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Medicine & Science in Sports & Exercise:
Roundtable Introduction

Introductory comments for the consensus on physical activity and obesity


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Pennington Biomedical Research Center, Baton Rouge, LA; and Cooper Institute, Dallas, TX

Address for correspondence: Claude Bouchard, Ph.D., Pennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road, Baton Rouge, LA 70808-4124. E-mail:

Roundtable held February 4–7, 1999, Indianapolis, IN.

Adocument developed by a group of experts from many disciplines over a period of about 2 years at the initiative of the National Heart, Lung and Blood Institute with the collaboration of several other NIH components was published in 1998 (10). Its purpose was to propose guidelines for the prevention and treatment of obesity and its comorbidities. One of the lessons learned in the course of the development of these guidelines was that the body of knowledge on physical activity and relevant obesity outcomes is extremely limited. There are few randomized clinical trials that have lasted 1 year or more, with reasonable statistical power, adequate monitoring of intervention protocols, high levels of compliance, and proper measurement of the outcome variables. The net result is a general lack of a solid research database regarding the role of physical activity in the prevention and treatment of overweight and obesity as well as their comorbidities. The evidence-based approach taken in the NIH Report is one that will have a growing influence on health-related issues, and all exercise specialists concerned with these topics, including physical activity and obesity, would do well to become familiar with it.

Another important publication published in 1998 was that of the World Health Organization consultation report on the worldwide obesity epidemic (20). It proposed a classification of body weight based on the body mass index (BMI) defined as weight in kilograms divided by height in meters squared (kg/m2). The main merits of the classification are that it is simple, it is based on a large body of epidemiological and clinical data, and it provides a useful tool for international comparisons, for monitoring changes over time in a given country as well as changes associated with major lifestyle alterations, implementation of new public health policies, or other relevant interventions. The BMI classification scheme is reproduced in Table 1. We would like to emphasize that overweight is defined as a BMI ranging from 25 to 29.9 and obesity is set at a BMI of 30 and above. We have asked the participants at the Consensus Conference to use these cutoff points and the related terminology in their papers.

Table 1
Table 1
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The organizers of the Consensus Conference proposed early on to build on the foundations that proved to be so useful for the NIH Report (10). First, invited experts were asked to undertake the review of the topic assigned to them by drawing from the studies that had been retained by the NHLBI Panel and then expand their literature search to other sources when applicable. Second, participants were instructed to use the four evidence categories as defined in the NHLBI Report to assess the level and quality of evidence for each particular issue they were addressing and in developing a series of summary statements on the levels of evidence.

Table 2 reproduces the NHLBI report table on evidence categories. Evidence Category A is attained when there is a rich body of data from randomized controlled trials (RCT). The evidence is from endpoints of well-designed RCT that provide a consistent pattern of findings. Category A therefore requires substantial number of studies involving substantial number of participants (10).

Table 2
Table 2
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Evidence Category B is reached when there is a limited body of data from RCT. It is applicable if few randomized trials exist, they are small in size, trial results are somewhat inconsistent, or trials were undertaken in populations that differ from the target population. Category B may also be attained based on the results of meta-analysis of RCT (10).

Evidence Category C is granted when the data supporting the conclusion are from uncontrolled or nonrandomized trials, or from cross-sectional or prospective observational studies (10).

Finally, Evidence Category D can be given when the provision of some guidance is deemed valuable but there is no compelling scientific or clinical data to justify the use of categories A to C. Category D results from the expert judgment of participants and panel members (10).

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Body weight is a function of energy balance over an extended period of time. Positive energy balance over weeks and months results in weight gain, whereas negative energy balance has the opposite effect. The increase in the prevalence of overweight and obesity cases worldwide is occurring against a background of a progressive reduction in the energy expended for work and occupational activities as well as for the accomplishment of personal chores and daily necessities (8,12,17). The reduction in energy expenditure associated with physical activity brought about by automation and changing job and professional environmental circumstances has been nothing but dramatic in the second half of this century. In contrast, the energy expenditure of leisure time physical activity may have increased slightly but not enough to keep pace with the changes brought about by urbanization and automation.

