Journal Logo

Roundtable Consensus Statement

Overview of the determinants of overweight and obesity: current evidence and research issues


Author Information
Medicine & Science in Sports & Exercise: November 1999 - Volume 31 - Issue 11 - p S515
  • Free


Obesity occurs when energy intake exceeds energy expenditure, and an understanding of how obesity occurs must begin with an understanding of how energy balance is regulated. Individuals reach energy balance and achieve stability of body weight when there is a balance between energy intake and energy expenditure and between the intake and oxidation of each macronutrient (27). The body weight and body composition that is maintained at the point of reaching energy balance is determined by many genetic and environmental factors that are incompletely understood.

Within any given environment, there will be a variation in body fatness among people who are in energy balance. Although genetic factors contribute to some of this variation (6,10,57,58), we cannot state the contribution of genetic factors with certainty. The available data indicate that the genetic contribution to variability in body fatness lies somewhere between 25 and 70%; studies in monozygous twins suggest this may be on the order of 50–70%, but family studies suggest it may be closer to 25–50%. Understanding the way in which genes contribute to this variation in body fatness is important and is the subject of much investigation.

It is clear that substantial changes in the environment can affect body fatness (14,45). As the environment becomes more obesity-conducive (as has the environment in the United States), the average body weight and fatness of the population will increase. Genes may protect some individuals from becoming obese and contribute to differences in the extent to which obesity occurs, but environmental factors may be overwhelming our genetic defenses against obesity.

Body weight is remarkably constant in many people over long periods of time, suggesting that the body has some capacity to adjust energy intake and/or energy expenditure to maintain its current state of energy balance (31,62). However, such studies suggest that the capacity to maintain a constant body weight and composition is limited, and can be overcome with a sufficient challenge (e.g., extended periods of over- or underfeeding). It is only when environmental pressure toward positive energy balance produces a sufficient challenge to exceed the capacity of the body to adapt that weight and fat gain occurs. When the organism is faced with a sufficient challenge, such as chronic overfeeding, the increases that occur in body fat mass seem to help restore energy and macronutrient balance (3,19). This results in a new steady-state of body weight but at a higher body weight.

We cannot, at present, determine the degree or pattern of positive energy balance required to overcome the body’s energy balance regulatory capacity and produce weight gain. Obesity is not a disease that develops quickly; rather, the typical pattern is gradual weight gain over a period of several years. This could be attributed, for example, to a chronic small positive energy balance or to episodic periods of more pronounced positive energy balance. In either case, we are dealing with very small degrees of energy imbalance that may not be detectable even with our most sophisticated techniques for assessing energy intake and energy expenditure.


Given that the American genotype has not changed substantially over the past two to three decades, we must look to the environment as the primary cause of the obesity epidemic. The most likely explanation for the high prevalence of obesity in the United States is an environment that produces constant pressure toward positive energy balance by promoting energy intake and discouraging physical activity. This is illustrated in Figure 1. A recent report from the World Health Organization concluded that “… behavioral factors tend to overwhelm an individual’s normal subconscious adjustments in food intake and metabolism that occur as part of a biological capacity to maintain energy balance” (66). The report identifies a fall in spontaneous, work-related physical activity and the availability of high fat, energy dense foods as two principal environmental factors that promote behaviors that lead to positive energy balance.

Figure 1:
The effect of environmental factors on energy balance. When energy intake (Ein) equals energy expenditure (Eout), the system is in energy balance and body fat mass stable. In the current environment, factors (in circles) on the left are driving Ein up, whereas factors on the right are driving Eout down, creating a state of positive energy balance, leading to an increase in the body fat mass.

A Low Level of Energy Expenditure as a Cause of Obesity

Daily energy expenditure consists of three components—resting metabolic rate (RMR), the thermic effect of food (TEF), and the energy expended in physical activity (EEact). The major determinant of EEact is the amount of physical activity performed, but there are also variations between subjects in the energy cost of physical activity.

