric bypass may benefit selected adults who are morbidly obese,112-114 but other procedures such as intragastric balloon insertion have not been shown to be effective.115-118

Certain weight reduction methods may cause important adverse effects. Very-low-calorie diets can cause fatigue, hair loss, dizziness, and symptomatic cholelithiasis.76,119 Pharmacologic agents may cause palpitations, dizziness, insomnia, headache, and gastrointestinal discomfort.120 Surgical therapies such as gastroplasty and balloon insertion can lead to gastric ulceration, perforation, and bowel obstruction.121 Some cohort studies have reported that weight change or fluctuation in weight (weight cycling) among adults is associated with increased cardiovascular morbidity and mortality, but a review by the National Task Force on the Prevention and Treatment of Obesity concluded there is insufficient evidence that weight cycling is associated with adverse effects.122 There is conflicting evidence regarding the potential adverse effects of caloric restriction and weight loss on growth velocity and development in obese children and adolescents.123-127 

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The American Academy of Family Physicians, 128 the American Heart Association,129 the Institute of Medicine,130 the American Academy of Pediatrics,131 the Bright Futures guidelines,132 and the American Medical Association guidelines for adolescent preventive services (GAPS)133 all recommend measurement of height and weight as part of a periodic health examination for patients. Bright Futures and GAPS also recommend the determination of BMI for all adolescents.132,133 The Canadian Task Force on the Periodic Health Examination concluded that there is insufficient evidence to recommend the inclusion or exclusion of height, weight, BMI, or skinfold measurement to screen for obesity in a routine health examination of either children or adults.134 The Canadian Task Force does, however, recommend measuring and plotting the height and weight of infants and children in order to identify those who are failing to thrive. 

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Evidence is limited that screening for obesity and implementing weight-reducing or weight maintenance strategies are effective in decreasing long-term morbidity and mortality. This is unlikely to improve in the near future due to the difficulty and cost of conducting controlled trials of weight loss with these outcome measures and of separating the effect of obesity from that of other risk factors. An additional obstacle is the low rate of long-term success in maintaining weight loss. Obesity is a chronic disorder that requires continuing treatment, which could explain the failure of short-term interventions in achieving long-term success. Although losing weight has not been proven to reduce morbidity and mortality, it is clear that weight loss reduces an individual's risk for major chronic diseases such as hypertension and coronary artery disease, and it also improves the management of both hypertension and diabetes. Periodic height and weight measurements are inexpensive, rapid, reliable, and require minimal training to perform. They may also be useful for the detection of medical conditions causing unintended weight loss or weight gain, such as cancer or thyroid disorders, and the detection of growth abnormalities in childhood. Once height and weight have been determined, the BMI or standard height and weight tables may be used as a means of evaluating adolescents and adults for obesity. In addition, determination of the WHR may be useful for assessing some adults, particularly those whose weight or BMI is borderline for classification as overweight and who have personal or family medical histories placing them at increased health risk. There are inadequate data to determine the optimal frequency of obesity screening, and this is best left to clinical discretion. 

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Periodic height and weight measurements are recommended for all patients ("B" recommendation). In adults, BMI (body weight in kilograms divided by the square of height in meters) or a table of suggested weights e.g.,43-45 may be used, along with the assessment of other factors such as medical conditions or WHR, as a basis for further evaluation, intervention, or referral to specialists. In adolescents, a BMI exceeding the 85th percentile for age and gender may be used as a basis for further assessment, treatment, or referral.54 The height (or length if appropriate) and weight of infants and children may be plotted on a growth chart e.g.,2 or compared to tables of average weight for height, age, and gender to determine the need for further evaluation, treatment, or referral. The optimal frequency for measuring height and weight in the clinical setting has not been evaluated and is a matter of clinical discretion. There is insufficient evidence to recommend for or against determination of the WHR as a routine screening test for obesity ("C" recommendation).

All patients should receive appropriate counseling to promote physical activity (see Chapter 55) and a healthy diet (see Chapter 56). 