The availability of relatively inexpensive and highly palatable foods in almost unlimited abundance is undoubtedly contributing to the epidemic as some of the affected individuals eat many times a day and consume large portions (6). The proportion of calories derived from fats is also potentially involved (1,5), particularly in those who consume a high-fat diet while living a sedentary life (16) although the exact contribution of a high-fat diet to the current obesity epidemic remains controversial (15,18).

The increase of the last decades in the prevalence of overweight and obesity is thought to result from the following circumstances: a) a large proportion of the population is consuming more calories than individuals of past generations with no change in habitual daily energy expenditure; b) for a large number of people, there is an abnormally low daily energy expenditure for a normal caloric intake; or c) for others, caloric intake per capita is actually lower than expected in comparison with previous generations but daily energy expenditure is, on the average, even lower (3). In all three scenarios, energy expenditure of physical activity is a major determinant.

There are several prospective studies that have demonstrated the presence of a significant and inverse relationship between the level of habitual physical activity and weight gain over a number of year. It is not infrequent in these studies to observe that the level of physical activity is a better predictor of weight gain than estimates of caloric or fat intake. One can hypothesize that the contribution of a diminished energy expenditure to the current overweight and obesity epidemic is determined by the decrease in the level of habitual physical activity associated with work and chores of daily living and by the growing amount of time spent in a very sedentary mode, such as watching TV, working on the computer, playing video games, etc. It is not associated with decreases in resting metabolic rate or in dietary-induced thermogenesis. Indeed, there is absolutely no indication that there is a downward secular trend for these two components of daily energy expenditure.

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Can Overweight and Obesity Be Prevented?

It would seem judicious to consider the prevention of obesity as an important agenda item (11). The rationale supporting the view that a good fraction of the obesity cases could have been prevented is based on the following considerations (2). First, the level of heritability of obesity or body fat content is only moderate. Second, most intermediate phenotypes that can be defined as determinants of body fat content are also characterized by low to moderate levels of heritability. Third, the prevalence of overweight and obesity has been steadily increasing over the last 50 years or so, and population studies in the Western countries seem to indicate that the prevalence is still rising. This increase has occurred over a period of time that is too short to be caused by changes in the frequency of obesity genes or susceptibility alleles.

A more physically active lifestyle is likely to be the cornerstone of a prevention strategy centered on the concept of the promotion of healthy weights (4). Moreover, there are reasons to believe that energy balance will be easier to achieve in the long term if the physically active lifestyle is associated with a moderate level of dietary fat (about 30% of calories). Energy balance, and particularly balance between lipid intake and lipid oxidation, is quite difficult and perhaps impossible to sustain for most people when dietary fat intake is high (16).

Two lines of evidence support the concept that overweight or obesity can be prevented. The first results from the comparison of the Arizona Pima Indians and Mexican Pima Indians living in Maycoba, a poor and remote area of Mexico (7,13). Pima Indians living in Arizona exhibit one of the highest prevalence rates of obesity and Type II diabetes in the world. In contrast, the 208 Mexican Pima Indians measured, among a total population of about 600 according to a recent census, had mean BMI of 25.9 for women (mean age of 34.1 yr) and 23.6 for men (mean age of 39.8 yr) (7), values that are markedly lower than their Arizonian kin. These data are admittedly preliminary, but they strongly suggest that environment and lifestyle have a strong impact on body mass for height.

The second observation comes from the survey of monozygotic twins discordant for BMI. Rönnemaa and collaborators surveyed monozygotic twin pairs of the Finnish Twin Cohort registry (14). A total of 1453 such pairs born between 1932 and 1957 responded to a mail questionnaire in 1990. Among them, 50 pairs were identified as being discordant for BMI. The latter was defined as a BMI difference between the two identical brothers or sisters of at least 4 kg/m2, with one twin having a BMI of at least 27. Hence, about 3% of this sample of identical twins were markedly discordant for an indicator of overweight or obesity. In a subgroup of 23 of these pairs who were extensively studied under controlled laboratory conditions, the mean body weight difference between the overweight or obese co-twin and the lean brother or sister reached 16 kg in men and 19 kg in women (14). Such data indicate that for the same genetic characteristics, it is possible to remain normal weight or become obese. There is no doubt that dietary and physical activity habits can have a major contribution to body weight regulation over and above those imposed by the genotype.