The available data do not support a role for a metabolic defect in resting energy expenditure as a significant cause of obesity. There is substantial variation in RMR, some of which appears due to genetic factors (8,46), but based on results of several prospective studies, it appears that a low RMR is not a major factor involved in the etiology of human obesity (24,52,65). RMR is primarily determined by body composition (68), and there is no indication that RMR has declined over the past few decades.

TEF varies within and between individuals, and the question of whether TEF is lower in obesity is controversial (15). Differences in TEF between lean and obese subjects, where found, have been small and there is no evidence that differences in TEF play a role in the development of obesity. Further, there is no indication that TEF has declined over the past few decades.

Finally, there is little evidence to suggest that differences in the energy cost of physical activity play a major causal role in obesity (29). It is worth noting that as obesity develops, the energy cost of weight bearing physical activity increases (41,42).

Some investigators have suggested that a relatively high respiratory quotient (RQ), reflective of reduced fat oxidation, may be a cause of obesity (69). In individuals eating similar diets, those with lower rates of fat oxidation could require larger fat mass in order to achieve energy and fat balance. However, the extent to which “defects” in substrate utilization cause obesity versus contribute to normal variation in body fatness is unclear and deserves further research.

In contrast, there are substantial data to suggest that differences in amount of physical activity contribute to differences in body weight and body fatness, and play an important role in whether obesity develops. Most evidence comes from cross-sectional and population studies that consistently show a negative relationship between level of physical activity and indices of obesity, such as body mass index (BMI) (23,53,67). Additionally, cohort studies, where subjects were studied periodically over years, consistently show that high levels of physical activity are protective against obesity (47,67). Although we lack a definitive prospective study to show that a low level of physical activity is a risk for obesity development and that a high level of physical activity is protective against obesity, an overwhelming amount of indirect evidence suggests this is the case. The amount of physical activity that protects against obesity is not known, but some have suggested that a physical activity level of 1.75 (daily energy expenditure of 1.75 times the basal metabolic rate) should be our target (66). We need more information in order to provide guidance to the public on this issue.

Environmental Influences on Physical Activity

If a low level of physical activity is a major determinant of low energy expenditure, it is useful to understand more about this component of energy expenditure. Genetics may affect amount of physical activity (7), but it is generally accepted that genetic influences on this component of energy expenditure are less than on other components. Thus, we must consider how changes in the environment over the past few decades may have influenced the levels of daily physical activity.

First, how have changes in our environment affected the amount of physical activity required in daily living? Although it is intuitively obvious that improvements in technology over the past few decades have substantially reduced the energy expenditure required for daily living, this has not been definitively documented. All indications are that work-related physical activity has declined. The only data available come from Finland, where work-related physical activity reportedly declined by 225 kJ·d1 between 1982 and 1992 (21). Similarly, there is reason to believe that household related physical activity has declined rapidly over the past two to three decades. One can, for example, estimate the energy savings due to proliferation of energy-saving devices such as washing machines, dishwashers, computers, remote control devices, and microwave ovens. Daily energy expenditure has also likely declined due to an increased use of prepared foods. Although each may reduce physical activity only slightly, together these energy savings accumulate and can have a significant impact upon total energy expenditure. There is a great need for developing methods for assessing lifestyle physical activity to determine the extent of this decrease over time.

Second, what are the secular trends of participation in leisure time physical activity (LTPA)? Most data suggest that participation in LTPA has remained relatively constant over the past few decades (54,63). Analysis of the NHANES III data suggests that about 22% of United States adults do not participate in LTPA, with higher rates in Hispanic (46%) and African-American (40%) women, groups with a particularly high prevalence of obesity (13). Although the overall prevalence of individuals reporting no LTPA is low, most indications are that the rate has remained relatively constant over the past two to three decades and, thus, has not likely contributed to a decline in total energy expenditure. The available data suggest that there has not been a systematic increase in this component of physical activity. It is therefore very likely that on a secular basis, participation in LTPA has not increased enough to offset significant declines in other aspects of physical activity, leading to a situation that favors positive energy balance in a large percentage of the population. This is not limited to adults, as it is also likely that significant declines have occurred in the amount of physical activity that children receive in schools. It is not possible to quantify the extent of this decline over the past two to three decades, but the requirement for physical education has declined in most schools as has the number of school children participating in physical education classes (50). A decline in mandatory physical education from 200 min·wk1 (40 min·d1, 5 d·wk1) to 60 min·wk1 (30 min, 2 d·wk1) could result in a decline in energy expenditure of approximately 100 kcal·d1.