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The draft update of this chapter was prepared for the U.S. Preventive Services Task Force by Barbara Albert, MD, MS, and Carolyn DiGuiseppi, MD, MPH, based in part on background papers written for the Canadian Task Force on the Periodic Health Examination by James Douketis, MD, William Feldman, MD, FRCPC, and Brenda Beagen, MA. 

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1. Institute of Medicine. Washington, DC; 1995. Weighing the options: criteria for evaluating weight-management programs.
2. Najjar MF, Rowland M. Washington, DC; 1987. Anthropometric reference data and prevalence of overweight, United States, 1976-80. Vital and health statistics; series 11, no 238. [PubMed]
3. Kuczmarski RJ, Flegal KM, Campbell SM, et al. Increasing prevalence of overweight among US adults. JAMA. 1994;272:205–211. [PubMed]
4. Kumanyika SK. Special issues regarding obesity in minority populations. Ann Intern Med. 1993;119:650–654. [PubMed]
5. Centers for Disease Control and Prevention. Prevalence of overweight among adolescents—United States, 1988-91. MMWR. 1994;43:818–821. [PubMed]
6. Dietz WH. Childhood obesity: susceptibility, cause, and management. J Pediatr. 1983;103:676–686. [PubMed]
7. Gortmaker SL, Dietz WH, Sobol AM, et al. Increasing pediatric obesity in the United States. Am J Dis Child. 1987;141:535–540. [PubMed]
8. Foster WR, Burton BT, eds National Institutes of Health consensus conference: health implications of obesity. Ann Intern Med. 1985;103:977–1077. [PubMed]
9. Van Itallie TB, Kral JG. The dilemma of morbid obesity. JAMA. 1981;246:999–1003. [PubMed]
10. Hubert HB, Feinleib M, McNamara PM, et al. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation. 1983;67:968–977. [PubMed]
11. Rhoads GG, Kagan A. The relation of coronary disease, stroke, and mortality to weight in youth and middle age. Lancet. 1983;1:492–495. [PubMed]
12. Wilcosky T, Hyde J, Anderson JJ, et al. Obesity and mortality in the Lipid Research Clinics Program Follow-up Study. J Clin Epidemiol. 1990;43:743–752. [PubMed]
13. Harris T, Cook EF, Garrison R, et al. Body mass index and mortality among nonsmoking older persons: the Framingham Heart Study. JAMA. 1988;259:1520–1524. [PubMed]
14. Manson JE, Stampfer MJ, Hennekens CH, et al. Body weight and longevity: a reassessment. JAMA. 1987;257:353–358. [PubMed]
15. Lee IM, Manson JE, Hennekens CH, et al. Body weight and mortality: a 27-year follow-up of middle-aged men. JAMA. 1993;270:2823–2828. [PubMed]
16. Javier Nieto F, Szklo M, Comstock GW. Childhood weight and growth rate as predictors of adult mortality. Am J Epidemiol. 1992;136:201–213.[PubMed]
17. Must A, Jacques PF, Dallal GE, et al. Long-term morbidity and mortality of overweight adolescents: a follow-up of the Harvard Growth Study of 1922 to 1935. N Engl J Med. 1992;327:1350–1355. [PubMed]
18. Epstein LH, Wing RR, Valoski A, et al. Childhood obesity. Pediatr Clin North Am. 1985;32:363–379. [PubMed]
19. Guo SS, Roche AF, Chumlea WC, et al. The predictive value of childhood body mass index values for overweight at age 35 years. Am J Clin Nutr. 1994;59:810–819. [PubMed]
20. Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med. 1993;119:655–660. [PubMed]
21. Van Itallie TB. Health implications of overweight and obesity in the United States. Ann Intern Med. 1985;103:983–988. [PubMed]
22. Manson JE, Colditz GA, Stampfer MJ, et al. A prospective study of obesity and risk of coronary heart disease in women. N Engl J Med. 1990;322:882–889. [PubMed]
23. Willett WC, Manson JE, Stampfer MJ, et al. Weight, weight change, and coronary heart disease in women: risk within the "normal" weight range. JAMA. 1995;273:461–465. [PubMed]