The tools available to reverse this unhealthy trend are remarkably simple in appearance as they center on the promotion of eating regular and healthy meals, avoiding high caloric density snacks, drinking water instead of energy-containing beverages, keeping dietary fat at about 30% of calories, cutting down on TV viewing time, walking more, participating more in sports and other energy-consuming leisure activities, and other similar measures (2). However, it will be a daunting task to change the course of nations that have progressively become quite comfortable with an effortless lifestyle in which individual consumption is almost unlimited. It will require massive resources and an unprecedented level of cohesiveness among all public health agencies and private organizations to begin reversing the trends that have emerged over the last decades (20). Foreyt and Goodrick (6) have argued that the increase in the prevalence of overweight and obesity appears to be unstoppable as a side effect of modernization.

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Physical Activity and the Comorbidities

Because the health consequences of excess body fat do not become immediately manifest, the current epidemic of obesity in children, adolescents, and young adults will translate later in unprecedented prevalence of Type II diabetes, hypertension, cardiovascular disease, gallbladder disease, postmenopausal breast cancers, osteoarthritis at the knees, back pain, and physical and mental disabilities. It has been estimated that Americans alone are currently spending about $100 billion annually as a result of the direct and indirect costs of obesity (19). The health consequences of a situation in which obesity is ever becoming more prevalent will be catastrophic.

It is well established that regular physical activity has favorable effects on several of the comorbidities of obesity, particularly those pertaining to cardiovascular diseases and Type II diabetes. Some data also indicate that mortality rates are lower in the overweight and moderately obese men and women who are physically fit compared with the unfit (9). Thus, regular physical activity plays an important role not only because of its contribution to the regulation of energy balance but also because it reduces the risk of being affected by the comorbidities of obesity and results in lower all-cause and cardiovascular death rates.

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The focus of the February 1999 Conference was on the development of a consensus document concerning the role of physical activity in the prevention and treatment of obesity and its comorbidities and to identify the most important research issues to be addressed. The specific goals were defined as follows: a) to summarize the relevant scientific literature, b) to develop a consensus statement, c) to prepare a series of recommendations for research, and d) to publish a document summarizing the proceedings of the conference.

The various texts published in this supplement of Medicine and Science in Sports and Exercise pertain to the realization of these goals. After this introductory chapter, the Evidence Report of the Independent Panel is presented. This consensus statement covers all the topics that were discussed during the conference and identifies a series of research questions to be pursued. This is followed by a series of papers dealing with the magnitude of the overweight and obesity epidemic (K. M. Flegal), the determinants of overweight and obesity (J. O. Hill and E. L. Melanson), the assessment of physical activity level and energy expenditure (K. R. Westerterp), and the current levels of physical activity and of inactivity in children and adults (M. Pratt, C. A. Macera, and C. Blanton). Subsequently, the papers on physical activity in the prevention and treatment of overweight and obesity are presented: contribution of a sedentary lifestyle (S. A. Jebb and M. S. Moore), prevention (L. DiPietro), treatment in adults (R. R. Wing), treatment in children (L. H. Epstein and G. S. Goldfield), pregnancy (S. Rössner), and menopause (A. Astrup). These papers are followed by others dealing with mobilization of abdominal fat (R. Ross and I. Janssen), regulation of food intake (J. E. Blundell and N. A. King), selection of macronutrients (A. Tremblay and V. Drapeau), and aging (M. J. Toth, T. Beckett, and E. T. Poehlman). Finally, a whole series of papers deal with the role of physical activity in the prevention and treatment of health outcomes in those who are overweight or obese: epidemiological background (J. C. Seidell, T. L. S. Visscher, and R. T. Hoogeveen), comorbidities (F. X. Pi-Sunyer), dislipoproteinemia (M. L. Stefanick), impaired glucose tolerance and diabetes (D. E. Kelley and B. H. Goodpaster), hypertension (R. H. Fagard), thrombogenic factors (R. Rauramaa and S. Väisänen), other morbid conditions and impairments (A. Rissanen and M. Fogelholm), mortality rates (S. N. Blair and S. Brodney), and economic costs (G. A. Colditz).