The amount of energy expenditure required for daily living also appears to be declining due to an increase in attractive sedentary activities such as television watching, video games, and computer interactions. Again, we do not have good measures of sedentary activity that would allow us to examine changes over time. Although it is likely that increases in sedentary activities are not reducing time spent in LTPA, increases in time spent in sedentary activities likely represents a lower energy expenditure than would occur otherwise.

A High Energy Intake as a Cause of Obesity

Energy intake can only be evaluated in relation to energy expenditure. If we accept that total energy expenditure has declined over the past two to three decades, obesity would have occurred unless there has been an equivalent decline in energy intake. The available data are problematic in that is has been obtained from self-reports, which have been shown to misrepresent the actual amount of energy consumed (33). If, however, we assume that measures taken over time accurately reflect change in energy intake, the available data suggest there has been either an increase or a very modest decline in total energy intake over the past two to three decades (17,18). This suggests the increase in obesity may have resulted from a decline in energy expenditure that was not matched by an equivalent reduction in energy intake.

Environmental Influences on Energy Intake

We must therefore consider which factors in the environment are promoting energy intake and thus making it difficult for most individuals to accurately match intake to a low level of energy expenditure. Environmental factors that have been implicated include excess dietary fat, the energy density of consumed food, sugar intake, large portion sizes, meal patterns (i.e., frequency of eating), and availability and cost of food.

Diets high in fat have been suggested to increase the risk of overeating and obesity (40,55,56,59). It is important to realize that most of these studies have measured voluntary food intake in subjects eating very low (e.g., <20%) and very high (>40%) fat diets. There is a need for information regarding the effect of dietary composition on voluntary energy intake for diets varying in %fat over the range of usual consumption (e.g., 20–40% fat).

Several studies suggest that reducing dietary fat intake may help reduce total energy intake (9,34,36). Additionally, when dietary fat is covertly reduced with noncaloric fat substitutes, most subjects do not compensate by increasing voluntary fat intake or by increasing intake of other macronutrients (30). Dietary obesity can be reversed by switching rodents from a high fat to a low fat diet (26,49). However, the extent to which this occurs depends on the extent and duration of the dietary obesity (28).

It is misleading to conclude that high fat diets are a sole cause of obesity. It would be more accurate to consider a high fat diet as a factor increasing the probability of overeating, or alternatively, to consider a low fat diet as decreasing the probability of overeating. Again, whether overeating occurs with a high fat diet may depend on genetic factors as well as on nongenetic factors such as the level of physical activity. The available data would suggest that as the food supply increases in fat, the percentage of people experiencing sustained or episodic overeating is also increasing. Reducing the fat content of the food supply should reduce the likelihood of overeating and could be a useful means of reducing the prevalence of obesity.

There are substantial data to suggest that energy intake is influenced by the energy density (energy per weight of food) of the diet (48). Because diets high in fat are also high in energy density, some have suggested that it is energy density and not the fat in the diet per se that produces overeating. If people tend to eat a constant volume of food, more total energy will be consumed when the diet is high in energy density than when it is low in energy density. Even if energy density is an important determinant of total energy intake, are variations in dietary fat still the major determinant of energy density? This question is currently being studied in a number of laboratories. An important research question is whether fat-and calorie-modified foods, which may be low in fat but high in energy density, contribute to increased energy intake.