24. Smoak CG, Burke GL, Webber LS, et al. Relation of obesity to clustering of cardiovascular disease risk factors in children and young adults. Am J Epidemiol. 1987;125:364–372. [PubMed]
25. Aristimuno GG, Foster TA, Voors AW, et al. Influence of persistent obesity in children on cardiovascular risk factors: the Bogalusa Heart Study. Circulation. 1984;69:895–904. [PubMed]
26. Burns TL, Moll PP, Lauer RM. The relation between ponderosity and coronary risk factors in children and their relatives: the Muscatine Ponderosity Family Study. Am J Epidemiol. 1989;129:973–987. [PubMed]
27. Ohlson LO, Larsson B, Svardsudd K, et al. The influence of body fat distribution on the incidence of diabetes mellitus: 13.5 years of follow-up of the participants in the study of men born in 1913. Diabetes. 1985;34:1055–1058. [PubMed]
28. Kaye SA, Folsum Folsom AR, Sprafka JM, et al. Increased incidence of diabetes mellitus in relation to abdominal adiposity in older women. J Clin Epidemiol. 1991;44:329–334. [PubMed]
29. Freedman DS, Jacobsen SJ, Barboriak JJ, et al. Body fat distribution and male/female differences in lipids and lipoproteins. Circulation. 1990;81:1498–1506. [PubMed]
30. Larsson B, Svärdsudd K, Welin L, et al. Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow-up of participants in the study of men born in 1913. BMJ. 1984;288:1401–1404. [PMC free article] [PubMed]
31. Lapidus L, Bengtsson C, Larsson B, et al. Distribution of adipose tissue and risk of cardiovascular disease and death: a 12 year follow-up of participants in the population study of women in Gothenberg, Sweden. BMJ. 1984;289:1257–1261. [PMC free article] [PubMed]
32. Ducimetiere P, Richard J, Cambien F. The pattern of subcutaneous fat distribution on middle-aged men and the risk of coronary heart disease: the Paris prospective study. Int J Obesity. 1986;10:229–240. [PubMed]
33. Kannel WB, Cupples LA, Ramaswami R, et al. Regional obesity and risk of cardiovascular disease: the Framingham study. J Clin Epidemiol. 1991;44:183–190. [PubMed]
34. Folsom AR, Prineas RJ, Kaye SA, et al. Incidence of hypertension and stroke in relation to body fat distribution and other risk factors in older women. Stroke. 1990;21:701–706. [PubMed]
35. Folsum AR, Kaye SA, Sellers TA, et al. Body fat distribution and 5-year risk of death in older women. JAMA. 1993;269:483–487. [PubMed]
36. Bjorntorp P. Regional patterns of fat distribution. Ann Intern Med. 1985;103:994–995. [PubMed]
37. Bray GA Obesity: basic considerations and clinical approaches. Dis Month. 1989;35:449–537. [PubMed]
38. Wadden TA, Stunkard AJ. Social and psychological consequences of obesity. Ann Intern Med. 1985;103:1062–1067. [PubMed]
39. Klesges RC, Klem ML, Hanson CL, et al. The effects of applicant's health status and qualifications on simulated hiring decisions. Int J Obesity. 1990;14:527–535. [PubMed]
40. Gortmaker SL, Must A, Perrin JM, et al. Social and economic consequences of overweight in adolescence and young adulthood. N Engl J Med. 1993;329:1008–1012. [PubMed]
41. Lukaski HC. Methods for the assessment of human body composition: traditional and new. Am J Clin Nutr. 1987;46:537–556. [PubMed]
42. National Institute of Diabetes and Digestive and Kidney Disease and the NIH Office of Medical Applications of Research. Bioelectrical impedance analysis in body composition measurement. Technology assessment conference statement, 1994 Dec 12-14. Bethesda: National Institutes of Health, 1994.
43. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Washington, DC; 1996. Dietary guidelines for Americans. 4th ed. [PMC free article] [PubMed]
44. Metropolitan Life Insurance Company. New weight standards for men and women. Stat Bull Metropol Life Insur Co. 1959;40:1–4.