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1. Astrup, A., S. Toubro, A. Raben, and A. R. Skov. The role of low-fat diets and fat substitutes in body weight management: what have we learned from clinical studies? J. Am. Diet. Assoc. 97: S82–S87, 1997.

2. Bouchard, C. Can obesity be prevented? Nutr. Rev. 54: S125–S130, 1996.

3. Bouchard, C. L’obésité est-elle une maladie génétique? Médecine Thérapeutique 4: 283–289, 1998.

4. Bouchard, C., J. P. Després, and A. Tremblay. Exercise and obesity. Obes. Res. 1: 133–147, 1993.

5. Bray, G. A., and B. M. Popkin. Dietary fat intake does affect obesity! Am. J. Clin. Nutr. 68: 1157–1173, 1998.

6. Foreyt, J., and K. Goodrick. The ultimate triumph of obesity. Lancet 346: 134–135, 1995.

7. Fox, C. S., J. Exparza, M. Nicolson, et al. Is a low leptin concentration, a low resting metabolic rate, or both the expression of the “thrifty genotype”? Results from Mexican Pima Indians. Am. J. Clin. Nutr. 68: 1053–1057, 1998.

8. Haskell, W. L. Physical activity, sport, and health: toward the next century. Res. Q. Exerc. Sport 67: S37–S47, 1996.

9. Lee, C. D., S. N. Blair, and A. S. Jackson. Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men. Am. J. Clin. Nutr. 69: 373–380, 1999.

10. National Institutes of Health and National Heart, Lung, and Blood Institute. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the Evidence Report. Obes. Res. 6(Suppl. 2): 51S–209S, 1998.

11. National Task Force on Prevention and Treatment of Obesity. Towards prevention of obesity: research directions. Obes. Res. 2: 571–584, 1994.

12. Prentice, A. M., and S. A. Jebb. Obesity in Britain: gluttony or sloth? Br. Med. J. 311: 437–439, 1995.

13. Ravussin, E., M. E. Valencia, J. Esparza, P. H. Bennett, and L. O. Schulz. Effects of a traditional lifestyle on obesity in Pima Indians. Diabetes Care 17: 1067–1074, 1994.

14. Rönnemaa, T., M. Koskenvuo, J. Marniemi, et al. Glucose metabolism in identical twins discordant for obesity: the critical role of visceral fat. J. Clin. Endocrinol. Metab. 82: 383–387, 1997.

15. Seidell, J. C. Dietary fat and obesity: an epidemiologic perspective. Am. J. Clin. Nutr. 67: 546S–550S, 1998.

16. Stubbs, R. J., P. Ritz, W. A. Coward, and A. M. Prentice. Covert manipulation of the ratio of dietary fat to carbohydrate and energy density: effect on food intake and energy balance in free-living men eating ad libitum. Am. J. Clin. Nutr. 62: 330–337, 1995.

17. Weinsier, R. L., G. R. Hunter, A. F. Heini, M. I. Goran, and S. M. Sell. The etiology of obesity: relative contribution of metabolic factors, diet, and physical activity. Am. J. Med. 105: 145–150, 1998.

18. Willett, W. C. Is dietary fat a major determinant of body fat? Am. J. Clin. Nutr. 67: 556S–562S, 1998.

19. Wolf, A. M., and G. A. Colditz. Current estimates of the economic cost of obesity in the United States. Obes. Res. 6: 97–106, 1998.

20. World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation on obesity. Geneva: World Health Organization, 1998.

© 1999 Lippincott Williams & Wilkins, Inc.


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