Several authors have pointed out an apparent paradox whereby obesity in the United States has increased over the past few decades while dietary fat as a percentage of total calories has slightly declined (25). In fact, self-reported food intake from NHANES surveys suggests that dietary fat intake in absolute terms has remained relatively constant over this period, but since total energy intake has increased, the proportion of intake from fat has declined (17). It is very misleading to conclude from this that dietary fat intake is not likely to play a role in the recent increase in the prevalence of obesity. It may be because the diets are high in fat that the additional increase in energy intake has occurred.

Despite the common perception that sugar contributes to overeating and obesity, the available data suggest this is not the case (2). The portions in which food is presented to Americans, however, has increased over the past few decades and could be contributing to overeating. This can be seen in “supersizing” in fast-food restaurants, in the larger portions served in other restaurants, and in the increase in the size of products such as candy bars and soft drinks. Although there is insufficient research to definitely implicate portion size as a contributor to overeating, it is reasonable to think this might be the case. The likelihood of overeating at any given meal will likely be related to the portions of food served at that meal. This is especially likely if the food served is high in fat and high in energy density.

Some researchers have suggested that the pattern of food consumption may relate to obesity. However, a recent review concluded that based on available data, there does not appear to be a relationship between meal patterning and obesity (5). Finally, our current environment is one is which food is abundant and relatively inexpensive. Very little systematic research has been conducted relating energy intake to the cost and availability of food. The extent to which this promotes energy intake and overeating deserves further study.


We have specified the influence of the environment on increasing energy intake and on decreasing physical activity. However, to understand the development of obesity, we must consider the two together. A low daily energy expenditure would not necessarily be a cause of obesity unless there was an inability to adjust energy intake appropriately. This indeed seems to be the case. If total energy expenditure has declined over the past two to three decades, avoiding obesity would have necessitated a comparable decline in energy intake. Unfortunately, our measurement devices are not sufficiently accurate to determine whether this has been the case; in fact, the rise in obesity argues that it has not.

Physiologically, we may not have a good ability to restrict energy intake to match a low level of energy expenditure. In fact, there has previously been survival value in the opposite ability—to secure sufficient energy intake to avoid depletion of body energy stores. The fact that we are not all obese within our current environment suggests either that many people are maintaining a relatively high level of energy expenditure through regular physical activity or that these individuals have a good ability to restrict energy intake to meet a low rate of energy expenditure.

The most likely explanation for the high prevalence of obesity in the United States today is that our environment requires low levels of energy expenditure. Our species has not evolved with the ability to restrict energy intake to match a low level of energy expenditure. This creates degrees of positive energy balance (either sustained or episodic) that exceed our ability to adjust energy intake or energy expenditure and require an increase in the body fat mass. Whether and to what extent an increase in body fat mass is required may be influenced by genetic factors.

Individuals who engage in high levels of physical activity and who consume habitual diets low in fat and low in energy density may be protected against developing obesity. In fact, it may be the case that either behavior can protect against obesity. There is evidence, for example, that animals or humans who engage in regular physical activity may avoid weight gain on a high fat diet (4,39,61) and that sedentary individuals can avoid obesity by consuming a low fat diet (39,43).

There is a need for substantial research in this area. If regular physical activity and a low fat, low energy density diet are protective against obesity, how much of each is required to prevent obesity? It makes sense to work toward obesity prevention guidelines that combine diet and physical activity. The optimum diet to prevent obesity in a sedentary person is likely to be different than in an active person, and the physical activity needed to prevent obesity is likely different in a person whose habitual diet is high in fat versus low in fat.


Obesity presents a particular problem for some minority groups. Obesity is higher, for example, in Hispanic and African-American women than in Caucasian women (20). This increased prevalence has been associated with metabolic and behavioral factors. RMR is lower in African-Americans than Caucasians (1,11,22,32), and a low RMR has been suggested to be a cause of the high prevalence of obesity in African-American women. However, RMR is also lower in African-American men than in Caucasian men, but the prevalence of obesity is not different (20). The high prevalence of obesity in minorities may be due to greater environmental pressures that promote greater excess energy intake and reductions in physical activity (38,44). Black women, for example, are less active and eat a diet higher in fat than Caucasian women (13,44). It could be that the combination of low RMR and low physical activity interact to affect the high prevalence of obesity in African-American women. We do not have enough data on behavioral and metabolic factors that may contribute to the higher prevalence of obesity in Hispanic women and men.