45. Metropolitan Life Insurance Company. Metropolitan height and weight tables. Stat Bull Metropol Life Insur Co. 1983;64:2–9.
46. Schulz LO. Obese, overweight, desirable, ideal: where to draw the line in 1986? J Am Diet Assoc. 1986;86:1702–1704. [PubMed]
47. Willett WC, Stampfer M, Manson J, et al. New guidelines for Americans: justified or injudicious? Am J Clin Nutr. 1991;53:1102–1103. [PubMed]
48. Stewart AW, Jackson RT, Ford MA, et al. Underestimation of relative weight by the self-reported height and weight. Am J Epidemiol. 1987;125:122–126. [PubMed]
49. Keys A, Fidanza F, Karvonen MJ, et al. Indices of relative weight and obesity. J Chronic Dis. 1972;25:329–343. [PubMed]
50. Deurenberg P, Westrate Weststrate JA, Seidell JC. Body mass index as a measure of body fatness: age- and sex-specific prediction formulas. Br J Nutr. 1991;65:105–114. [PubMed]
51. Roche AF, Sievogel RM, Chumlea WM, et al. Grading body fatness from limited anthropometric data. Am J Clin Nutr. 1981;34:2831–2838. [PubMed]
52. Gray DS, Fujioka K. Use of relative weight and body mass index for the determination of adiposity. J Clin Epidemiol. 1991;44:545–550. [PubMed]
53. Schey HM, Michielutte R, Corbett WT, et al. Weight-for-height indices as measures of adiposity in children. J Chronic Dis. 1984;37:397–400. [PubMed]
54. Himes JH, Dietz WH. Guidelines for overweight in adolescent preventive services: recommendations from an expert committee. Am J Clin Nutr. 1994;59:307–316. [PubMed]
55. Bray GA, Greenway FL, Molitch ME, et al. Use of anthropometric measures to assess weight loss. Am J Clin Nutr. 1978;31:769–773. [PubMed]
56. Kispert CP, Merrifield HH. Interrater reliability of skinfold fat measurements. Phys Ther. 1987;67:917–920. [PubMed]
57. Kushi LH, Kaye SA, Folsum AR, et al. Accuracy and reliability of self-measurement of body girth. Am J Epidemiol. 1988;128:740–748. [PubMed]
58. Pi-Sunyer FX. Short-term medical benefits and adverse effects of weight loss. Ann Intern Med. 1993;119:722–726. [PubMed]
59. Tuck ML, Sowers J, Dornfeld L, et al. The effect of weight reduction on blood pressure, plasma renin activity, and plasma aldosterone levels in obese patients. N Engl J Med. 1981;304:930–933. [PubMed]
60. Kannel WB, Brand N, Skinner JJ, et al. The relation of adiposity to blood pressure and the development of hypertension. Ann Intern Med. 1967;67:48–59. [PubMed]
61. Fagerberg B, Berglund A, Andersson OK, et al. Weight reduction versus antihypertensive drug therapy in obese men with high blood pressure: effects upon plasma insulin levels and association with changes in blood pressure and serum lipids. J Hypertens. 1992;10:1053–1061. [PubMed]
62. Weinsier RL, James LD, Darnell BE, et al. Obesity-related hypertension: evaluation of the separate effects of energy restriction and weight reduction on hemodynamic and neuroendocrine status. Am J Med. 1991;90:460–468. [PubMed]
63. Hypertension Prevention Trial Research Group. The Hypertension Prevention Trial: three-year effects of dietary changes on blood pressure. Arch Intern Med. 1990;150:153–162. [PubMed]
64. Davis BR, Blaufox MD, Oberman A, et al. Reduction in long-term antihypertensive medication requirements: effects of weight reduction by dietary intervention in overweight persons with mild hypertension. Arch Intern Med. 1993;153:1773–1782. [PubMed]