The reduced-obese have been studied as a population at high risk for obesity development. It has been suggested that reduced-obese individuals may suffer from a low relative RMR and an impaired capacity to oxidize fat (35,37). However, this is highly controversial, with many reports that RMR and fat oxidation are not impaired in the reduced-obese (16,65). This is a valuable population that needs further study.

Aging is also associated with an increase in obesity. Several investigators have shown that a reduction in physical activity may be a key component in initiating the positive energy balance that leads to obesity with advancing age (12,51). Individuals who maintain high levels of physical activity as they age are able to avoid storing excess body fat (60,64).


The cause of the worldwide obesity epidemic is an environment that encourages excessive energy intake and discourages physical activity. These pressures are sufficient to create a state of positive energy balance that requires an increase in the body fat mass in order to reestablish energy balance. The data available suggest that declining levels of physical activity may be a key factor in the development of obesity. In our current environment, energy expenditure is low in most people, due to a low level of physical activity. Obesity can only be avoided if energy intake is restricted to meet low energy requirements. It is difficult for most people to do this consistently, and more and more people are becoming obese. Becoming obese is a natural response to our current environment and without changes in the environment, obesity will likely become a characteristic of our species.

There are two major environmental strategies to preventing obesity—increasing physical activity or decreasing food intake. Either strategy will be difficult to implement. However, given that human physiology is aimed at ensuring sufficient energy intake through multiple redundant pathways, we suggest that increasing physical activity may be the strategy of choice for public health efforts to prevent obesity.


1. Albu, J., M. Shur, M. Curi, L. Murphy, S. B. Heymsfield, and F. X. Pi-Sunyer. Resting metabolic rate in obese, premenopausal black women. Am. J. Clin. Nutr. 66: 531–538, 1997.
2. Anderson, G. H. Sugars, sweetness, and food intake. Am. J. Clin. Nutr. 62: 195S–201S; 1995.
3. Astrup, A., B. Buemann, P. Western, S. Toubro, A. Raben, and N. J. Christensen. Obesity as an adaptation to a high-fat diet: evidence from a cross- sectional study. Am. J. Clin. Nutr. 59: 350–355, 1994.
4. Bell, R. R., M. J. Spencer, and J. L. Sherriff. Voluntary exercise and monounsaturated canola oil reduce fat gain in mice fed diets high in fat. J. Nutr. 127: 2006–2010, 1997.
5. Bellisle, F., R. McDevitt, and A. M. Prentice. Meal frequency and energy balance. Br. J. Nutr. 77(Suppl. 1): S57–S70, 1997.
6. Bouchard, C., R. Savard, J. P. Despres, A. Tremblay, and C. Leblanc. Body composition in adopted and biological siblings. Hum. Biol. 57: 61–75, 1985.
7. Bouchard, C., and A. Tremblay. Genetic effects in human energy expenditure components. Int. J. Obes. 14: 49–55, 1990.
8. Bouchard, C., A. Tremblay, A. Nadeau, et al. Genetic effect in resting and exercise metabolic rates. Metabolism 38: 364–370, 1989.
9. Boyd, N. F., M. Cousins, M. Beaton, V. Kriukov, G. Lockwood, and D. Tritchler. Quantitative changes in dietary fat intake and serum cholesterol in women: results from a randomized, controlled trial. Am. J. Clin. Nutr. 52: 470–476, 1990.
10. Cardon, L. R., D. Carmelli, R. R. Fabsitz, and T. Reed. Genetic and environmental correlations between obesity and body fat distribution in adult male twins. Hum. Biol. 66: 465–479, 1994.
11. Carpenter, W. H., T. Fonong, M. J. Toth, et al. Total daily energy expenditure in free-living older African-Americans and Caucasians. Am. J. Physiol. 274: E96–E101, 1998.
12. Coakley, E. H., I. Kawachi, J. E. Manson, F. E. Speizer, W. C. Willet, and G. A. Colditz. Lower levels of physical functioning are associated with higher body weight among middle-aged and older women. Int. J. Obes. 22: 958–65, 1998.
13. Crespo, C. J., S. J. Keteyian, G. W. Heath, and C. T. Sempos. Leisure-time physical activity among US adults: results from the Third National Health and Nutrition Examination Survey. Arch. Intern. Med. 156: 93–98, 1996.
14. Curb, J. D., and E. B. Marcus. Body fat and obesity in Japanese Americans. Am. J. Clin. Nutr. 53: 1552S–1555S, 1991.
15. de Jonge, L., and G. A. Bray. The thermic effect of food and obesity: a critical review. Obes. Res. 5: 622–631, 1997.
16. de Peuter, R., R. T. Withers, M. Brinkman, F. M. Tomas, and D. G. Clark. No differences in rates of energy expenditure between post-obese women and their matched, lean controls. Int. J. Obes. 16: 801–8, 1992.
17. Ernst, N. D., E. Obarzanek, M. B. Clark, R. R. Briefel, C. D. Brown, and K. Donato. Cardiovascular health risks related to overweight. J. Am. Diet. Assoc. 97: S47–S51, 1997.
18. Federation of American Societies for Experimental Biology, L. S., Research Office. Food Consumption and Nutrient Intake. Third Report in Nutrition Monitoring in the United States. In: Third Report in Nutrition Monitoring in the United States. Washington, DC: U.S. Government Printing Office, 1995, pp. 148–149.
19. Flatt, J. P. The difference in the storage capacities for carbohydrate and for fat, and its implications in the regulation of body weight. Ann. N. Y. Acad. Sci. 499: 104–123, 1987.
20. Flegal, K. M., M. D. Carroll, R. J. Kuczmarski, and C. L. Johnson. Overweight and obesity in the United States: prevalence and trends, 1960–1994. Int. J. Obes. 22: 39–47, 1998.
21. Fogelholm, M., S. Mannisto, E. Vartiainen, and P. Pietinen. Determinants of energy balance and overweight in Finland 1982 and 1992. Int. J. Obes. 20: 1097–1104, 1996.
22. Forman, J. N., W. C. Miller, L. M. Szymanski, and B. Fernhall. Differences in resting metabolic rates of inactive obese African- American and Caucasian women. Int. J. Obes. 22: 215–221, 1998.