65. Deleted in proof.
66. Stevens VJ, Corrigan SA, Obarzanek E, et al. Weight loss intervention in phase 1 of the Trials of Hypertension Prevention. The TOHP Collaborative Research Group. Arch Intern Med. 1993;153:849–858. [PubMed]
67. Wing RR, Marcus MD, Salata R, et al. Effects of a very-low-calorie diet on long-term glycemic control in obese type 2 diabetic subjects. Arch Intern Med. 1991;151:1334–1340. [PubMed]
68. Kirschner MA, Schneider G, Ertel NH, et al. An eight-year experience with a very-low-calorie formula diet for control of major obesity. Int J Obesity. 1988;12:69–80. [PubMed]
69. Fitz JD, Sperling EM, Fein HG. A hypocaloric high-protein diet as primary therapy for adults with obesity-related diabetes: effective long-term use in a community hospital. Diabetes Care. 1983;6:328–333. [PubMed]
70. Jalkanen L. The effect of a weight reduction program on cardiovascular risk factors among overweight hypertensives in primary health care. Scand J Soc Med. 1991;19:66–71. [PubMed]
71. Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr. 1992;56:320–328. [PubMed]
72. Wolf RN, Grundy SM. Influence of weight reduction on plasma lipoproteins in obese patients. Arteriosclerosis. 1983;3:160–169. [PubMed]
73. Smith PL, Gold AR, Meyers DA, et al. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med. 1985;103:850–855. [PubMed]
74. Wittels EH, Thompson S. Obstructive sleep apnea and obesity. Otolaryngol Clin North Am. 1990;23:751–760. [PubMed]
75. Stunkard AJ. Conservative treatments for obesity. Am J Clin Nutr. 1987;45:1142–1154. [PubMed]
76. NIH Technology Assessment Conference Panel. Methods for voluntary weight loss and control: Technology Assessment Conference Statement. Ann Intern Med. 1993;119:764–770. [PubMed]
77. Bennett WI. Beyond overeating. N Engl J Med. 1995;332:673–674. [PubMed]
78. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995;332:621–628. [PubMed]
79. Wadden TA. Treatment of obesity by moderate and severe caloric restriction: results of clinical research trials. Ann Intern Med. 1993;119:688–693. [PubMed]
80. National Task Force on the Prevention and Treatment of Obesity. Very low-calorie diets. JAMA. 1993;270:967–974. [PubMed]
81. Wadden TA, Syernberg Sternberg JA, Letizia KA, et al. Treatment of obesity by very low calorie diet, behavior therapy, and their combination: a five-year perspective. Int J Obesity. 1989;13(Suppl 2):39–46. [PubMed]
82. Karvetti RL, Hakala P. A seven year follow up of a weight reduction programme in Finnish primary health care. Eur J Clin Nutr. 1992;46:743–752. [PubMed]
83. Perri MG, McAllister DA, Gange JJ, et al. Effects of four maintenance programs on the long-term management of obesity. J Consult Clin Psychol. 1988;56:529–534. [PubMed]
84. Ginsberg-Fellner F, Knittle JL. Weight-reduction in young obese children. I. Effects on adipose tissue cellularity and metabolism. Pediatr Res. 1981;15:1381–1389. [PubMed]
85. Nuutinen O, Knip M. Long-term weight control in obese children: persistence of treatment outcome and metabolic changes. Int J Obesity. 1992;16:279–287. [PubMed]
86. Holden J, Darga LL, Olson SM, et al. Long-term follow-up of patients attending a combination very-low calorie diet and behavior therapy weight loss programme. Int J Obesity. 1992;16:605–613. [PubMed]
87. Hakala P, Karvetti RL, Ronnemaa T. Group vs. individual weight reduction programmes in the treatment of severe obesity--a five year follow-up study. Int J Obesity. 1993;17:97–102. [PubMed]
88. Wing RR. Behavioral treatment of severe obesity. Am J Clin Nutr. 1992;55(Suppl 2):545s–551s. [PubMed]
89. Epstein LH, McCurley J, Wing RR, et al. Five year follow-up of family-based behavioral treatments for childhood obesity. J Consult Clin Psychol. 1990;58:661–664. [PubMed]
90. Epstein LH, Valoski A, Wing RR, et al. Ten-year follow-up of behavioral, family-based, treatment for obese children. JAMA. 1990;264:2519–2523. [PubMed]