23. French, S. A., R. W. Jeffery, J. L. Forster, P. G. McGovern, S. H. Kelder, and J. E. Baxter. Predictors of weight change over two years among a population of working adults: the Healthy Worker Project. Int. J. Obes. 18: 145–54, 1994.
24. Goran, M. I., W. H. Carpenter, A. McGloin, R. Johnson, J. M. Hardin, and R. L. Weinsier. Energy expenditure in children of lean and obese parents. Am. J. Physiol. 268: E917–E24, 1995.
25. Heini, A. F., and R. L. Weinsier. Divergent trends in obesity and fat intake patterns: the American paradox. Am. J. Med. 102: 259–264, 1997.
26. Hill, J. O., J. Dorton, M. N. Sykes, and M. Digirolamo. Reversal of dietary obesity is influenced by its duration and severity. Int. J. Obes. 13: 711–722, 1989.
27. Hill, J. O., M. J. Pagliasssotti, and J. C. Peters. Nongenetic determinants of obesity and fat topography. In: Genetic Determinants of Obesity, C. Bouchard (Ed.). Boca Raton, FL: CRC Press, Inc., 1994, pp. 35–48.
28. Hill, J. O., and J. C. Peters. Environmental contributions to the obesity epidemic. Science 280: 1371–1374, 1998.
29. Hill, J. O., and W. H. M. Saris. Energy expenditure in physical activity. In: Handbook of Obesity, G. A. Bray, C. Bouchard, and W. P. T. James (Eds.). New York: Marcel Dekker, Inc., 1998, pp. 457–474.
30. Hill, J. O., H. M. Seagle, S. L. Johnson, et al. Effects of 14 days of covert substitution of olestra for conventional fat on spontaneous food intake. Am. J. Clin. Nutr. 67: 1178–1185, 1998.
31. Horton, T. J., H. Drougas, A. Brachey, G. W. Reed, J. C. Peters, and J. O. Hill. Fat and carbohydrate overfeeding in humans: different effects on energy storage. Am. J. Clin. Nutr. 62: 19–29, 1995.
32. Jakicic, J. M., and R. R. Wing. Differences in resting energy expenditure in African-American vs Caucasian overweight females. Int. J. Obes. 22: 236–242, 1998.
33. Jebb, S. A. Aetiology of obesity. Br. Med. Bull. 53: 264–285, 1997.
34. Kasim, S. E., S. Martino, P. N. Kim, et al. Dietary and anthropometric determinants of plasma lipoproteins during a long-term low-fat diet in healthy women. Am. J. Clin. Nutr. 57: 146–153, 1993.
35. Larson, D. E., R. T. Ferraro, D. S. Robertson, and E. Ravussin. Energy metabolism in weight-stable postobese individuals. Am. J. Clin. Nutr. 62: 735–739, 1995.
36. Lee-Han, H., M. Cousins, M. Beaton, et al. Compliance in a randomized clinical trial of dietary fat reduction in patients with breast dysplasia. Am. J. Clin. Nutr. 48: 575–586, 1988.
37. Leibel, R. L., M. Rosenbaum, and J. Hirsch. Changes in energy expenditure resulting from altered body weight. N. Engl. J. Med. 332: 621–628, 1995.
38. Lewis, C., J. Raczynski, G. Heath, R. Levinson, and G. Cutter. Physical activity of public housing residents in Birmingham, Alabama. Am. J. Public Health 83: 1016–1020, 1993.
39. Lissner, L., B. L. Heitmann, and C. Bengtsson. Low-fat diets may prevent weight gain in sedentary women: prospective observations from the population study of women in Gothenburg, Sweden. Obes. Res. 5: 43–48, 1997.
40. Lissner, L., D. A. Levitsky, B. J. Strupp, H. J. Kalkwarf, and D. A. Roe. Dietary fat and the regulation of energy intake in human subjects. Am. J. Clin. Nutr. 46: 886–892, 1987.
41. Miller, A. T., and C. S. Blyth. Influence of body type and body fat content on the metabolic cost of work. J. Appl. Physiol. 8: 139–141, 1955.
42. Passmore, R. Daily energy expenditure in man. Am. J. Clin. Nutr. 4: 692–708, 1956.
43. Prewitt, T. E., D. Schmeisser, P. E. Bowen, et al. Changes in body weight, body composition, and energy intake in women fed high- and low-fat diets. Am. J. Clin. Nutr. 54: 304–310, 1991.
44. Ransdell, L., and C. Wells. Physical activity in urban white, African-American, and Mexican- American women. Med. Sci. Sports Exerc. 30: 1608–1615, 1998.
45. 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.
46. Rice, T., A. Tremblay, O. Deriaz, L. Perusse, D. C. Rao, and C. Bouchard. Genetic pleiotropy for resting metabolic rate with fat-free mass and fat mass: the Quebec Family Study. Obes. Res. 4: 125–131, 1996.