91. King AC, Tribble DL. The role of exercise in weight regulation in nonathletes. Sports Med. 1991;11:331–349. [PubMed]
92. Blair SN. Evidence for success of exercise in weight loss and control. Ann Intern Med. 1993;119:702–706. [PubMed]
93. Sweeney ME, Hill JO, Heller PA, et al. Severe vs moderate energy restriction with and without exercise in the treatment of obesity: efficiency of weight loss. Am J Clin Nutr. 1993;57:127–134. [PubMed]
94. Epstein LH, Wing RR, Koeske R, et al. The effects of diet plus exercise on weight change in parents and children. J Consult Clin Psychol. 1984;52:429–437. [PubMed]
95. Epstein LH, Wing RR, Penner BC, et al. Effect of diet and controlled exercise on weight loss in obese children. J Pediatr. 1985;107:358–361. [PubMed]
96. Reybrouck T, Vinckx J, Van den Berghe G, et al. Exercise therapy and hypocaloric diet in the treatment of obese children and adolescents. Acta Paediatr Scand. 1990;79:84–89. [PubMed]
97. Pavlou KN, Krey S, Steffee WP. Exercise as an adjunct to weight loss and maintenance in moderately obese subjects. Am J Clin Nutr. 1989;49:1115–1123. [PubMed]
98. Sikand G, Kondo A, Foreyt JP, et al. Two year follow-up of patients treated with a very low calorie diet and exercise training. J Am Diet Assoc. 1988;88:487–488. [PubMed]
99. Wood PD, Stefanick ML, Williams PT, et al. The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med. 1991;325:461–469. [PubMed]
100. Bray GA. Use and abuse of appetite-suppressant drugs in the treatment of obesity. Ann Intern Med. 1993;119:707–713. [PubMed]
101. Goldstein DJ, Rampey AH, Enas GG, et al. Fluoxetine: a randomized clinical trial in the treatment of obesity. Int J Obesity. 1994;18:129–135. [PubMed]
102. Toubro S, Astrup AV, Breum L, et al. Safety and efficacy of long-term treatment with ephedrine, caffeine and an ephedrine/caffeine mixture. Int J Obesity. 1993;17(Suppl 1):S69–S72. [PubMed]
103. Weintraub M, Sundaresan PR, Schuster B, et al. Long-term weight control study: I-VII. Clin Pharmacol Ther. 1992;51:581–646.
104. Gray DS, Fujioka K, Devine W, et al. Fluoxetine treatment of the obese diabetic. Int J Obesity. 1992;16:193–198. [PubMed]
105. Darga LL, Carroll-Michals L, Botsford SJ, et al. Fluoxetine's effect on weight loss in obese subjects. Am J Clin Nutr. 1991;54:321–325. [PubMed]
106. Levine LR, Enas GG, Thompson WL, et al. Use of fluoxetine, a selective serotonin-uptake inhibitor, in the treatment of obesity: a dose-response study. Int J Obesity. 1989;13:635–645. [PubMed]
107. Guy-Grand B, Crepaldi G, Lefebre P, et al. International trial of long-term dexfenfluramine in obesity. Lancet. 1989;2:1142–1145. [PubMed]
108. Enzi G, Crepaldi G, Inelman EM, et al. Efficacy and safety of dexfenfluramine in obese patients: multi-centre study. Clin Neuropharmacol. 1988;11(Suppl 1):S173–S178. [PubMed]
109. Weintraub M, Hasday JD, Mushlin AI, et al. A double-blind clinical trial in weight control: use of fenfluramine and phentermine alone and in combination. Arch Intern Med. 1984;144:1143–1148. [PubMed]
110. Mathus-Vliegen EM, Van De Voore K, Kok AM, et al. Dexfenfluramine in the treatment of severe obesity: a placebo-controlled investigation of the effects on weight loss, cardiovascular risk factors, food intake and eating behavior. J Intern Med. 1992;232:119–127. [PubMed]
111. Andersen T, Astrup A, Quaade F. Dexfenfluramine as adjuvant to a low-calorie formula diet in the treatment of obesity: a randomized clinical trial. Int J Obesity. 1992;16:35–40. [PubMed]
112. MacLean LD, Rhode BM, Sampalis J, et al. Results of the surgical treatment of obesity. Am J Surg. 1993;165:155–162. [PubMed]
113. MacGregor AM, Rand CS. Gastric surgery in morbid obesity: outcome in patients aged 55 years and older. Arch Surg. 1993;128:1153–1157. [PubMed]