47. Rissanen, A. M., M. Heliovaara, P. Knekt, A. Reunanen, and A. Aromaa. Determinants of weight gain and overweight in adult Finns. Eur. J. Clin. Nutr. 45: 419–430, 1991.
48. Roberts, S. B., F. X. Pi-Sunyer, M. Dreher, et al. Physiology of fat replacement and fat reduction: effects of dietary fat and fat substitutes on energy regulation. Nutr. Rev. 56: S29–S41, 1998.
49. Rolls, B. J., E. A. Rowe, and R. C. Turner. Persistent obesity in rats following a period of consumption of a mixed, high energy diet. J. Physiol. 298: 415–427, 1980.
50. Ross, J. G., and R. R. Pate. The National Children and Youth Fitness. Study II: a summary of findings. J. Phys. Educ. Recreat. Dance 58: 51–56, 1987.
51. Ryan, A. S., B. J. Nicklas, and D. Elahi. A cross-sectional study on body composition and energy expenditure in women athletes during aging. Am. J. Physiol. 271: E916–E921, 1996.
52. Seidell, J. C., D. C. Muller, J. D. Sorkin, and R. Andres. Fasting respiratory exchange ratio and resting metabolic rate as predictors of weight gain: the Baltimore Longitudinal Study on Aging. Int. J. Obes. 16: 667–674, 1992.
53. Slattery, M. L., A. McDonald, D. E. Bild, et al. Associations of body fat and its distribution with dietary intake, physical activity, alcohol, and smoking in blacks and whites. Am. J. Clin. Nutr. 55: 943–949, 1992.
54. Stephens, T. Secular trends in adult physical activity: exercise boom or bust? Res. Q. Exerc. Sport 58: 94–105, 1987.
55. Stubbs, R. J., C. G. Harbron, P. R. Murgatroyd, and A. M. Prentice. Covert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. Am. J. Clin. Nutr. 62: 316–329, 1995.
56. 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.
57. Stunkard, A. J., T. T. Foch, and Z. Hrubec. A twin study of human obesity. JAMA 256: 51–54, 1986.
58. Stunkard, A. J., T. I. Sorensen, C. Hanis, et al. An adoption study of human obesity. N. Engl. J. Med. 314: 193–198, 1986.
59. Thomas, C. D., J. C. Peters, G. W. Reed, N. N. Abumrad, M. Sun, and J. O. Hill. Nutrient balance and energy expenditure during ad libitum feeding of high-fat and high-carbohydrate diets in humans. Am. J. Clin. Nutr. 55: 934–942, 1992.
60. Thune, I., I. Njolstad, M. L. Lochen, and O. H. Forde. Physical activity improves the metabolic risk profiles in men and women: the Tromso Study. Arch. Intern. Med. 158: 1633–1640, 1998.
61. Tokuyama, K., M. Saito, and H. Okuda. Effects of wheel running on food intake and weight gain of male and female rats. Physiol. Behav. 28: 899–903, 1982.
62. Tremblay, A., J. P. Despres, G. Theriault, G. Fournier, and C. Bouchard. Overfeeding and energy expenditure in humans. Am. J. Clin. Nutr. 56: 857–862, 1992.
63. U. S. Department of Health and Human Services. Physical activity and health: a report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Promotion, 1996, pp. 175–207.
64. Van Pelt, R. E., K. P. Davy, E. T. Stevenson, et al. Smaller differences in total and regional adiposity with age in women who regularly perform endurance exercise. Am. J. Physiol. 275: E626–E634, 1998.
65. Weinsier, R. L., K. M. Nelson, D. D. Hensrud, B. E. Darnell, G. R. Hunter, and Y. Schutz. Metabolic predictors of obesity: contribution of resting energy expenditure, thermic effect of food, and fuel utilization to four-year weight gain of post-obese and never-obese women. J. Clin. Invest. 95: 980–985, 1995.
66. WHO. Obesity: Preventing and Managing the Global Epidemic. Geneva: World Health Organization, 1998.
67. Williamson, D. F., J. Madans, R. F. Anda, J. C. Kleinman, H. S. Kahn, and T. Byers. Recreational physical activity and ten-year weight change in a US national cohort. Int. J. Obes. 17: 279–286, 1993.
68. Zurlo, F., K. Larson, C. Bogardus, and E. Ravussin. Skeletal muscle metabolism is a major determinant of resting energy expenditure. J. Clin. Invest. 86: 1423–1427, 1990.
69. Zurlo, F., S. Lillioja, A. Esposito-Del Puente, et al. Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ. Am. J. Physiol. 259: E650–E657, 1990.


© 1999 Lippincott Williams & Wilkins, Inc.