114. Mason EE, et al. Impact of vertical banded gastroplasty on mortality from obesity [abstract]. Obes Surg. 1991;1.
115. Kramer FM, Stunkard AJ, Spiegel TA, et al. Limited weight losses with a gastric balloon. Arch Intern Med. 1989;149:411–413. [PubMed]
116. Meshkinpour H, Hsu D, Farivar S. Effects of gastric bubble as a weight reduction device: a controlled, cross-over study. Gastroenterology. 1988;95:589–592. [PubMed]
117. Benjamin SB, Maher KA, Cattau EL, et al. Double-blind controlled trial of the Garren-Edwards gastric bubble: an adjunctive treatment for exogenous obesity. Gastroenterology. 1988;95:581–588. [PubMed]
118. Lindor KD, Hughes RW, Ilstrup DM, et al. Intragastric balloons in comparison with standard therapy for obesity: a randomised, double-blind trial. Mayo Clin Proc. 1987;62:992–996. [PubMed]
119. Everhart JE. Contributions of obesity and weight loss to gallstone disease. Ann Intern Med. 1993;119:1029–1035. [PubMed]
120. Physicians' desk reference Montvale, NJ: Montvale, NJ; 1994. 48th ed.
121. Kral JG. Overview of surgical techniques for treating obesity. Am J Clin Nutr. 1992;55:552S–555S. [PubMed]
122. National Task Force on the Prevention and Treatment of Obesity Weight cycling. JAMA. 1994;272:1196–1202. [PubMed]
123. Mallick MJ. Health hazards of obesity and weight control in children: a review of the literature. Am J Public Health. 1983;73:78–82. [PMC free article] [PubMed]
124. Dietz WH, Hartung R. Changes in height velocity of obese preadolescents during weight reduction. Am J Dis Child. 1985;139:705–707. [PubMed]
125. Paige DM. Obesity in childhood and adolescence: special problems in diagnosis and treatment. Postgrad Med. 1986;79:233–245. [PubMed]
126. Epstein LH, McCurley J, Valoski A, et al. Growth in obese children treated for obesity. Am J Dis Child. 1990;144:1360–1364. [PubMed]
127. Epstein LH, Valoski A, McCurley J. Effect of weight loss by obese children on long-term growth. Am J Dis Child. 1993;147:1076–1080. [PubMed]
128. American Academy of Family Physicians. Kansas City, MO; 1994. Age charts for periodic health examination. (Reprint no. 510.)
129. Grundy SM, Greenland P, Herd A, et al. Cardiovascular and risk factor evaluation of healthy American adults. A statement for physicians by an ad hoc committee appointed by the Steering Committee, American Heart Association. Circulation. 1987;75:1340A–1362A. [PubMed]
130. National Academy of Sciences, Institute of Medicine. Washington, DC; 1978. Preventive services for the well population.
131. American Academy of Pediatrics, Committee on Practice and Ambulatory Medicine. Recommendations for preventive pediatric health care. Pediatrics. 1995;96:373–374. [PubMed]
132. Green M, ed. Arlington, VA; 1994. Bright Futures: national guidelines for health supervision of infants, children, and adolescents.
133. American Medical Association. Guidelines for adolescent preventive services (GAPS): recommendations and rationale. Chicago: American Medical Association. 1994.
134. Canadian Task Force on the Periodic Health Examination. Canadian guide to clinical preventive health care. Ottawa: Canada Communication Group. 1994:334–344, 574-584.

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